text:
Steroid hormones: how do they travel through the cytoplasm (not just the blood plasma) if they're hydrophobic?
I get that steroid hormones need hydrophilic plasma protein carriers (eg albumin, TBG) to travel in the plasma because they're not soluble in the plasma. However, I don't see any sources talking about how these hormones can then traverse through the (presumably also hydrophilic) cytoplasm to get to their receptors either in the cytoplasm or nucleoplasm. Anyone have any clarifications on this?

Firstly not all steroid hormones travel inside the cell and regulate the gene expression.
Basically there are two pathways- direct and indirect.
Steroid hormones are lipid-soluble, which allows them to cross the extracellular membrane to the inside of the cell.

Classical models of steroid action suggest that steroid hormones bind to specific nuclear receptor proteins once inside the cell. Reference

Once inside the cell, a steroid hormone binds with receptor proteins in the cytoplasm. The steroid hormone and its receptor form a complex, called a steroid complex, which moves into the nucleus where it influences the expression of genes.
Reference

In the indirect pathway,

The traditional nuclear steroid receptors can also indirectly regulate gene transcription by serving as signal transduction proteins that interact with various signaling pathways in the cytoplasm of a cell. In particular, ER can activate kinases, enzymes that phosphorylate and thereby activate other proteins. This sets in motion a signaling cascade that eventually ends in the nucleus with the induction of gene transcription.
Reference

I am not an expert in this area, but found a summary of and illustration from a textbook — Karen Lounsbury, Pharmacology, 2009 — on a Science Direct summary page.
Apparently for the glucocorticoid hormones there is a cytoplasmic glucocorticoid receptor protein (GR in the diagram) they bind to, presumably keeping them soluble in the aqueous environment. This causes heat-shock proteins (HSP90 in the diagram) associated with the receptor to be released from it, which allows the complex to be translocated to the nucleus where it binds to a glucocorticoid response element (GRE in the diagram), triggering transcription of appropriate genes.

More detail is given in a paper by Bledsoe et al. (2002) in which the structure of the dimeric GR bound to a steroid analogue was determined. To quote from the introduction to that paper:

Like most nuclear receptors, GR is a modular protein that is organized into three major domains: an N-terminal activation function-1 domain (AF-1), a central DNA binding domain (DBD), and a C-terminal ligand binding domain (LBD).
…
Within the context of the full-length receptor, both the AF-1 function
and the DNA binding activity of GR are dependent on hormone binding.
In the absence of ligand, GR is retained in the cytoplasm by
association with chaperone proteins such as hsp90 and p23, which bind
to the LBD (ref). The chaperone activity of the hsp90
complex has been shown to be critical for hormone binding by GR
(refs). Hormone binding
initiates the release of chaperone proteins from GR, allowing
dimerization and translocation of the receptor into the nucleus. In
the nucleus, GR binds to DNA promoter elements…

A image of their structure is shown below:

I suspect the issue is mainly one of diffusion distance. Steroid hormones are not that insoluble as they are compact and have multiple oxygen functional groups. Checking predicted log octanol/water partition coefficients on PubChem gives 3-4ish for steroid hormones compared to 6+ for a typical fatty acid, despite the latter having an ionizable headgroup.
These hormones are present in the body at nanomolar concentrations or even lower, and at that concentration, almost anything is soluble. The problem with them being in the plasma at any concentration, though, is that as soon as a molecule would collide with the lipid membrane of a cell in the wall of the vessel, it would tend to stick, and therefore the vessels would act sort of like a chromatography column that drastically reduces the apparent diffusion coefficient and generates steep gradients. While this might actually be desirable for a local mediator like a prostaglandin that has a range of a few cell diameters, it is very undesirable for something like steroid hormones that travel to completely different organs from where they are produced. Therefore, a hydrophilic carrier is essential.
On the scale of the cytoplasm of a single cell, this is not likely to be an issue, especially since there are receptors inside that act as a "sponge" or "sink" to catch and trap molecules that diffuse in.


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Are these springtails and isopods?
G'day!
I'm based in Victoria, Australia.
I'm hoping to culture springtails for my terrariums, so I went out and tried to collect some. I found them underneath a rock, which was sitting on damp ground. They certainly look like springtails, and gee they're tiny! 1-2mm. But they don't jump at all.
My first question is -- is this little fella a springtail?

