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What caused the Mesozoic-Cenozoic radiation?
The Phanerozoic eon has had 5 major extinction events and 3 major radiation events. After the Cambrian and Ordovician radiations came all five of the major extinction events, the last of which (Cretaceous-Paleogene) occurred during the last major radiation event (Mesozoic-Cenozoic). This timeline suggests the freeing of previously occupied ecological niches isn't the primary driver of major radiations. (However, the Cretaceous-Palaeogene extinction freed niches during the Mesozoic-Cenozoic radiation, and this may be part of why it continued for so long rather than being a purely Mesozoic event.) Although Wikipedia generally gives a good account of suggested reasons for major extinctions, and also for the Cambrian and Ordovician radiation events, it provides no real such detail for the Mesozoic-Cenozoic radiation. What are its conjectured causes?

I'm confused. I always thought that the impact separating the mesozoic from the Cenozoic, which killed the non-avian dinosaurs, and many other lineages freed niches for mammals and birds to fill. Is this no longer the explanation?

@KarlKjer I thought so too, but to quote Wikipedia, "The Mesozoic–Cenozoic Radiation began in the mid-Mesozoic and extends through the Cenozoic". So it seems that, however much the extinction event may have helped the radiation event continue, it started somewhat earlier.

Oh yes. For example, pterosaurs were on the decline. There were a variety of non-impact-related causes. But the impact finished the deal, and it was (as far as I know) mostly the opening of new niches made possible by mass extinction.

@KarlKjer In which case, I suppose, it was some minor extinctions that started the radiation.

There is no real start to a radiation event.
First there are many mass extinctions and many radiation events, what you are referring to are just the most notable ones. also the big five do not occur after the odrivian the first occurs directly before.  Radiation events happen after every mass extinction even minor ones, the amount of radiation corresponds well with the severity of the extinction. The big five and the big three are just the ones we find the most interesting, not the largest, note graph below). The ordovician radiation event happened directly after the cambrian–ordovician extinction event for instance. And there was a massive diversification after the P_T extinction, it just does not get as much press because almost all the major players become extinct in later extinction events and becasue there are  fewer fossils from that time period. Every extinction event is followed by a radiation event. the Mesozoic-Cenozoic radiation is a large radiation because of the KT mass extinction otherwise it would just be the normal background biodiversity turnover.
Essentially radiations are always happening, there is always some radiation going one in some clades.  But if you suddenly wipe out a large number of species and organisms, many of those what survive will be the ones that were radiating simple becasue they were small fast breeding generalists which is also the group that radiate a lot. Small fast breeding generalists are what what best survive mass extinctions and a group that does a lot of radiating. There is also a large anthropomorphic component to this, if you take the tree of life and make a radom slice across it anywhere it sill look like many of the groups that survive are radiating becasue all the other radiation events are cut off, while we ignore stable groups becasue they are stable. You can even notice that the radiation of different groups start at different times but then explode after the event. Almost as if our artificial lines between groups is not a great predictor of diversification events. Radiation events are not one off occurrences with clear cut beginnings and ends but a prolonged uptick in an ongoing system with a lot of variation. there is no clear cut start to radiation events imagine trying to pick the exact second summer or winter begins using nothing but temperature data, there is just to much noise due to local and daily condition to make any such point anything but arbitrary.
So the large scale radiations is still caused by the extinction event, it however will almost always look like it was happening earlier becasue on a small scale it never really stops, and where we draw the lines for groups does not correlate well with radiation events, yet we still use it to decide which "groups" are radiating.
Sources

If you look at this paper and its graph you can see this effect in angiosperms. The group originates and begins to diversify before the KT but a massive upswing in diversity happens after (actually fairly long after, once the climate/extinction has stabilized)

The Big 5 are OS, LD, PT, TJ and KT, so they do all occur after the Ordovician began. You're right that extinction events drive radiation to some extent. But that leaves open the question of which extinctions encouraged MC, and overlooks the possibility other factors drove it too. Explanations of the Cambrian & Ordovician radiations are much broader than then-recent extinction.

And those five are not the largest just the ones we pay the most attention to.

Is it your contention that extinction events are the only causes of the Mesozoic-Cenozoic radiation? Because while extinctions may have contributed to earlier radiation events, they were often not their only cause.

no if you read my post I mention that radiation is always occuring they become major eents when extinction clears a wide swath of niches.Radiation events are not one off occurrences but a prolonged uptick in and system with a lot of variation. there is no clear cut start to radiation events.


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What is meant by Gene Expression Level?
I am new to BioInformatics, I want to know what is gene expression level and how it is determined.. Anyone who can answer this silly question.

Are you familiar with the concept of gene expression but not gene expression level or you're not familiar with the concept of gene expression? You might want to have a look at wikipedia > gene expression or at any intro course to molecular genetics.

“Gene expression level” is an imprecise and partially ambiguous term
  that should be avoided.

Many (but not all) genes have the information to produce proteins†, but there is no need for this information to be used at any given time — it depends on the requirements of the organism or cell. For example the DNA of lung cells contains the information to produce the protein chains of haemoglobin, but it is never used in those cells. We can say that “the gene is not expressed”.
So the absence of expression is fairly easy. However, for a protein-coding gene the meaning and quantitation of expression is more difficult. That is because in expressing the information in the gene the DNA is first transcribed into mRNA by RNA polymerase, and then that information that encodes a protein can be translated into protein on the ribosome.
The word level refers to quantification, and is a sloppy substitute for quantity or perhaps rate (quantity produced in unit time) or perhaps relative quantity.
But the main difficulty is whether in quantifying gene expression you measure the quantity of mRNA synthesised under standard conditions or the quantity of protein produced.
If you are a bioinformatician encountering this term, my bet is that it is in relation to the currently (2018) popular RNA-Seq technique, which in fact provides relative measurements of the quantity of RNAs of different types produced under standard conditions. This is generally expressed in units called FPKM — Fragments Per Kilobase of transcript per Million mapped reads. The difference between this technique and the northern blotting mentioned by @Hawkeye, is that the latter is used to detect a single mRNA, whereas RNA-Seq applies to all the mRNAs that are present in a sample.
In the field of proteomics, it is possible that the term is being used in relation to the amount of protein produced, which may be roughly quantified by two-dimensional gel electrophoresis.
†Some genes encode RNAs that do not encode proteins (ribosomal RNAs, transfer RNAs, RNAs involved in splicing and in modification of rRNA, microRNAs etc.). The expression of the genes for these will end with the synthesis of the RNA.

source: Stack Exchange

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Have there been any successful studies showing that it is possible to increase IQ?
I am curious if there have been any leading studies that show improvement in general IQ. For example, an adult with an IQ of 130 reaching an IQ of 140, over many different IQ tests and then averaged, after some sort of practice (perhaps playing video games, reading books, taking lots of IQ tests, or doing memory exercises).
It would be interesting to know. If you can, please reference sources with your answer, so that I may look at the studies myself.

When talking about increasing intelligence there are a few things you have to keep in mind. Can you increase your IQ score? Probably, yes. Just take the same test twice, or more realistically practice a lot of IQ-type problems. You will probably raise a few points.
But this is just a score. When experts are talking about raising intelligence, they are talking about raising the underlying ability that tests can only estimate. Raising your test score does not necessarily mean that you raised your intelligence. What you want is something that transfers over to some general ability.
Richard Haier, the editor-in-chief of the journal Intelligence, has written extensively on this topic. In his 2014 article Increased Intelligence Is A Myth (So Far) he writes about this very subject of increasing intelligence (Haier, 2014). You can probably guess what the conclusion is from the title of the paper. This topic is also a substantial portion of his book The Neuroscience of Intelligence (Haier, 2016).
Technically, when you ask whether there are any studies that purport to have found a way to increase intelligence, then the answer is definitely yes. There are many (hundreds, probably thousands). The correct question to ask is whether any of these ways consistently replicate. At the moment, the answer to this question appears to be no. One of the most infamous "ways of increasing intelligence" was the supposed Mozart Effect. The hypothesis was that listening to Mozart music would increase intelligence, and there were studies providing evidence for this. Fairly silly, yes. It was not until a meta-analysis came out of Mozart Effect studies that this hypothesis was finally laid to rest (Pietschnig et al, 2010). There is a history of many supposed ways of increasing intelligence being suggested, but typically the more scientific scrutiny they are put under they tend appear less and less impressive. Therefore, whenever a new way of increasing intelligence is suggested, it may be good to have some scepticism.
Given the current body of evidence, the most plausible way of raising intelligence is probably education (Ritchie & Tucker-Drob, 2017). However, it is unclear whether education really increases general intelligence or just specific skills (Ritchie, Bates & Deary, 2015).
The best  non-genetic way to get high intelligence is probably not to increase your intelligence per se, but just to avoid decreasing it. This means avoiding things like lead exposure, don't suffer from iodine deficiency (Qian et al, 2005), get decent nutrition and so on. Anything that realistically could interfere with the development of the brain may be implicated in intelligence.

See also my answer to a similar question on the Psychology & Neuroscience Stack Exchange, which is slightly more comprehensive.

Mostly agree with this, but it's worth noting that the question explicitly asks about increasing IQ, rather than intelligence - it's not entirely clear whether OP understands that IQ is a poor indicator of this. So paragraphs 2-3 maybe should go first (with some sources).

@arboviral I made a change as you advised, putting the paragraphs about the clarification about increasing IQ scores versus increasing intelligence first. I agree that this makes most sense. I will try to find some sources later today (Not able to at the moment). I wouldn't say that IQ is necessarily a poor indicator of general intelligence, but rather it is a non-perfect one. (We also have to be fair and compare to other psychological measures. In this comparison, intelligence tests are probably the best measured psychological trait despite its imperfections.)

Thanks - that looks fine. I think IQ is a tricky one - I'd say it's a reasonable attempt to measure something that's inherently difficult to reduce to a single number, but it has a history of misuse for purposes other than psychological research that makes a lot of people quite skeptical of its value, and it discriminates against some groups.