Fast forward a few weeks, and these little critters still seem to be alive in a jar. However, what I believe are isopods appear to have joined them. They're super tiny though, < 2mm. And they're always hovering around what appears to be eggs.
Here's two pictures:

I read online about the lifecycle of isopods. They don't lay eggs; rather, the mother keeps them in a pouch on her underside. I also read that, absent better food sources, they can feed on the eggs of other insects.
So what I suspect is, that these are springtail eggs, and the isopods are eating them. Is that a correct assessment? And are these indeed isopods?
Thank you in advance for your help!
TLDR

Is the first picture of a springtail?
Are the second/third pictures of isopods eating springtail eggs?

Look in thick, damp, leaf mulch for springtails

Thank you! The rock I found them underneath was nestled among a fair bit of damp leaf litter and mulch, so I'm hoping they're springtails (other than the fact they don't jump).

All three photos feature springtails (two different families, though).  The last photo shows only three pairs of legs, eliminating Isopoda.

It seems like they're both springtail species, as suggested by Arthur's comment.
The white one appears to be a type of folsomia, which is easy enough to guess from the appearance (mine don't jump though, I guess ruling out folsomia candida?).
You can compare it to this image of one, from Wikipedia:

I purchased a cheap USB microscope to inspect the second one further. Indeed, as Arthur suggested, it only has three sets of legs:

Additionally, I turned it around and got a look at the underside. I can only guess this is the furcula (though, interestingly, this one doesn't jump either!)?

I'm not sure what the genus is. Could be folsomia, or perhaps hypogastruridae? Either way, they're both springtails! Great news!

source: Stack Exchange

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

sort: votes


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Are all dead plant cells (that die to do a job), have secondary wall?
Can we say that all plant cells that die to do a job (they are dead now), like the outer cell surface of the root cap, have secondary cell wall?

Not all plant cells perform a function when they die.
But a lot do.
Sclerenchyma is refereed to as:

Sclerenchyma is the tissue which makes the plant hard and stiff...

Mature sclerenchyma is composed of dead cells with extremely thick cell walls (secondary walls).

Plant cell death includes necrosis, apoptosis and autophagy and studying how and why they occur is an active area of plant research.
Some plant cells die because they are not provided enough energy. Plants garner energy via the sun and biochemical process known as photosynthesis.
When the days start to become shorter there is less sunlight and parts of some plants die.
E.g. Leaves die.

I add an answer since Andrew's answer "Do all plant cells that die do it while fullfiling a function" and the question asks wheater all plants cells that die to fulfill a function have a secondary wall.
Hyper-virulence response is a plant defence mechanism from pathogenes similar to "scortched earth" strategy. The plant kills all cells near the infection to prevent the proliferation of the pathogen.
If you consider this as a "job" than no, not all cells that fall in the line of duty have secondary walls
Root cap cells are parenchyma cells that undergo programed cell death.
By definition parenchyma cells do not have a secondary wall

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


text:
How many hematopeietic stem cells (in percentage) does the bone marrow contains?
I've found out that the body marrow of an adult weights about 5% of it's total weight. How much (%) of the bone marrow consists of hematopeietic stem cells and how much consists of other non-hematopoietic cells, i. e. "stroma" (%) ? I've also found that in adults, ~70% of bone marrow consists of adipocite cells.

What research have you done to try to find the answer? Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

Im not a biology student. My baby girl was diagnosed with AML - M5a (FAB) and I am trying to understand better What's going on in her bone marrow and how the hematopoesis works in a healthy organism. The doctors explains it, but they don't go so deep. It helps me psihologicaly to understand better the underlying mechanisms.

In the bone marrow usually, the amount of stem cells is very low less than 99% of cells. You can check that on the Williams haematology book. It shouldn't be hard to find online.


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What are the long term consequences of settling an isolated territory with an extremely limited gene pool?
I remember reading about a discredited theory - I'm afraid that, despite some frantic Googling, I've been unable to track down a link - which stated that Australia was first settled by a woman, pregnant with a son, who washed up on a beach. It struck me as surprising that such a theory was ever proposed; I know very little about genetics, but it seemed implausible that all Aboriginal Australians, who seem about as physically healthy as any other race, are descended from just a mother and her son. But could just one woman be the progenitor of a healthy nation? And, if not, what is the minimum number of distantly-related individuals required?
As was stated in the answers to a related question: the more immediate consequences of inbreeding are a dramatic rise in inherited diseases, as well as, perhaps, some mild intellectual disabilities. But what are the consequences over several generations? The Pitcairn Islands and Easter Island/Rapa Nui spring to mind when thinking of historical examples of isolated territories with limited gene pools: both seem to have been settled by around two dozen individuals. Did either community experience specific problems over the centuries due to a small gene pool?