I won't comment on whether it has historically been misused. I'm only here to address scientific questions, not moral questions. Whether it discriminates against some groups is an empirical question, one that would take an entire new post to address. However, I can definitely say that it is not the scientific consensus among intelligence researchers that the tests are biased towards any groups (The fact that different groups score differently on average is not evidence of bias. There are systematic ways to interrogate whether there is bias).

Well, every lecturer we had who mentioned it at undergrad highlighted  those concerns and limitations, so it isn't a particularly minority view. Sounds like we'll have to agree to disagree on this one.

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What is the animal in this video?
I made some research however there seems to be a conflict with this animal's translation to my language and the original. So I couldn't find it. Do you mind helping me out ?
https://static.59saniye.com/videos/2018/04/21/20180421080742-6014_720.mp4
Some resources say pufferfish or Porcupinefish. Are these the same thing ?

You can do a search by common name (possibly in your language) in http://www.fishbase.org/search.php This site also has images for species in a family, like here for tetraodontidae: http://www.fishbase.org/identification/specieslist.php?famcode=448&areacode=

This is a Northern pufferfish. It is called Sphoeroides maculatus.

  Source: https://www.flickr.com/photos/vims_photos/3570935564

You can confirm this on FishBase.

I'm no expert in the field, so I can't identify the fish in your video; but it seems that pufferfish belong to the family Tetraodontidae, while porcupinefish are of the family Diodontidae. So, no, they are not the same thing.


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Using different polysaccharides for coagulation
Would a particular type of polysaccharide be better at coagulation than another? For example, would the presence of cellulose in a bio-coagulant be more effective at coagulation than the presence of starch or glycogen? I would like to know as I am doing an experiment about it and since nobody has done this before, I don't know whether having a higher concentration or ratio of a certain polysaccharide in a bio-coagulant compared to other polysaccharides will have an effect on coagulation efficiency?


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What is linkage?
If two genes are on the same chromosome, are they always “linked”? What if they are more than 50 cM apart? Then they would follow Mendalian pattern of inheritence. So are they still linked?

The centimorgan is not a measure of the physical distance between gene loci, but a measure of the linkage between loci.
Suppose that you have two genes located adjacent to each other, at the tip of a chromosome. The likelihood of their recombination is almost zero, since it is very unlikely that the two genes will be segregated in a crossover event during meiosis.
In contrast, if you have two genes as far apart from each other, but still on the same chromosome (i.e. they are on opposite tips), their likelihood of recombination is as close to 100%---this means a 1:1 ratio of parental type to recombinant type gamates.
So, if a 0% likelihood of recombination implies that the genes are right next to each other, and a 100% likelihood of recombination implies that they are as far away from each other, we will be able to approximate how far away a gene is from another gene by their likelihood of recombination.
Now, the likelihood of recombination is measured through the calculation of a recombination frequency. Genes that are unlinked give you a 1:1 parental to recombinant type in the offspring, which is a recombinant frequency of 50%. Genes that are 'perfectly linked', i.e. always segregated together, gives offspring of the parental type all the time, so they have a recombinant frequency of 0%.
Having said all that, we are able to associate,
$$\text{0% likelihood of recombination} \implies \text{0% recombinant frequency}\\
\text{100% likelihood of recombination} \implies \text{50% recombinant frequency}$$
And relating that to the loci of two genes on a chromosome,
$$\text{Adjacent genes} \implies \text{0% recombinant frequency}\\
\text{Perfectly Distant Genes} \implies \text{50% recombinant frequency}$$
And if we represent the length of a chromosome as 50 centimorgans, then
$$1\text{ centimorgan} \approx 1\%\text{ recombinant frequency} \approx 1\%\text{ likelihood of recombination}$$
That is to say, the theoretical maximum distance between two genes on a chromosome is the length of the chromosome itself, which is 50 centimorgans.

Note that there are many implicit assumptions in the explanations above. The first is that there are no random fluctuations in calculating the recombinant frequency. The second is that exactly one crossover event takes place during meiosis, and the loci that it acts on is uniformly random. When I say 'likelihood of recombination', I refer to the possibility of a single crossover event between two homologous chromosomes, resulting in a 1:1 parental to recombinant type gamete.


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Bird identification by sound; midwestern US
This one's been bugging me for a couple of years. Location is southwest Michigan.
Here are a couple of song samples (I couldn't separate it from the Titmouse... they're pretty chatty these days):

Unidentified Bird 1
Unidentified Bird 2

Closest I can come up with is an Eastern Towhee, but the trill doesn't seem quite right. All the samples I've been able to find have it pretty constant in pitch and tempo, but this one gets a little higher and slower as it goes on.
This is a rural area. Our property is about half grass/prairie, half wooded. The sounds seem to come from a line of tall evergreens at the front of our property (an otherwise more open area), but I have yet to actually find the bird, so I can't be sure. A creek runs behind our house in a wooded area, about 400 feet from where the sounds appear to be emanating. These clips were taken about an hour after sunrise.
Can anyone identify this bird?

Can't really help, but if you aren't already aware of it, xeno-canto provides a good database of bird calls.

Xeno-Canto (fm ning's comment) seems to be a good site with well-versed users, and has a "mysteries" page where you can submit.


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Neuron repair inhibition in the CNS
Evolution provides different myelin sheathing cells (Oligodendrocyte and Schwann cells) in mammalian CNS and PNS. Damaged neurons in the CNS have little chance of recovery whereas damaged neurons in the PNS have an excellent chance of recovery. When ruptured, olidodendrocytes release Nogo that signals the damaged neuron cell body to stop any attempt at regrowing its axonal stump. Ruptured Schwann cells in the PNS do not release Nogo. Why should nature behave like this? Is it because the wiring density of the CNS is orders of magnitude greater than that of the PNS?
Or could it be because in the PNS the nerve is encased in a perineurial sheath that can readily self-repair and provide a framework for axon regeneration? There doesn't appear to be any similar sheath in the tightly packed CNS. Therefore to prevent unstructured axon regrowth, that could cause chaos in the brain, such a possibility is actively prevented?

Your question is a bit unclear. I can't understand your point about how having oligodendrocyte in CNS is detrimental.

You are misquoting me, what I said was "to the detriment of CNS neuron damage recovery" which of course is of extreme importance to many CNS injuries not the least being spinal cord injuries.

So, you are saying that having two different types of sheathing cells may be a detrimental factor in neuron repair. I still do not get your question. Please [edit] your question so that it is more clear. Comments should not be used for providing clarifications for many technical and logistic reasons.

I think you are taking a huge leap by saying "Oligodendrocytes vs Schwann cells == the reason why CNS damage recovery is more difficult than PNS recovery"... Correlation does not imply causation.

Now that’s a very interesting refutation Bryan. How would you interpret the quotations in my answer, the science seems so imperative.

I almost got it right. The consensus as of 2018 appears to be that it's a Faustian pact between providing the CNS with our unique mental powers at the cost of poor damage repair. This is not an issue in the PNS where damaged neuron repair is, in the main, impressive.
Quote (1): Principles of Neural Science 5th Ed (2013) (Eric R Kandel et al)
“ ... the regenerative capacities in the peripheral nervous system are impressive.
In contrast, in the central nervous system regeneration after injury is poor.”
“Is it the ability of peripheral axons to regenerate that is unusual, or the inability of central axons to do so? It is in fact the latter.”
“Maintaining constancy in the face of small perturbations in connectivity may therefore have the unavoidable consequence of limiting the ability of central connections to regenerate in response to injury. In this view our limited regenerative capacity is the Faustian biological bargain we have made for the possession of many precisely wired circuits that underlie our superior intellectual powers.”
Quote (2): Transl Psychiatry (2017) 7, e1214; doi:10.1038/tp.2017.170 www.nature.com/tp
“Reticulon 4 receptor (RTN4R) [aka NgR and NgR1] plays an essential role in regulating axonal regeneration and plasticity in the central nervous system ...”
Quote (3): A.R. Walmsley, D. Bourikas And A.K. Mir, 15 - Myelin Neutralization For Spinal Cord Injury And Stroke, In CNS Regeneration (Second Edition 2008)
“ ... the environment of the CNS is highly inhibitory to axonal regeneration and plasticity. In recent years, great advances have been made in our understanding of the molecular components contributing to the inhibitory environment of the CNS. The majority of these have been identified as membrane proteins present in CNS myelin, such as myelin-associated glycoprotein, Nogo-A and oligodendrocyte-myelin glycoprotein, that inhibit neurite outgrowth by binding to the multimeric Nogo-66 receptor (NgR1) complex on the neuron ...”
Quote (4): https://en.wikipedia.org/wiki/Reticulon_4_receptor
Reticulon 4 receptor (RTN4R) also known as Nogo-66 Receptor (NgR) or Nogo receptor 1 is a protein which in humans is encoded by the RTN4R gene. This gene encodes the receptor for reticulon 4, oligodendrocyte myelin glycoprotein and myelin-associated glycoprotein. This receptor mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult central nervous system.


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Species that murder their own counterparts when put in captivity
Mary Midgley writes in her book, Beast and Man (p. 54 in this eBook: https://goo.gl/3NnhtP):

Lorenz gives chilling examples from roe deer and doves, in both of which species stronger members will slowly murder weaker ones if kept in captivity with them[...]

I find this fascinating but I was not successful in finding any more info on this phenomena on the internet.
Can any biologists point me into a good direction? I do not have the work of Konrad Lorenz at hand, and would not know where to exactly look for in them.
Thanks a lot!

Some individuals kill their own offspring (https://en.wikipedia.org/wiki/Infanticide) or eat their offspring (https://en.wikipedia.org/wiki/Filial_cannibalism) or their own siblings (https://en.wikipedia.org/wiki/Siblicide).  See this article about siblicide and fratricide in bacteria:  https://www.webmedcentral.com/article_view/4804.
Other conflict and killing between members of a population occurs in many species, including humans (https://en.wikipedia.org/wiki/Homicide), mice (https://sci-hub.tw/10.1111/j.1469-185X.1991.tb01147.x), and other primates (https://www.sciencedirect.com/science/article/pii/S0140175082920632).
Search "intraspecific killing" on Google or Google Scholar.
See also a similar question here:  Why social animals attack odd members of their own group?


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Where are eosinophils and basophils phagocytic?
It seems known that neutrophils circulate and are phagocytic within the blood stream, but I'm having trouble finding similar conconclusions about where eosinophils and basophils are phagocytic which are less common.

Eosinophils and basophils are broadly referred to as non-professional phagocytes, in that they can use phagocytosis, but don't primarily function like this. Rather, they tend to de-granulate to kill their targets. They lack the abundance of receptor complexes for efficient phagocytosis that professional phagocytes like monocytes and neutrophils express, like opsonin receptors.
There's some data to suggest that macrophages control non-professional phagocytes like epithelial and endothelial cells (ref), but it's a bit of a jump to generalize that to eosinophils and basophils.
My intuition is that these specialized types of cells uptake debris and extracellular antigen, since they do partake in non-professional class-II antigen presentation, rather than larger bodies or microorganisms like macrophages uptake.

Also to add to this - lets not forget that these cells can function differently in circulation, compared to when they enter in tissue. They look morphologically different, and often one can see phagocytic vacuoles present in the cytoplasms..meaning they probably do participate in some minor "cleaning up" , but like the above poster mentioned, primarily they release granules into the environment wherever they detect damage, or antibody reactions.


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What is the difference between silent and synonymous mutations?
Several sources all caution that silent mutations and synonymous substitutions are not the same thing and should not be confused. But they seem to draw different actual distinctions between the terms:

This Wikipedia page and this biology dictionary entry define a silent mutation as a point substitution that replaces a single codon by another codon that codes for the same amino acid, and therefore does not directly change the amino acid sequence that is coded for. It defines a synonymous substitution as a silent mutation that occurs in an exon. Under these definitions, a synonymous substitution is a special case of a silent mutation.
This Wikipedia page and this blog post define a silent mutation as any mutation that does not have any phenotypic effects, and defines a synonymous substitution as a point substitution to a degenerate codon (anywhere in the genome, as far as I can tell). It points out that such synonymous substitutions can still have indirect phenotypic ("nonsilent") effects by affecting translation and transcription. Under these definitions, a silent mutation is a special case of a synonymous substitution (namely, one that doesn't have any indirect phenotypic effects).
This Wikipedia page uses similar definitions to the one in #2, except it explicitly requires that a synonymous substitution occurs in an exon.

Clearly these definitions are not all compatible. (#2 and #3 are very similar and could perhaps be excused as minor variants on the same definition, but they clearly conflict strongly with #1 - they disagree on which of "silent mutation" and "synonymous substitution" is a special case of the other!) Is there a standardized distinction in the biology community between these terms, or is it just the case that everyone uses conflicting definitions and we should ask people to clarify the senses in which they're using these terms?

Silent mutations are those which have no phenotypic effect and it seems important to note that these could occur in coding regions and non-coding regions alike. Synonymous mutations, on the other and, are confined to coding regions. Because these mutations, by definition, do not change the amino acid sequence, they are nominally silent. However, due to codon bias, etc.,, a synonymous mutation may not always be silent. Therefore, my non-authoritative opinion is that it is not entirely accurate to classify one as a subset of the other. All you can really say is that silent mutations have no phenotypic effect, and synonymous mutations can be silent or not.

"Silent mutations are those which have no phenotypic effect".. the definition should have ideally been so. However, the existing definition pertains only to changes in amino acid sequences. In fact, you can have non-synonymous mutations that are "silent".

@WYSIWYG I seemed to remember, for some reason, that silent mutations need not necessarily refer to mutations in a coding sequence, but I struggled in vain to find more than a few papers that used it this way. Your answer certainly captures its actual usage better than mine.

Your definition does make real sense but unfortunately the real definition is a bit obsolete.

I would say that silent mutations, as they have been defined, are a subset (or perhaps even same as) of synonymous mutations. However, the term, "silent mutation", is not used so much these days. Almost every research paper that I have read pertaining to this topic has always used the term "synonymous mutation" irrespective of whether or not it has a phenotypic effect. It seems that the term, "silent mutation", is confined only to textbooks.
If you consider silent mutations are mutations that are not reflected in the phenotype then there some points that you should consider.

As canadianer mentioned, these mutations can be present in non-coding region. However, mutations in non-coding regions can also affect the phenotype. Moroever, as they mention, synonymous mutations can cause changes in translation rates because of the codon bias which in turn can lead to phenotypic differences (Kimchi-Sarfaty et al, 2007; Waldman et al, 2011; Buhr et al, 2016). These phenotypic differences can arise due to altered protein concentration or altered folding states. So a synonymous mutation is not essentially "silent"
A non-synonymous mutation may not affect the phenotype (neutral mutation).

I would say that this definition should not be used unless the majority of the scientific community agrees on redefining the term. Till then, you can possibly use the term, "neutral mutations", to mean mutations that do not affect the phenotype. Remember that neutrality of "neutral mutations" is defined with respect to fitness. However, if your measure of fitness pertains to the molecular function of the gene then this definition works.

I don't understand your last paragraph, I thought that there's a standardized definition that "neutral mutation" only means neutral with respect to evolutionary fitness, not to phenotype. What do you mean "your measure of fitness pertains to the molecular function of the gene"?

@tparker Fitness is a relative term. If you are selecting for the molecular function of a gene, lets say an enzyme, then the enzyme activity is your fitness. Check this out.

Oh, I thought that "fitness" always refers to reproductive success.

@tparker Let's say in a lab you want to engineer an enzyme with high activity and you are selecting the E.coli cells that show high activity of this enzyme. In that case the fitness (under the selection) is proportional to enzyme activity (unless there are pleiotropic effects). In fact there are (many?) research articles that have used the term in the context of molecular phenotypes.

I meant to say that I thought that "fitness" always refers to reproductive success under natural selection. But I suppose that if you also include reproductive success under artificial selection, then indeed any trait (even normally "bad" ones) could improve fitness.

But the following sites (Nature and Science) use the "silent mutation" as synonymous mutation.
https://www.nature.com/scitable/definition/silent-mutation-10
https://www.sciencemag.org/news/2006/12/sound-silent-mutation

Please provide more ocntext in case your links go dead. If possible, please include the formal citations of each article you link as well as a quote or page number where you are pulling from. Thanks.


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Can someone identify this plant
Growing in a garden in the philippines
Photo from above notice the unusual leaves

Photo showing bloom... In peak bloom...

Photo showing pod that plant produced at the same time blooms appeared

What is the word for the leaf structure - meaning secondary terminal leaf at the end of a "tendril"? The plant form somehow reminds me of a Nepenthes, but the terminal growth is a leaf not a pitcher.

@user22542 I thought this could be called "mucron" in French, but I don't know in English (from what I've found, "mucron" exists in English but has a different meaning).


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Database of predicted protein-ligand binding/docking score
Is there a database of computationally determined "binding scores" across protein-ligand pairs in the PDB?
My phrase "binding score" is deliberately generic, since any such score would be fine. In particular, some docking energy, i.e. scoring function, would be great. (Don't worry, I am aware that these docking energies are not perfect :) ).
I am looking for comprehensive coverage and the same score across bound pairs, meaning that experimental measures are obviously impossible; however, I am hoping there are people who ran some docking scoring function across all the protein-ligand pairs in the PDB, or at least some large number of them.
I am aware of the many database which hold experimentally determined binding data of protein-ligand structural complexes.
For instance, Binding Moad, Binding DB, PDB-Bind, and SC_PDB are all good for what they are meant to do.
However, they have (1) poor coverage (i.e. not all the complexes have affinity data or they don't include some complexes) and (2) use heterogeneous scores/measures (e.g. IC50, KD, etc...).
This is not the same as this question, since I am looking for comprehensive coverage and computationally determined scores, not experimentally determined ones.


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Why is there an increase of diagnoses of Lyme disease?
On the Center for Disease Control page for Lyme disease, you can see the progression of reported cases of Lyme disease from 2001 until 2016 and see that over time, there are more reported cases of Lyme Disease.

I am wondering if there is an actual increase in incidence or if, perhaps, there is an increased awareness of the disease causing doctors to be more likely to test for it (and diagnose it) than they were in 2001.
Is there any information supporting one or the other?

Most likely higher standards for public health surveillance and reporting, as well as population increase. For the site you link, there are articles/publications that analyze and interpret the data. If you haven't read them already, that would be a good place to start (they're listed on the left side of the CDC page).

One of the opinions expressed on the CDC website is that the increase of diagnosis of the Lyme disease could be accounted to expansion of ticks:

Since the late 1990s, the number of reported cases of Lyme disease in the United States has tripled and the number of counties in the northeastern and upper Midwestern United States that are considered high-risk for Lyme disease has increased by more than 300%. One explanation for this trend is that the ticks that can transmit Lyme disease have expanded their geographic range and are now being found in places they weren’t seen 20 years ago. --Rebecca Eisen, Ph.D. (source)

I have also found a report containing another possible explanation:

Areas of patchy woods, which are very common in cities and suburban and rural areas, may have higher populations of Lyme-disease carrying ticks than forest fragments, which generally have fewer species than continuous habitat. This is because some species thrive in smaller places.
White-footed mice, for example, are more abundant in forest fragments in some parts of the country, likely because fewer predators and competitors remain there. These mice are particularly abundant in patches smaller than about five acres, which could spell trouble for people living nearby: the mice are the main carriers of Lyme disease-causing bacteria. In the eastern and central United States, Lyme disease is contracted via blacklegged ticks that feed on infected mice, then transmit the bacteria when the ticks bite people. As a result, says biologist Felicia Keesing of Bard College in Annandale, New York, Lyme disease is concentrated in areas where people live near forests with blacklegged ticks.
Keesing, scientist Richard Ostfeld of the Cary Institute in New York and other researchers found that smaller forest fragments had more infected ticks, which could translate to more Lyme disease. Forest patches that were smaller than three acres had an average of three times as many ticks as did larger fragments, and seven times more infected ticks. As many as 80 percent of the ticks in the smallest patches were infected, the highest rate the scientists have seen. These ticks may also be infected with other emerging diseases--Babesiosis, Anaplasmosis and Powassan encephalitis--therefore, forest fragmentation might also be contributing to other serious illnesses, Ostfeld says.
"Our results suggest that efforts to reduce the risk of Lyme disease should be directed toward decreasing fragmentation of deciduous forests of the northeastern United States, particularly in areas with a high incidence of Lyme disease," says Keesing. "The creation of forest fragments smaller than five acres should especially be avoided."