The above, obviously, is concerned with our own species, but I'd be very interested to hear about this topic with respect to other species too. I seem to remember, in one of his "Dark Horse" podcasts, Bret Weinstein talked about how a particular species of Hawaiian bat colonised those islands by way of a single pregnant female being blown off course and/or washing up on a beach. Again, is such a thing plausible, and, if so, what would be the long term consquences for the colonisers?

I think this is a potentially interesting question that I will have a go at answering, but I think the section about whether or not the 'unsavoury goings on' in the history of those islands are related to inbreeding depression needs to go; fitting culture and history in terms of genetics in this way isn't a good avenue to go down, in my view.

@4galaxy7 I am wholeheartedly on board with the point of view that 'fitting culture and history in terms of genetics... isn't a good avenue to go down', and I'll do my best to amend my question along the lines you suggest. I think the way I phrased the question leant itself to being misunderstood. What I meant was: "Did the Rapa Nui community  experience specific problems over the centuries due to a small gene pool?" And not, "Was [insert racist stereotype here] caused by inbreeding?" As I said, I'll amend the question.

Minimum number of individuals needed to start a population

But could just one woman be the progenitor of a healthy nation? And,
if not, what is the minimum number of distantly-related individuals
required?

Healthy is a pretty subjective term, and it's perhaps easier to think of things in terms of a minimum viable population, which is more about straight survival than population health. However, Marin & Beluffi (2018) performed some simulations of humans in a multi-generational space exploration scenario, using 'healthy population' as a desired outcome and found:

A initial amount of 25 breeding pairs of settlers drives the mission
towards extinction in 50 +/- 15% of cases if we completely forbid
inbreeding. Under the set of parameters described in this publication,
we find that a minimum crew of 98 people is necessary ensure a 100%
success rate for a 6300-year space travel towards the closest telluric
exoplanet known so far.

So according to this simulation, it seems quite unlikely that a single woman could be the progenitor for some kind of colony. However, as I discuss a bit further down, some human populations went through bottlenecks of ~20 individuals and remained viable. They may have incurred some health costs, but they would be able to propagate the population.
Long term consequences of founder effects
There are several different case studies of modern human populations relating to the founder effect.
Achromatopsia Pingelap
The atoll of Pingelap in the Pacific Ocean is extremely remote, and up until the late 18th century had around 500 inhabitants. Around then, it was hit by a devastating typhoon which reduced the population size to around 20 individuals. In following generations, it was estimated by that 10% of the estimated 3,000 Pinglapese had Achromatopsia (Carr et al 1971), an autosomal recessive form of colour blindness that otherwise has an extremely low frequency of about 0.003% in other populations (Thiadens 2011).
Subsequent studies used homozygosity mapping in order to determine the genetic basis of the high levels of Achromatopsia. Sundin et al (2000) demonstrated that Pingelapese achromats are homozygous for a missense mutation (serine to phenylalanine) in a highly conserved membrane-spanning domain. This is quite solid evidence for the deleterious consequences of the founder effect in modern human populations.
Jewish populations
There is also reasonable evidence of a severe bottleneck in the ancestors of the global Ashkenazi Jew population. Carmi et al (2014) estimated that the total population fell as low as 350 individuals:

The AJ population is much larger and/or experienced a more severe
bottleneck than other founder populations, such as Amish, Hutterites
or Icelanders.

Other studies have suggested that the high incidence of particular diseases found in Ashkenazi Jew populations was the result of genetic drift following the bottleneck, rather than subsequent co-sanguinity (Bray et al 2010):

We identified genomic regions under selection that account for lactose
and alcohol tolerance, and although we found evidence for positive
selection at some AJ-prevalent disease loci, the higher incidence of
the majority of these diseases is likely the result of genetic drift
following a bottleneck

Rapa Nui
Since you asked about Rapa Nui. Gonzalez-Martin et al (2006) have this to say:

The population of Easter Island is one of the most interesting extant
human communities due to its unique demographic history, its geographic
isolation, and the development of an incomparable culture
charac-terized by the towering ‘‘Moais’’ and its enigmatic writing.
Following the colonization of its population by Polynesians from the
Mangarevan Islands in the 5th century AD, the island remained isolated
up until the middle ofthe 20th century. Under these conditions, with
endogamy levels ﬂuctuating between 61.04–96.54% and given such a small
population, a high rate of inbreeding, and consequently, an elevated
level of genetic relationships would be expected. Using data from
church and civil records, we calculated the consanguinity of the
population of Rapa Nui. The results of this analysis do not support
the hypothesis of a high level of consanguinity.

That said, I have heard some unverified rumours that there was a high incidence of having 6 toes on Rapa Nui, but I can't find anything solid to back it up with.
Norfolk Island
One last example. I've taken this text from a nice paper by Macgregor et al (2009):

The population of Norfolk Island, located off the eastern coast of
Australia, possesses an unusual and fascinating history. Most
present-day islanders are related to a small number of the ‘Bounty’
mutineer founders. These founders consisted of Caucasian males and
Polynesian females and led to an admixed present-day population. By
examining a single large pedigree of 5742 individuals, spanning >200
years, we analyzed the influence of admixture and founder effect on
various cardiovascular disease (CVD)-related traits.

Further...

Marker-derived homozygosity was computed and agreed with measures of
inbreeding derived from pedigree information. Founder effect
(inbreeding and marker-derived homozygosity) significantly influenced
height

Non-human species
I think the last part of your answer is referring to the Hoary Bat, which colonised Hawaii from mainland USA. It was originally hypothesised that the population was the result of a single founding event, but this has been disputed by mtDNA markers (Russell et al, 2015):

Our results point to the colonization of Hawai'i by hoary bats on two
occasions by lineages that experienced distinct evolutionary
trajectories

There is some evidence of single-individual founder events occurring, however (Clegg et al 2002);

Here we undertake a genetic analysis of a series of historically
documented, natural colonization events by the silvereye
species-complex (Zosterops lateralis), a group used to illustrate the
process of island colonization in the original founder effect model.
Our results indicate that single founder events do not affect levels
of heterozygosity or allelic diversity, nor do they result in
immediate genetic differentiation between populations

Further..

A Bayesian analysis based on computer simulation allows inferences to
be made on the number of effective founders and indicates that founder
effects are weak because island populations are established from
relatively large flocks.

There is a lot of literature on this in wild populations which might be of interest, e.g. https://link.springer.com/content/pdf/10.1007/s10592-010-0049-0.pdf
References
Thiadens, Alberta. "Genetic etiology and clinical consequences of cone disorders." (2011). APA
Carr, Ronald E., Newton E. Morton, and Irwin M. Siegel. "Achromatopsia in Pingelap islanders: study of a genetic isolate." American journal of ophthalmology 72.4 (1971): 746-756.
Sundin, O.H. et al. Genetic basis of total colourblindness among the Pingelapese Islanders. Nature Genet. 25, 289– 293 (2000).
Carmi, Shai, et al. "Sequencing an Ashkenazi reference panel supports population-targeted personal genomics and illuminates Jewish and European origins." Nature communications 5.1 (2014): 1-9.
Bray, Steven M., et al. "Signatures of founder effects, admixture, and selection in the Ashkenazi Jewish population." Proceedings of the National Academy of Sciences 107.37 (2010): 16222-16227.
APA
Marin, Frédéric, and Camille Beluffi. "Computing the minimal crew for a multi-generational space travel towards Proxima Centauri b." arXiv preprint arXiv:1806.03856 (2018).
Russell, Amy L., et al. "Two tickets to paradise: multiple dispersal events in the founding of hoary bat populations in Hawai'i." PLoS One 10.6 (2015): e0127912.
Clegg, Sonya M., et al. "Genetic consequences of sequential founder events by an island-colonizing bird." Proceedings of the National Academy of Sciences 99.12 (2002): 8127-8132.
Macgregor, Stuart, et al. "Legacy of mutiny on the Bounty: founder effect and admixture on Norfolk Island." European Journal of Human Genetics 18.1 (2010): 67-72.

I'm always impressed by the answers I receive on SE for my malformed "shower thoughts". But this one stands head and shoulders above the others in its breadth and rigour. Thank you.