EDIT: Another article on Vox also provides some possible explanations including the global warming, reforestation of farms and increase in the number of deers (caused by hunting protections).

My understanding is that there is a population increase of ticks, due to the milder winter temperatures.
Testing for Lyme disease is done with a specialized and somewhat expensive procedure called ELISA. Also as the prevalence of lyme disease has increased, physicians have become more aware and are making preliminary diagnosis , based on typical symptoms.
So its a two-part situation, increase in tick populations, and increased sensitivity for making diagnosis.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Where different types of proteins can be found in food?
According to https://www.youtube.com/watch?v=KSKPgaSGSYA (created by one of the largest supermarket chains in the UK), different proteins have different roles in human body:

(Group 1) They’re like building blocks of you body, they help grow and repair your muscles, skin, hair, and nails.
(Group 2) They help protect you from getting ill by attacking germs of bacteria that might make you unwell.
(Group 3) They help you breathe by carrying oxygen around your body.

The following food is rich in proteins: meat (e.g. chicken, ham, beef), fish (e.g. salmon), eggs, tofu, lentils, beans, etc. but I couldn't find out which food is rich in which specific group of proteins, e.g. "eggs - Groups 1 & 3".

It does not really matter what “protein groups” are in a food, as during digestion they are broken down into smaller peptides. The main thing is to make sure you are getting the correct amount of the different amino acids for the body to then make those proteins you are describing.

Thank you for your answer! My question was purely out of scientific curiosity as I'm a quantum chemist and would love to learn more when it comes to nutrients. I'm trying to explain proteins to my little daughter.

@Hawkeye perhaps you should expand your comment into an answer.

I@WYSIWYG — wouldn't it be better if this question was migrated to a nuitrition/health list, as it is incredibly naive and, as pointed out, is  based on the misconception that the proteins in one's food preserve their functions after human consumption. The poster is as well reading her daughter the blurb on the back of cereal packets.

Possible duplicate of How a vegan can consume all the needed varied proteins / amino acids?

Having watched the video listed I see the confusion. Actually protein from different sources is interchangeable.
The video FIRST talks about what foods are high in protein like meat, fish, eggs and tofu
THEN about the different ways we use proteins in the body which it lists a few of not meant as a formalised 3 group system.
These two sections of information are meant separately. All the proteins are made up from only 20 discrete amino acid building block types (sometimes with a few modifications), when digested the body returns the proteins to their amino acids building blocks and reuses them. This effectively cycles left to right and back in the diagram below.

Amino Acid building block makeup is not identical between different foods but is usually roughly comparable. So all the sources of protein are interchangeable like a pile of 20 different colours of Lego brick, especially in a western diet it is very unlikely you would run short of any of them. The body uses spare amino acids as a food source and or can switch their types for reuse.
For more info and an interesting read on the amino acid make up of different foods have a look at the USDA database here https://ndb.nal.usda.gov/ndb/
And a more detailed look at the protein digestion itself in a good video "Protein Digestion and Absorption" by Armando Hasudungan https://www.youtube.com/watch?v=HL7-fYBtJ1Y


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What species of arthropod is in this picture?
I've found exactly one of these, dead, on my kitchen floor most mornings this past week.
It looks like a large flea, is about 1 cm long (picture compares it to a British 10 pence coin, approx. 24.5 mm in diameter) and 2 mm thick with a laterally flattened body.
I believe it to be of the order Siphonaptera, but am unsure as to what exactly it is.
Can anybody identify the exact species of this arthropod?
If it helps, I live in the South-West of the UK.

Doesn't look like a flea, to me. Fleas have saliently long hindlegs.

Don't worry, it is not a flea, nor is it an insect. Looks like a crustacean to me (like a pillbug), but I am not sure of the species.

This is an amphipod, or "scud" (think of a pillbug that's flattened side-to-side rather than top-to-bottom); they're usually aquatic.  Getting past that point will probably be difficult (impossible for me, as I don't know the British fauna of the group).


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Meiosis pairing of chromosomes
How do the X and Y chromosomes synapse during the zygotene stage of when they have almost no homology between them?

There is 'homology' at the pseudo-autosomal region, a recombining region of the X and Y chromosomes.


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Do B/T cells form from lymphoid tissue or bone marrow?
This website says lymphocytes are produced in bone marrow https://courses.washington.edu/conj/immune/lymphoid.htm
But if that's true, then what cells do lymphoid tissues produce? It could make sense if bone marrow is a lymphoid tissue, but red blood cells are also produced from bone marrow.

This is a good question and I can see where some confusion can arise. Lymphocytes are a class of cells that include both B and T cells among others. They both have the same precursor cell that being a small lymphocyte [1,2]. The small lymphocyte will grow into a large lymphocyte then differentiate into a pro-B-cell or a pro-T-cell [3]. After differentiation the pro-B-cells are "trained" in the bone marrow and the pro-T-cells are "trained" in the thymus [4,5]. The processes of training for both B and T cells are active areas of research and are quite interesting if a bit confusing.
from [6]
"Lymphoid tissue has several different structural organizations related to its particular function in the immune response. The most highly organized lymphoid tissues are in the thymus and lymph nodes, which are well-defined encapsulated organs with easily identifiable architectures. In the spleen (a soft, purplish organ lying high in the abdomen), the lymphoid tissue is a cylinder of loosely organized cells surrounding small arteries. In the bone marrow this tissue is mixed with the blood-forming cells, and no organization is apparent."
It is true that red blood cells are produced in the bone marrow and are somewhat related to lymphocytes. They are cousins to each other in some way [7].
I hope this helped show the differences in the maturation of T and B cells and cleared up some confusion for you. If you would like to know more I would recommend picking up an immunology book. I used this one [8] and quite liked it when I was taking immunology.
[1] https://en.wikipedia.org/wiki/Lymphocyte
[2] https://medical-dictionary.thefreedictionary.com/small+lymphocyte
[3] https://www.researchgate.net/figure/Life-and-death-decisions-during-B-and-T-cell-developmenta-This-panel-is-a_fig2_8014354
[4] https://www2.nau.edu/~fpm/immunology/Exams/Tcelldevelopment-401.html
[5] https://www.researchgate.net/publication/6196234_B-cell_anergy_From_transgenic_models_to_naturally_occurring_anergic_B_cells
[6] https://www.britannica.com/science/lymphoid-tissue
[7] https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022042/?figure=1
[8]https://www.amazon.com/Basic-Immunology-Functions-Disorders-Immune/dp/032339082X/ref=sr_1_7?ie=UTF8&qid=1524514359&sr=8-7&keywords=immunology

Thank you for your detailed input. But, what is the direct answer? Does lymphoid tissue actually produce any cells? Because I encountered a biology professor who seems to think T and B lymphocytes "form" in lymphoid tissue.

@JohnJoe To clarify T and B cells are "trained" inside of lymphatic tissue but are not generated from the tissue itself.


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Strange fast growing mushroom like entity
I found this in my lounge today.
This room was cleaned less than 48hours ago, with no sign of this growth.
We sweeped and mopped, using the same floor cleaner we always do.
The two images below is of the same corner, but with the growth lifted in one image.
The consistency is like a fungus or mushroom and can probably be removed from the wall as one piece without much effort.
One of the walls close by do suffer from damp on occasion, but we have been in this house for over two years and have not had anything like this appear.
Please help!

How weird. Could it be leaking insulation foam or sealant or something? What makes you think it's fungal?

The way it's spreading looks like dry rot (Serpula lacrymans, Meruliporia incrassata or Fibroporia vaillantii), but the color doesn't look quite right. Did it stay that color or go darker at the center?

It is/was dry rot. The pictures were taken when these "flowers" just appeared, so it hasn't yet opened to show the orange/brown spores.

Builders have been in and ripped it all out, including our 100-year-old floorboards and fireplace :(
It is what it is... Thanks for the assistance though!

@Lizzie or Johan: please write up an answer so that this question can be marked as such. Thanks!

@theforestecologist Done!

This is dry rot. It could be one of several species, including Serpula lacrymans, Meruliporia incrassata and Fibroporia vaillantii. It is a fungus that feeds on and decomposes wood. Despite the name, some moisture is required for growth, so
it makes sense that your wall suffered from damp. The fruiting body will darken at the center as the spores appear.
Example images of dry rot fruiting bodies:

Photo by Seabrooke Leckie

Photo by Dave Brown


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Questions on DNA structural motifs
In the recent Nature Chemistry paper I-motif DNA structures are formed in the nuclei of human cells (open access link in LATimes) figure 1a shows "Schematic of i-motif and G4 structures."

I'm not a biologist, nor a chemist, so please forgive if the answer to my  questions seems obvious. I've looked at Wikipedia's Structural Motif article but there's little there about nucleic acids.

The length of the unlinked strand seems shorter, is this just because it is a schematic, and in reality the two branches would have the same number of bases?
What does the presence of the dual left and right arrows in G4$\ce{<-->}$ iM in the figure mean in this case? Does it suggest that a single molecule can change configuration back and forth between two distinct structures, or something else?