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Are there any thermogenic plants which are suitable as houseplants?
I have been wanting to supplement my heating system with some plants that produce heat! I have become aware that there are around 14 species which generate significant amounts of heat for example the eastern skunk cabbage.
However I have also read that many species which are thermogenic release odours such as the smell of rotting flesh. I would rather avoid plants which will make my house smell like this!
Are there any plants which produce heat which would be suitable for storing in my house?

I never knew there were such plants, thank you for educating me! Insulating the walls with plants or moss might be the most effective way, though. You want any structure that creates cusions of small air pockets along a surface. Like wall carpets that are used in some cultures, but green and pretty and happy.

Philodendron bipinnatifidum is a thermogenic houseplant. It is somewhat toxic, so not pet- or small-child-friendly, but commonly grown as a houseplant. However, I do not know if the heat generated would be enough to significantly impact your house; my impression is that most thermogenic plants merely warm their immediate surroundings (so you may need a LOT of plants). As a side note, your scheme to use plant-based-heating would probably also have good effects on air quality :)

Well, this is really more of a fun experiment than a serious project but I am not opposed to having many plants! I will investigate this species further thank you.

The heat the plant produces ultimately comes from the light it uses. Unless the plant produces heat just in the wanted time (winter?) from light absorbed another time; then you would be just as warm by letting the light directly warm your environment regardless of plants.

I don't see how this can be true. Light reflected off my white walls could be better spent absorbed by the plants and used to generate heat.

Yes basically I believe they do not release heat immediately after obtaining the energy from the sun so they would be "smoothing" variation in temperature in the room by releasing heat e.g. at night. From what I understand some species are capable of melting snow in this way.


text:
What fish is this?
I was out snorkeling at Biscayne Bay in Miami, Florida in the shallow waters near the shore when I saw this fish.

What fish is this?
I see it has black spots at the bottom and five white lines along its posterior fin.

I think this is probably a checkered puffer Sphoeroides testudineus based on your location and picture, with the wave-reflection patterning on the dorsal surface and ventral speckling the most obvious features.

(image from https://biogeodb.stri.si.edu/caribbean/en/thefishes/species/4403 )
Could be a different Sphoeroides, but I looked through other species found off Florida and none had similar patterning.

Would you please let the community know how did you find that?

@JossieCalderon I recognized it as a puffer fish from being familiar with puffer fishes more generally, but had no idea of the genus or species. At that point I went to geography, and got a list of puffer fish found off Florida. I started with this one since it seemed most common (showed up first and often in search), then looked at others found in Florida and tried to rule them out. Some of those are found on this page, too: https://biogeodb.stri.si.edu/caribbean/en/gallery/gspecie/4403

Wonderful. It does resemble a pufferfish. Thank you!


text:
is ventricular depolarisation same as depolarisation during nerve impulse conduction?
Does the change in membrane charge accumulation occur in a similar way in heart and nerves cells?

Depolarisation of nerve (here Purkinje fibres) causes Action Potential (bcoz of opening of voltage gated Na channels) which causes opening of Ca++ channels in membrane of heart muscle- results in ventricular contraction
So ventricular depolarisation is actually action potential in heart muscle of ventricles
So both terms are related
Ventricular depolarisation is a consequence of nerve impulse(depolarisation of nerve here Purkinje fibres )
Thnks
Ps: read bracket portion separately

thanks. I assume that the phenomenon takes place in the atria as well during arterial depolarisation .

True Correction atrial depolarisation not arterial

SHORT ANSWER: They are basically the same thing physically.
LONG ANSWER: Depolariation is a feature of any excitable tissue. Heart is no exception.
But the striking feature of Heart is that it can produce periodic depolarisation waves (With a defined Time Period). This ability of heart is due to certain modified myocardial cells, which are called conducting tissue of heart (SAN, AVN, Internodal Tracts, Bundle of His, Purkinje system).
The pattern of Action potential in different tissues is different. In pacemaker tissues we observe mainly a 'SLOW TYPE AP' (Due to L-Type $Ca^{2+}$ Channel); whereas the autorhythmicity is majorly due to an HCN Cation Channel. This eventually travels through Gap Junction from cell to cell to initiate depolarisation. Thus Depolarisation gradually moves from Atria to Ventricles (P $\longrightarrow$ Q-R-S Waves of ECG). In working myocardial cells AP is of 'FAST TYPE', due to VG $Na^+$ Channels)
Note that: Heart's oscillatory AP can be controlled (I mean modified) by ANS intervention.

References: HCN Channels—Modulators of Cardiac and Neuronal
Excitability Stefan Herrmann,* Sabine Schnorr, and Andreas Ludwig*
Jens Schlossmann, Academic Editor ;
Cardiology Explained. Ashley EA, Niebauer J. London: Remedica; 2004.


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How Does The Presence of Livestock on Land Increase Net Methane Production?
It's a hot topic, and I've just read this article that debunks the claim I'm about to make - But even though I read it, I still don't really understand it. I'm happy to change my opinion if I understand the facts.
Suppose we have a closed system, imagine a pasture in an aquarium. Light goes in, grass grows, dies, decays, is recycled, all that good stuff. I imagine the air going into the aquarium is pretty atmospheric, and the air exiting has been changed depending on the amount of CO2 that is absorbed through photosynthesis, the amount of O2 is absorbed through plant respiration, and the amount of greenhouse gasses produced from decaying plant material in the thatch/soil.
(I think I have that right - my biology education doesn't go past high school level)
Now suppose we add a cow into the mix. If anything, to me, the cow reduces net emissions while it grows because less grass decays, and is instead turned into cow. Once the cow is mature, in this closed system, it's only eating and "processing" the grass that was already part of this natural cycle of growth/decay.
Here's where I think I am possibly going wrong:

Does the cow increase the amount of "decay"? Does eating the grass make it re-grow faster, thus speeding up that natural cycle?
Or, does the cow output different (more harmful) greenhouse gasses than the grass would normally produce through decay?

In short, how does the cow increase emissions? It can only have eaten what has already been grown -  And what has grown is doomed to someday decay and be re-released into the atmosphere anyway. I don't particularly like having contrary opinions, so help me out!

Are you familiar with the phrase "gut microbiome"?

@Cell I am -- Is the bacteria in our gut so different from the bacteria in the soil that would break down the plant material? Do they release different gasses? If so, that's probably the answer I'm looking for

Consider that the methane problem isn't really about cows grazing on land, it's cows in factory feedlots.  After all, a couple of centuries ago North America had a similar biomass (estimated 30-75 million, and they're bigger than domestic cattle) of buffalo grazing, without apparent problems.  Buffalo are similar enough to cows that they can interbreed, producing "beefalo".

@jamesqf I had just looked up bison populations then vs. cattle now, funny that you mention it. I understand the process has been industrialized, but they're still consuming organic compounds, right? We're just moving them elsewhere.

@Aww_Geez: I don't know why buffalo grazing, or FTM open range cattle grazing, should result in different amounts of methane being emitted, or even if it does.  Maybe it's a different diet, feedlot animals eating hay or silage instead of fresh grass.  Or maybe it's just statistical manipulation by anti-meat people.  I just think it's something that seems to have been overlooked, and needs explanation.

Ruminant digestion produces a lot of methane.
Cows are ruminants, and ruminants produce a LOT of methane. Sheep and goats are also ruminants but their are far fewer of them. Ruminants use methanogenic bacteria to breakdown their food, these bacteria, as there name implies release methane as a byproduct.  Ruminants produce a lot more methane than other herbivores becasue of this.
Decaying grass normally produces CO2 as do many native herbivores. Cows like most herbivores only convert a very small amount of the grass they eat into cow. Herbivore digestion is not terribly efficient, not surprising the grass does not what to be easy to digest.
Farming also puts a lot more herbivore mass on a piece of land than it would normally have, further increasing the effect, that is the purpose of farming to get more out of the land than simple hunter/gathering could. This is an issue becasue methane is a FAR more effective greenhouse gas than CO2.
Feeding cattle often involves replacing existing ecosystems which high yield feed crops and this can release a lot of CO2 and/or Methane depending on the original ecosystem just from the change, but it also means that feed is now producing methane instead of CO2 it would be if eat by non-ruminants.
Source
Source 2

I see, I think my error in thought was that "all decomposition will release carbon into the atmosphere, what does it matter if it comes from a cow or a pile of compost?". . . Turns out different methods of decomposition create different gasses, of varying harm.


text:
What kind of people are more likely to catch COVID-19?
It is well known that people of old age or with respiratory problems are more vulnerable by the effects of COVID-19. However, I wasn't able to find information on any similar trends on catching the disease in the first place.
So what are the factors predicting the most significant differences in the chance of catching COVID-19?
I'm looking for predictors of the immune system response, whether that would be smoking, age or gender, not obvious notions such as "people from populated areas".
I know the role of ethnicity is much debated but since there's no conclusive evidenence yet, I'm not interested in its role.