Double arrows represent reversible reactions. Your question is not really about biology but about the correctness of a schematic. Therefore I shall put this question on hold. BTW, both your guesses are right.

@WYSIWYG thanks for your comment. I'm trying to understand how all those bonds can re-arrange between those two configurations, and if this is actually known to happen. My intended question is to explore how DNA can do this but I wanted to check first if I was interpreting the diagram correctly or not, perhaps I was being overly methodical. If I rewrote to make this clearer, asking if DNA can do this, how, and if it is known to do this (move between these two configurations) would that be potentially on-topic?

Yes, if you edit your question such that it is about how DNA attains a certain configuration then your question is on topic. However, make sure that you are not asking a broad question.

@WYSIWYG thanks for your help, I'll take a day or so and try to do some additional reading.

When you edit the question ping me in the comment or vote to reopen. Ideally, the question should show up in the reopen review queue if it is edited post closure.

To answer point 1: The length of the unlinked strand is not represented accurately, it is shown shorter only because this is a schematic. In reality, the unlinked strand should be the same length, and would have the same number of bases as you have guessed.


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Is this bird a woodpecker?
This bugger is pecking on the side of my house. I don’t know anything about birds, but it doesn’t look like your typical woodpecker.

BTW, the pecking may be due to finding a plentiful supply of insects in your siding.

That is a red breasted nuthatch.(https://www.allaboutbirds.org/guide/Red-breasted_Nuthatch/id
Include a location next time,it helps with identification.

See how the top part of the beak is flatter than the bottom part of the beak. That helps them catch the insects that they eat.


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Insects emerging from vertical tube
I found a vertical mud tube about the thickness of a pencil in my garden with a series of metallic green insects coming out of it. They came out when I pulled a weed but stopped when I stopped, as if the vibrations were scaring them out. I think they were bees, wasps, or flies. They were 1/2" long or a little longer and thin. Head, thorax, and abdomen were all shiny green, wings transparent. What are they?
I live near Philadelphia and it was in the upper 60s F today.

Did you happen to take a picture of them?

alas, no camera available

Mud tube, metallic green, bee-like - sounds like a mason bee to me.
There are several metallic green mason bees (Osmia spp.). As Wikipedia explains:

Mason bees are named for their habit of using mud or other “masonry”
  products in constructing their nests, which are made in naturally
  occurring gaps such as between cracks in stones or other small dark
  cavities; when available some species preferentially use hollow stems
  or holes in wood made by wood-boring insects.

One example here:

Photos at http://www.laspilitas.com/insects/megachilidae/osmia-mason-bee.html


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How do we see and/or detect neurons?
I'm curious as to how we "see" neurons, for lack of a better term. Is it the detection of the neuro-transmitters? Can we literally see the electricity firing and moving throughout the pathways? Is it a combination of both, or something completely different, like scanners?
What kind of technology is used to do these things?
thank you!

Google is a good technology to find answers to these questions. Did you try it? Please try doing some looking up from your side before posting a question. Questions with no effort from the asker are usually not very useful to anyone (unless the question itself is quite good). Plus, your question is broad. If you are interested in these topics then you can check out the first few chapters of Principles of Neural Science by Eric Kandel et al.

Currently, the big thing in Neuroscience is imaging in vivo Calcium release which correlates with neuron action potentials, seen here. Each white speck is a neuron, the black lines and circles are blood vessels. Using this method you can visualize distribution and activity of neurons in real time.


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Why is gene finding in Eukaryotes such a difficult task?
Why is gene prediction in eukaryotes such a difficult task? Every gene starts with a codon and the non coding regions in between a coding region also has some specific base sequence(which are used by enzymes to recognize non coding regions during splicing). A computer program could simply search for start codon and then for stop codon. In between it could also search for those non coding regions since they start with specific base sequences. Why does gene finding need such complex things such as HMM?

What research have you performed to try to answer this question yourself?

The main problem is that while most of the things you describe are necessary to have a protein coding gene (introns, the non-coding regions within a coding region, aren't actually per se, even though they're common), they are not sufficient. Additionally there are also genes for non-coding RNAs (including tRNA and rRNA), which obviously don't have a 'coding region' (and also usually no introns).
In order to classify something as a functional gene we usually require that is actually made into (at least) RNA, which requires regulatory sequences that lead to transcription of the gene, these are called promotors. In eukaryotes there are many different promotor sequences, so its very hard to predict them computationally, additionally there are evolutionary remnants in our genomes, which are called pseudo-genes, and while they still have the general structure of a gene, they are not actively used any more.


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Proof of Darwinism( fossil records)
What logic do anti-darwinists provide for refuting the proofs( by proof I mean the fossil records) of darwinism ?
Is it the missing links?
If yes then , what do they make of the fossils which are present?
Note : I'm not being hostile to the anti-darwinists, I'm just very curious.Also I really want  to see it directly from an anti-darwinist (i.e. answer from an anti darwinist highly preferred)
If there's any problem in my question please inform me.

A terminological comment; Darwinism is a rather obsolete term, if you are referring to modern evolutionary theory. Sometimes it is used in contrast to the Modern synthesis or modern evolutionary theory. Especially by creationists, and in some popular use, it is seen as a general term for evolutionary theory though. However, it is rather inaccurate to label that as Darwinism, since much of modern evolutionary theory was completely unknown to Darwin (DNA, mechanisms of inheritance, Modern synthesis, much of EcoEvo etc).

Simply calling it Evolution or Evolutionary theory is better, when you are referring to the research field as a whole.

I would also downplay "theory". We never talk about the "theory of gravity". Evolution is the only series of facts that we insist on linking with "theory", which is misunderstood by non-scientists as some kind of guess.

@fileunderwater actually I meant darwinism specifically, not the modern theory of evolutions, like the neo- lamarckian model of evolution, symbiotic model of evolution, mendelian evolution etc.

@fileunderwater darwinism is actually pretty controversial , watch this----------https://www.youtube.com/watch?v=riqCx84rhfY

@KarlKjer This is a fundamental problem. Scientists have a complete different meaning for the word theory. For them a theory a system of scientifically proven statements. For the "lay public" it is seen as an unproven hypothesis.

@user545735 Darwinism is not controversial at all. Only people who don't understand evolution think it is.

Also, if you link people to an hour long lecture on a topic, they probably don't have time to listen to it all. It's better to summarise your points in writing.

I'm voting to close this question as off-topic because, on a scientific websites, one cannot list nonsense, undefined "arguments" from creationist philosophy. If you have a specific, well defined creationist argument, we can debunk it for you but we cannot safely list and explain what is nonsense. Unfortunately, the website nonesense.SE does not exist for you to ask your question.

Related: Is evolution a fact?

@user545735 If you are asking specifically about the historical theory Darwinism, you first need to define exactly what you mean by that, and how it differs from modern concepts of evolution. Everything expressed in The Origin of Species, 6ed? The question then also becomes an exercise in the history of science.

The word "Darwinism" is antithetical to science, because it implies a system of beliefs ("-ism"). Science is not a system of beliefs, but a method to test hypotheses and data. Scientists don't "believe" in evolution or climate change. They simply find that all the data are consistent with these explanations (theories are explanations that fit the observations and cannot be falsified).

I'm voting to close this question as off-topic because it is not a question about Biology, and hence off-topic here.

I'll try to approach this topic academically and undogmatically since skepticism is essential to scientific discourse. However, bear in mind that as of $2009$, $97\%$ of scientists believed in evolution (Pew Research Center, 2009). Although I can't find how many scientists were surveyed, nor what disciplines they studied.
I've not given many citations, since I'm questioning the counter-arguments to evolution, and not necessarily providing my own specific claims. I'll also avoid discussions in comments since this could be a contentious topic.
1. Missing Links
In theory, if there aren't fossil records forming a complete chain of species from early hominids to humans, then this could cast doubt on the theory of evolution. But the fossil records are convincing and there are many of them (Wikipedia, n.d.). Also, if there truly is a missing link and there is no relation between humans and early hominids, then why do their skeletons look so similar? And why did humans suddenly come into existence? Is there a better rational or empirical explanation?
2. Skepticism of Existence of Fossils
One could propose that there are no fossil records, or that they have been faked. But why would anyone want to make any fake fossils or lie about them? What possible conflict of interest would they have, and why would this benefit them? Why would tens of thousands of scholars want to support this theory? How does this explain how scientists are still discovering new fossils? If anything, a paper that shows that evolution is false would be groundbreaking and give instant publicity to whoever publishes it.
3. Inaccuracy of Techniques: Radiocarbon Dating
A variety of scientific techniques have been used to garner information about the fossil records. One such technique is radiocarbon dating, which tells us how old the fossils are. If this technique is inaccurate, we could be wrong about the fossils and they might not form a chain that leads from early hominids to humans. But the technique is broadly accepted. Also, how would this explain the fossils - why would humanoid fossils with such odd shapes occur at random points in time? The shapes of these fossils don't look like typical human mutations.
4. Skepticism of Age of the Earth
Another counter-argument proposed to evolution is that the age of the fossils doesn't allow for their beliefs of the age of the earth. But the age of the earth is accepted by the geological community to be ca. $5\;\mathrm{bn}$ years old (Wikipedia, n.d.).
5. Summary and Micro/Macroevolution
A related counter-argument to evolution that I'd like to cover, but isn't directly related to the accuracy of fossil records is that of microevolution vs. macroevolution. Some people argue that we can only see evolution on minute scales, and not on large scales. But then if a population does have small-scale changes, and there is a higher probability individuals with certain adaptations surviving, then wouldn't these micro-effects sum, over millions of years, to produce large-scale effects?
In my opinion, the counter-arguments for the fossil records of the fossil records for evolution are rather flimsy, which suggests that evolution is the best explanation we currently have for the evidence we've observed.


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Advanced Higher Biology 2017 - EPT Index
I was recently completing a biology past paper the Scottish SQA 2017 Advanced Higher Biology Qualifications. The question is as follows:

To solve this, I did:
EPT Index = 100*(striped stonefly + net spinning caddisfly + flathead mayfly)/(total number of taxa) = 100*(6+6+3)/(44)=34.09%
So, I answered C, however, the answer is B. What mistake have I made?

Do not post questions as graphics. They are unindexable and unreadable by people with sight problems.

The point of the question was to determine if you know what taxa are.  You don't; remedying that might give you the right answer.

Well, you made a mistake: The numbers in the second table are irrelevant to the question as it is not about taxa but about individuals. And the ETP number is calculated from number of EPT taxa (and not individuals).
The correct answer was 3*100/7 = 42.9% ==> B good quality of water.


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How are single-stranded binding proteins removed from the lagging strand during DNA replication?
The lagging strand, downstream of the Okazaki fragment, is covered in single-stranded binding proteins (SSBPs) during DNA replication. What is the mechanism which ensures that SSBPs are removed from the lagging strand to allow for the binding of the next Okazaki fragment?

Actually, there has been some evidence that the SSBPs keep the bases facing outwards so DNA polymerase can still replicate the lagging strand with the SSBPs on them. There has also been other evidence that they can pop off spontaneously.
You can learn more about this by watching the lectures on https://www.edx.org/course/molecular-biology-part-1-dna-replication-and-repair

Your answer may well be correct but there is no way for anyone to know without reference to some external source that supports your answer. At the moment it is likely to be automatically flagged as low quality by the system. Please take a moment to read the Help on writing the sort of answers that are appropriate here, and then edit your answer.


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Bacteria without plasmid
I am currently working on antibiotic resistance and I would be very interested to know which bacteria has no plasmid, in a similar way than M. tuberculosis.
This would help me a lot for my work and I did not succeed to get that much information online.
Thank you very much for your answer !

You might want to take a look at Bacillus subtilis. Most of the lab strains don't contain plasmids, though they have been found in some environmental isolates.
https://academic.oup.com/femsre/article/21/4/337/490925
All this depends on exactly what you're looking for: a species with no known plasmids in any isolates, or some commonly used lab strains with no plasmids?
M. tb is a pretty unique case. Most of the other species in the Mycobacterium genus do contain plasmids.

Thank you very much for the information, this will be very usefull !
I am looking for bacteria which, as MTB does not share (or sharing few) plasmids so the antibiotic resistance cannot be detected by mapping their genomes with common antibiotic resistance genes. Some just as MTB, which have developped SNP which induce resistance.

Another way to approach this is to do it by genes rather than organism. For instance, gyrase and topoisomerase proteins are targeted by some antibiotics. Because these are produced by essential genes, resistance has to arise from point mutations (more or less). So you could look at these genes across a wide range of organisms. Just depends on what your objective is.


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How do you keep track of past/new lab protocols?
Does there exist a list grouped my subject (e.g. 'microscopy') for keeping track of what protocols have been designed and used?
Closest I could find is http://www.protocol-online.org/ but it's fairly sparse and out of date.
Any recommendations/tips and tricks? Thanks!

The best match to what you're looking for is probably https://www.protocols.io/, which hosts protocols for free and generates a digital object identifier (DOI). It is not indexed by PubMed or other similar engines, however.
Some journals permit methods papers, but not a high proportion (and it sounds like you're looking for a place to find them, not to send them).

Looks interesting – I had in mind that someone would have built a crawler for finding method papers and indexed them, but perhaps not.


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What does "This variant falls on 11 transcripts in 3 genes" mean in the output from GnomAD?
The gnomAD browser provides information on variants of genes (in this link, for the SAMD11 gene.)   The report on a particular variant, like this one,  includes the information in the header that says (for example): "This variant falls on 5 transcripts in 2 genes."
What does this mean? In particular, how can a variant occur on more than one gene? Isn't such a variant a variant of a particular gene -- SAMD11 in this case?

In this particular case, there is another unannotated gene at the same locus, running in the opposite direction as SAMD11.
http://grch37.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000268179;r=1:865499-865579;t=ENST00000598827

How can 3 genes turn up?  As in this variant to SAMD1: http://gnomad.broadinstitute.org/variant/19-14198695-C-T

The SNP is in the upstream region of C19orf67, and the downstream region of PRKACA.  http://grch37.ensembl.org/Homo_sapiens/Variation/Mappings?db=core;r=19:14198195-14199195;v=rs534496627;vdb=variation;vf=67232947


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What is the pH of the mitochondrial intermembrane space?
The proton gradient is stored between the mitochondrial double membrane. More protons mean more hydronium ions and lower pH, but how much exactly?

I agree with @alina that it is well accepted that the pH difference across the inner membrane is ~0.5-1 units. However, the absolute value of the pH in the IMS will vary between organisms and even cells. It is experimentally difficult to measure it, therefore most of the times only the matrix pH has been reported. Using the output from the BioNumbers database as an example:
human endothelial cells ECV304: 6.88 (IMS), 7.78 (matrix)
human HeLa cells: 7.98 (matrix)
rat cardiomyocytes: 7.91 (matrix)

That does not look a lot, but now I realize that in the mitochondria of human endothelial cells the intermembrane space is about 8 times as acidic as the matrix [10^(-6.88-(-7.78)) = 10^0.9 = 7,94]. That's quite a gradient.

According to the authorities Roos and Boron the difference of pH across the inner-membrane of mitochondrion is  0.5 with pH outside the membrane equal 7.0 and inside the pH is 7.5 (pH-mit = 7.5, pH-out = 7.0) according to Intracellular pH


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What is the relatedness of sisters in a haplodiploid system if you mate virgin queens with 1 of their sons
So I'm having trouble wrapping my head around this. In haplodiploid insects, sisters are related by 75% on average due to all sharing 100% of dad's genetics and 1/2 of mom's. (males are produced from haploid eggs)
The question I have is, if you take a son of a queen and mate her with her own son, what is the genetic relatedness of her resulting daughters to one another?
Here is an illustration of the haplodiploid system in insects.

Thanks in advance!
source: https://en.wikipedia.org/wiki/Haplodiploidy

Possible duplicate of How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?

It is not a duplicate to me, it is related for sure but the question here is more precise. Maybe we sould rename the question so that it is easier to understand what is asked

This question may not be duplicate but I would reconmmend reading the answers of this question first How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?
I think an image is worth a lot of words so here it is:

To calcul relatedness, I used the formula
$ \text{relatedness} = \ce{prop_{mother}} \times \ce{shared_{mother}} + \ce{prop_{father}} \times \ce{shared_{father}}$
The little trick here is that we know the father (son of queen) is unique, so we can focus on either of the two possible son of the queen. This gives us a 0.875 relatedness between sisters with a father being the son of the mother.
I hope it is clearer now.


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Can cells show negative growth?
I know that growth is an irreversible increase in mass or overall size of a cell, organ or whole organism. I also found that growth occurs due to the net result of anabolism and catabolism.
My teacher said;
           When anabolism > catabolism - growth occurs
                 Anabolism = catabolism - no growth
                Catabolism > anabolism - negative growth
But on searching about this negative growth, I couldn't find any information. What is this negative growth? Where do you see it?

At what scale do you want to observe this 'negative growth' - cell or tissue level?

Could "negative growth" be listed as "shrinking"?

When you look at a certain mass of cells (in a petri dish, a tumor, whatever) which are in principle viable, growth can go in both directions. It can be poitive which means that the number of cells is growing over time.
It can also be negative, which results in a declining number of cells over time. We see this effect in cell growth assays, when we analyze the effect of certain treatments to our cells. Since we want to "kill" our cells with the treatment, a positive growth would indicate an unsuccessful treatment, a negative cell growth a positive treatment effect.


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gel band contrast
Is there any way to increase the contrast of my SDS PAGE gel. I want to increase the coomassie stained gel contrast of my gel bands a little bit as it looks little less for my thesis. Ive heard that it is legal and can be done. Is there any software for it or some other way.

The bands should be a bit clearer (blue background drag in the lanes). You can try improving the protein extraction protocol. Could also be a problem with the gel. Is the leftmost lane your protein ladder?

If you are asking how to alter the image to make it clearer then your question is off-topic.

I have made a standardised protocol for protein extraction... this is the best I could get for bands as protein content is less from my sample..I dont want to alter the image just increase the overall contrast....and yes the leftmost lane is my ladder...do you have any suggestion to improve this particular image?

If this is accepted or not depends on your institution. For publications, it is usually accepted to use adjustions of color, tonal values and contrast which are applied to the whole image and which do not alter the statement of the image. These changes are not ok if for example the contrast it raised so much that weak bands disappear.
Not accepted are changes which are only made to changes to parts of the image, partial adding or removal of parts of the image. Keeping this in mind, you can basically use any software which can be used to process images. Photoshop is kind of a standard but pretty expensive, free software like Gimp also does the job.
I adjusted the tonal values of your image and raised the contrast just a little to get this:

You got there first. I also took it into PhotoShop and did an "Image>Auto Contrast" (not quite as good) but then went into "Adjustment>Levels" and with the dropper selected an area between the lanes as the white point, which gave a slightly better result.

this looks much better than my posted image..and yes it is legal over here to adjust the gel as long as we do not tamper the bands...and thanks a lot...do you think this one is good to proceed with or should I tune it a little bit more.

@Kushal That depends on your desires for the image. For me, this looks fine.

@Chris okay I'll see to it. and thanks a lot for the help and suggestions.


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Is the common house gecko poisonous to touch?
I live in India. Sometimes some common house geckos came in house and my family members kill them and I feel very bad (I even cried once ). They told me that It is very poisonous and toxic. If they fell in food or water, the water or food becomes toxic and would kill you. They told me that if you want to save them then catch them and release somewhere else but should I touch it?
I just saw a man on YouTube who handled it like it was no big deal?
I am talking about this gecko :-

Actually, there are two poisonous lizards in the world. The other is Heloderma horridum, also from Mexico.

They are completely harmless. There are no poisonous lizards in India, and only one species of poisonous lizard in the world (Heloderma suspectum, from Mexico and SW U.S.). A gecko's skin is not toxic. They don't inflict a painful bite. The best way to hold a lizard without harming it is by the base of a hind leg.


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Is cruelty a human instinct?
I had started studying human behaviour and human instincts a few months ago, earlier the question was raised after seeing human behaviour with animals (his prey). Animals hunt their prey for eating, on the other hand, I have seen kids stone pelting at street cats and dogs. Again human approach towards life is more than survival, it is dominating his peer beings. Can I call this behaviour of mankind as a cruel? If so, is it instinctual?
I am very sorry for the late response. Hope this clears the question.

Can you expand a bit? As it stands, you only have the title question. To be able to talk about these things from a scientific point of view, it is important to define exactly what you mean by "cruelty", so that is can be viewed as a behaviour without all the negative connotations (as much as possible...). After that, it might be possible to draw comparisons to other species closely related to humans, as well as looking at results from neurobiology and psychology.

What made you think people are generally cruel? What cruelty even is from your POV?

I have edited the description, please revisit the question. @fileunderwater

I have edited the description, please revisit the question. @rus9384

It sounds like a philosophical question, but it also has evolutionary roots. All species are instinctually selfish, in that there is a drive to move their genes into the next generation. So misbehaviors (like "cruelty") should be held in check, because they are likely to be punished in a social species. We evolved as a social species that lives in family groups, with a high probability of meeting nearby family groups repeatedly. If you are cruel to your neighbors, you would expect to meet the points of their spears sometime in the future. This expectation of future encounters with neighbors can explain altruism as well. But its a balance. If cruelty to your neighbors is in your long term selfish interests, then you would expect it to be instinctual, just as you might expect kindness to be. Its all about different strategies to send our genes forward. As a side issue, chimps, our close relatives exhibit violence to their neighbors (but bonobos, equally close, are much less violent).


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Why don't cells of aquatic animals burst?
We know that if we keep plant cells in water, they don't burst because of a cell wall. But the cells of aquatic animals lack cell walls but they still survive. Why?

Comparative physiology of body fluid regulation in vertebrates
Cells are not passive components that always return to osmotic equilibrium. Through hormonal, cell signaling, and the number of pores for ion and water exchange marine animals can maintain osmoregulation in various aquatic environments. In land mammals osmoregulation is more passive since it is controlled by the endocrine system.


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What is it called when an animal only has one type/variation of dentition?
An example would be alligators that only have one type/shape of tooth. Not the variation in function and shape like seen in humans, which have canines, molars, incisors, etc

Homodont
You can find the term "homodont" used in Lambert et al. (2014) or on wikipedia > dentition for examples. The opposite of homodont is heterodont (wikipedia > heterodont). In mammals, a classical example of homodonts is the dolphin.

to reinforce heterodont dentition is fairly rare, only mammals with their limited number of teeth have it constantly across a large clade.


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Is a nature possible where animals do not kill each other?
like the title suggests, i always wondered if its possible that nature would work without animals killing each other. Where they just eat plants. Like one special plant for each animal. If they eat to much of them away they also will stop multiplying to much, so there will never be too much of one species etc, terefore balance. I am sure there could be other controlling mechanism for balances.
:)

I suppose your question could be rephrased, "how could predators never evolve?" This type of question should be asked on worldbuilding.SE, not on a science website. Note that plenty of points are unclear in your question. How about cells phagocyting? Is this allowed in your imaginary world? How about competition leading to death of other individuals?

Somewhat related: Are there any multicellular forms of life which exist without consuming other forms of life in some manner?

I'm voting to close this question as off-topic because it is unclear and in essence is not open to empirical testing and is therefore unsuitable on a scientific website.

No. Because a spiderwebs can't catch herbs.

I'm not sure how a spider would catch herbs in its web.

No, even herbivores will eat other animals, and predation goes down ot the cellular level.  Also something has to be ating your dead and will have a huge evolutionary pressure to evolve toward predation with no predators present.
Animals by definition have a much better profile of nutrients for other animals.
Deer routinely kill and eat birds, eggs and even dead rabbits. In nature food is food and evolution does not care where you get it from. Carnivores will and have evolved from an herbivorous ancestor when no carnivores are present.


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The effect of Atrazine on the LDR in Photosynthesis
The herbicide Atrazine causes inhibition within the Qb site in the D1 protein of photosystem 2.   Given this information, would Atrazine’s inhibitory effect halt the production of oxygen or ATP first?

Given that water is oxidized indirectly by P680+ and the build up of intermediates caused by inhibition in Qb  would not allow P680 to deposit its extra electron into the beginning of the electron transport chain, water would not be oxidized/split into 2H+ and (1/2)O2 because P680 would not become P680+.   So this inhibition would halt the production of oxygen, correct?
Given that, I would say that the production of O2 would be more immediately halted than that of ATP, especially since ATP synthase would continue to function until the electrochemical gradient between the stroma and thylakoid space was spent, and would not be immediately affected by inhibition in Qa (although the electron transport chain which maintains the electrochemical gradient would be compromised and thus indirectly ATP synthase would be affected).
Is my reasoning correct?


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Bacteria utilize short chain fatty acid as energy source
I'm doing research about the short chain fatty acid producing bacteria. I studied 7 short chain fatty acid (acetic propionic butyric isobutyric valeric isovaleric and captionic). and I found that the bacteria produced all acid in 8-12 hr incubation time  and after that all short chain fatty acid rapidly decreased, except acetic acid slightly decreased. How can I explain this results?  and I did my experiment under anaerobic condition.


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What metric(s) is a good proxy for relatedness?
In attempting to seed a simulation, where an individual foregoes resources that go r to same-type individuals and (1-r) to all members (including same-type individuals).  What commonly used metrics are a good proxy for r in this sense?  In other words, if I am seeing a simulation to replicate the parameters of the mean population for, for example, a zebra finch or a human or a house mouse, and I am looking in empirical reports of these species and r does not appear, are there other metrics that are convertible?

I'm not sure to understand what you are looking for. Are you seeking for a way to calculate genetic relatedness? If ris a value for giving food to same-type individuals how do you define same-type? Is it from genetic relatedness or other way?

Thank you for the reply.  No I'm not looking for a way to calculate genetic relatedness.  I have written a simulation and am looking to feed it realistic values for relatedness.  Emphasis upon populations of the zebra finch, human, house mouse, and also populations of trees.  But r is not reported commonly and other metrics are reported more typically, such as FST.  I don't know whether they are substitutable or convertible into r.

This article by Harpending would suggest that but I'm not seeing it in a textbook and am not familiar enough with these measures. Harpending, Henry (2002-11-01). "Kinship and Population Subdivision" (PDF). Population & Environment. 24 (2): 141–147. @Untitpoi

It would seem from the article, unless I am wrong, that 2*Fst is a good proxy for the Hamiltonian r (if benefits can be confined to within subpopulation).  Am I wrong?  @Remi.b


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What color does the other cone in Tetrachromacy correspond to?
Human with normal vision possesses 3 cones, which correspond to blue (S), green (M) and red (L). What about tetrachromacy, where people have 4 cones in their retinae? What is the fourth cone exactly, and what color does that other cone correspond to?

According to Deeb (2005), there are two relatively common types of causes for tetrachromacy in humans:

The common Ser180Ala polymorphism, which results in two spectrally different red pigments in the retina. This mutation also plays an important role in variation in normal color vision. This polymorphism most likely resulted from gene conversion by the green‐pigment gene.
Another common variation are several red/green pigment chimeras with different spectral properties. The red and green‐pigment genes are arranged in a head‐to‐tail tandem array on the X‐chromosome with one red‐pigment gene followed by one or more green‐pigment genes. The high homology between these genes has predisposed the locus to relatively common recombination events that give rise to red/green hybrids and deletions of green‐pigment genes. Such events constitute the most common cause of red‐green color vision defects. Only the first two pigment genes of the red/green array are expressed in the retina and therefore contribute to the color vision phenotype. The severity of red‐green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by the first two genes of the array. Women who are heterozygous for red and green pigment genes that encode three spectrally distinct photopigments have the potential for enhanced color vision.

Reference
Smeeb, Clin Gen (2005); 67:(5): 369-3
Further reading
- Color vision across species


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Could you identify which species of ant is this queen?
could you identify which species of ant is this queen. I caught it in Bangalore, India. I caught it after a rain at around five to six.
]2

You should probably add more information, such as the time and place where it was caught (including ecological context).

I caught it at around five to six. I also caught it directly after a rain storm. I live in a relatively warm place which is not to humid. Oh and I caught it just outside my house.

Oh I also caught it in Bangalore, India which is where I live.

@DarkGuardian2006 please [edit] your question to add the details. Do not reply in comments.

Although absolutely no formal criteria are visible on your photo, the general shape of the ant, especially the wide elongated head and low thorax, is typical of the ant genus Camponotus.
See ref below:

Bolton, B., Alpert, G., Ward, P. S., & Naskrecki, P. (2006). Bolton’s
  Catalogue of Ants of the World. Massachusetts, Harvard University
  Press (CD-ROM).


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Can ribosomes read ssDNA?
My question is whether translation can be done, either naturally or artificially, through a ribosome reading (single-stranded) DNA directly. If not, I would like to know what allows ssRNA to be translated but not ssDNA.

https://biology.stackexchange.com/questions/3678/can-dna-act-as-a-translation-substrate

Summary
Messenger RNAs that are recruited to the ribosome for protein synthesis in vivo, need to satisfy particular structural requirements and must interact with the protein initiation factors that deliver them to the ribosome. Generic single-stranded DNA (ssDNA) does not have these structural characteristics and so cannot be translated on ribosomes under natural conditions.
A single reported attempt to translate deoxyribose-based analogues of these mRNAs under conditions equivalent to those within the cell was unsuccessful. Thus, although experiments suggest that ssDNA may be able to bind transfer-RNA and allow some polypeptide synthesis under non-physiological conditions, this reflects only those aspects of protein biosynthesis that involve base-pairing interactions between the message and other RNAs involved in translation. In contrast, the stages involved in the selection of the first initiation codon and the recognition of termination codons involve interactions between protein factors and the message, where recognition of a hydroxyl group in the 2ʹ-position (and discrimination between thymine and uracil) may well occur and would prevent translation of a synthetic ssDNA message.
If, in fact, no discrimination against DNA has evolved for the ribosomal- and transfer-RNA components of the translation apparatus, this may be because the system arose in an ‘RNA World’ before DNA evolved, and because free ssDNA in the cell has never been a competitor with mRNA for ribosomes, especially after sophisticated protein-based systems arose for the selection of the appropriate initiation codon.
Contemporary physiological interactions of mRNA with ribosomes
Translation of mRNA by ribosomes (protein biosynthesis) is a complex process which can be divided into a number of stages, each generally involving a variety of RNA and protein molecules — initiation factors (IF), elongation factors (EF) and termination or release factors (RF). The reader who is not familiar with this is advised to read a text-book account such as that in Chapter 29 of Berg et al.. However, to summarize briefly, they are: selection of the correct AUG (usually) on the mRNA for initiation, IF-dependent binding of the initiator-tRNA to the P site, EF-dependent and codon-directed binding of an elongator-tRNA, peptide bond formation catalysed by the large ribosomal subunit, EF-dependent translocation, and eventually stop-codon directed and RF-dependent release of the completed polypeptide chain.
The first step, is crucial for the binding of natural mRNAs — the subject of this question. Under natural cellular conditions prokaryotes and eukaryotes have different methods of ensuring that the ribosome interacts with the correct mRNA codon to start translation. In prokaryotes a specific ribosome-binding signal (Shine and Dalgarno sequence) must interact with the 16S rRNA and a particular initiation factor protein is involved in this step. In eukaryotes the main method is recognition of a modified 5ʹ structure on the mRNA and unwinding of secondary structure, also modulated by protein initiation factors.
I am aware of one report of an attempt to translate a DNA-based analogue of such natural mRNA structures under any conditions. This was by Damian et al.  (Biochim. Biophys. Res. Commun 385, 296-301 (2009)), and was unsuccessful, even though physical methods indicated binding to the ribosome. I imagine that recognition by the protein initiation factors did not occur but I cannot be sure that base-pairing to the 16S rRNA was also hindered.
Regardless, one can answer the question posed:

The fact that ‘random’ single-stranded DNA would lack the structural features for selection of the correct initiation codon
  explains why it would not be translated under natural
  conditions — it could not bind to the ribosome.

Artificial systems of protein synthesis
The full details of the reactions on the ribosome only emerged gradually. Nevertheless the lack of understanding of the features of natural mRNA required for binding to the ribosome did not prevent either the dissection of subsequent steps of protein biosynthesis, nor the use of ribosomal systems to decipher the genetic code. This is because it was possible to bypass the initial steps by using suitable unphysiological conditions, that allowed polynucleotides or oligonucleotide triplets to bind to the ribosome, where further reactions were possible, albeit generally less efficiently than in the cell. Such conditions included high concentrations of magnesium ions and certain antibiotics that affect the accuracy of protein synthesis. It has been suggested that the neutralization of the charge on the backbone phosphates of the RNA by Mg2+ enhances (non-specific hydrophobic interactions at the mRNA-binding channel, and that the antibiotics stabilize a state of the ribosome in which amino-acyl tRNA can bind more easily (and hence promote the binding of polynucleotides by base pairing). Once bound with the codons hydrogen-bonded to the cognate anticodons of tRNA, subsequent elongation reactions depended on components of the ribosome other than the artificial messenger.
Thus, it was that the genetic code was deciphered using bacterial cell-free systems to which were added simple synthetic polynucleotides, lacking Shine and Dalgarno sequences or start (or stop) codons; and by experiments in which amino acyl-tRNAs were bound to triplet codons in the absence of both IFs and EFs. Other partial reactions of protein synthesis were similarly dissected artificially — the peptidyl transferase reaction was studied on isolated 50S subunits using just a fragment of tRNA and puromycin by conducting the reaction in 50% ethanol!
Experiments with single-stranded DNA
Understanding that ribosomes can be induced to bind and translate ‘non-mRNA’ oligo-ribonucleotides under certain artificial conditions, we are in a position to consider the significance of reports of translation of oligo-deoxyribonucleotides — ssDNA.
The original experiments in this area by McCarthy and Holland in 1965 showed that denatured DNA from various sources (including animal cells) could stimulate the incorporation of radioactive amino acids in a bacterial cell-free system, but this depended on the presence of antibiotics. Furthermore, it was shown in Khorana’s lab that only certain synthetic poly-deoxynucleotides  (analogous to the poly-ribonucleotides he used to decipher the genetic code) were active. Thus, it would appear that under the non-physiological conditions that favour promiscuous binding of poly- and oligo-ribonucleotides, there is some binding of ssDNA, and subsequent translation.
A paper by Ricker and Kaji mentioned by @Mesentery — reports that oligodeoxynucleotides could function in some partial reactions (fmet-tRNA binding) although not in others. In particular it was not possible to perform RF-dependent termination reaction with oligonucleotides containing termination codons, but — in the presence of antibiotics — termination independent of release factors did occur.
It is, thus, obvious that these experiments in which ssDNA is translated on ribosomes have no physiological significance. However it is still pertinent to ask the complement to the question of the poster, why does the system work at all?
Why are deoxyribose (and thymine) not discriminated against under artificial conditions?
Enzymes of synthesis and degradation of nucleic acids — RNA and DNA polymerases; ribonucleases and deoxyribonucleases — are specific for either RNA or DNA (or in some cases DNA/RNA hybrids). This is both important to ensure they fulfil their specific functions, and perhaps an inevitable consequence of the nature of their reactions — the making or breaking of sugar–phosphate bonds. Here we are dealing with catalysis by a protein enzyme that binds these structures at its active site.
In contrast, those reactions of protein synthesis for which certain requirements may be relaxed under non-physiological conditions involve base-pairing interactions. In modern ribosomes they may be optimized by associated proteins, but it is thought that the latter only evolved later. Artificial conditions, such as high concentrations of magnesium ions or antibiotics, may be thought of as allowing the essential interactions that existed in ‘ur-ribosomes’. And, of course as DNA/RNA hybrids readily form, the participation of DNA in such interactions is not so surprising. (In the RNA world of ‘ur-ribosomes’ — or even an RNA/protein world — there would be no need to discriminate against DNA, because it had not yet arisen. And chemically, the substitution of a hydrogen for a hydroxyl group could not hinder an interaction — at the worst it would only weaken it.)
It is pertinent that the contemporary AUG-selection and termination reactions depends on RNA–protein interaction. These might well involve recognition of ribose as well as base sequence, explaining the observations by Ricker and Kaji, and by Damian et al., mentioned above.

This answer attempts to address some of the considerations implicit in a simple factual answer to the question, even though they are perhaps not the primary concern of the poster. If anyone wishes further references or clarification, do ask.

I have now finished revising my answer. I have made a major change in considering the paper of Damian et al., which does use DNA analogues of natural mRNA.

My question is whether translation can be done, either naturally or artificially, through a ribosome reading (single-stranded) DNA directly.

Ribosomes participate into the translation of mRNA into proteins. See the wikipedia article for more information

If not, I would like to know what allows ssRNA to be translated and ssDNA not.

The "if not" makes no sense because answering yes or no to the first question does not really have much to do with the second question.
ssRNA and ssDNA refers to the genetic material of some viruses. Most of the time, I do not think we use the terms ssDNA and ssRNA to refer to a virus that reverse transcribe the RNA into DNA, so your question is unclear and confusing.
Some viruses do reverse transcribe RNA to DNA. They do so with a reverse transcriptase.

What I want to know with the second question is what structural or chemical characteristic allows the reading of RNA but not DNA.

Oh I think I understand your question...
Double stranded DNA cannot be translated by a ribosome for sure. I suppose ssDNA could eventually fit in a ribosome (or a slightly modified one), however, the tRNA should be adapted to using T and not U. I am not a molecular biologist and I can't say more than that.

I want to know how DNA lacking a 2-hydroxy group and using thymine instead of uracyl makes it unreadable to a ribosome

I don't know if it does and, if it does, then I don't know why! Sorry, I am not able to help more!


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Acetone–butanol–ethanol fermentation

Source

Source

Source
Acetoacetyl-CoA is a C3 unit.
3-Hydroxybutyryl-CoA / Butyryl is a C4 unit.
Where does the additional C atom come from? I'm suspecting it's another Acetyl-CoA -> CoA reaction, but I don't see it in the images.

What does ABE mean? Do not use non-standard abbreviations in titles and if you must use them in your question define them. This allows indexing and improves your chance of getting an answer. And edit your image so we can see the reaction you are concerned about. Have you tried other sources for an answer?

@David fixed the title and added additional images I looked at. Maybe I'm missing something obvious.

I think you are.

Well, I’m not sure I should answer this, as your question is predicated by an incorrect supposition:

Acetoacetyl-CoA is a C3 unit.
3-Hydroxybutyryl-CoA / Butyryl is a C4 unit.

Not according to Kegg:

However, my answer is worthwhile if I explain how I found this out. One way to check this sort of thing is to go to the Kegg website and search for the compounds of interest, find the appropriate pathway (shown below) and then click to check compounds and reactions.

There is also the Metacyc website for metabolic pathways, and you can check the formulae on Wikipedia.

Kind of embarrassing that I missed that. It was so fixed in my head that it's C3 that I didn't even thought of checking that assumption. But your answer, as you already suspected, is worthwhile nonetheless. I went over to KEGG and was successfully able to navigate to the same map as you did. This will be a helpful place to start searching for answers in the future.