Evidence suggests higher death rates from COVID-19 including
among racialised groups might be linked to higher levels of a cell
surface receptor molecule known as ACE2. But this can result from
taking drugs for diabetes and hypertension, which takes us back to the
point about the social causes of such diseases. (The Conversation)

might be worth looking at this for starters. I imagine that occupation is likely one of the biggest predictors of catching covid-19 - https://www.ons.gov.uk/employmentandlabourmarket/peopleinwork/employmentandemployeetypes/articles/whichoccupationshavethehighestpotentialexposuretothecoronaviruscovid19/2020-05-11

@AlexReynolds Can you make this into a full answer?

@AlexReynolds I'm looking for biological, not behavioral determinants.

There are populations that might be more vulnerable due to genetics surrounding the ACE2 receptor. For instance, men are more likely than women to get severe cases of COVID-19:

A growing body of evidence reveals that male sex is a risk factor for a more severe disease, including death. Indeed, globally, ~60% of deaths from COVID-19 are reported in men7,8, and a recent cohort study of 17 million adults in England reported a strong correlation between male sex and risk of death from COVID-19 (hazard ratio 1.99, 95% confidence interval 1.88-2.10)8

The ACE2 gene lies on the X chromosome. In addition to polymorphisms distributed by ethnicity, women have two X chromosomes and may gain some protection from differences in their two alleles of the ACE2 gene, which could make viral binding more difficult, or alter the signaling pathways which result in the subsequent autoimmune response that damages internal organs:

In addition to differential polymorphisms which may explain susceptibility and even outcome in different ethnic populations, the fact that ACE2 is localized to Xp22.2 may help explain the observed male-associated risk. As such, even in the absence of variation in this gene, the monoallelic versus biallelic presence of this gene may impact the natural history and prognosis of COVID-19 in males.

Additionally, in some ethnic populations, expression of the ACE2 gene (as measured by mRNA levels) is lower in women than in men, which may account for reduced infectivity or disease severity in women:

In the normal human lung, ACE2 is expressed on type I and II alveolar epithelial cells. Among them, 83% of the type II alveolar cells have ACE2 expression. Men had a higher ACE2 level in their alveolar cells than women. Asians have a higher level of ACE2 expression in their alveolar cells than the White and African American populations. The binding of SARS‐CoV‐2 on ACE2 causes an elevated expression of ACE2, which can lead to damages on alveolar cells. Damages to alveolar cells can, in turn, trigger a series of systemic reactions and even death.

This aspect of research seems to be ongoing. Region-specific behavior does seem to be the main driver for new infections, however: Ignoring public health guidelines and reopening economies early, calling the virus a hoax, giving healthcare workers garbage bags for PPE, etc. etc. Biology takes a backseat, when governments deliberately put people in harm's way.


text:
What is a subgenomic promotor?
I am looking for a good definition of the term "subgenomic promotor". Can someone help me out?

Welcome to SE Biology. Please read the [tour] and the Help on asking questions. Note that you are expected to research a problem first before posting here. Where are you looking, or, more precisely, where have you looked for this term? I find an immediate hit to a Wikipedia entry on Googling. If that did not solve your problem you need to explain why and describe (preferably link to) the context in which you met the term so we can check out the context.

The spelling promoter is most common in this context, which is important if your search mechanism does not return both spellings.

Can it be a DNA motif where the RNA polymerase will bind to create a subgenomic (m)RNA ?

A subgenomic promoter is a promoter added to a virus for a specific heterologous gene, resulting in the formation of mRNA for that gene alone. Many positive-sense RNA viruses produce these subgenomic mRNAs (sgRNA) as one of the common infection techniques used by these viruses and generally transcribe late viral genes. From doi:10.1128/jvi.74.13.5988-5996.2000
So it seems to be an added promoter that helps express certain genes. Often useful in viral engineering.


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Identify this black dragonfly with a bright bluish-white band around its body
I took these photos around noon in late July in Hsinchu county Taiwan. This particular stick in this particular pond is visited by many dragonfly species. This one was very high energy and nervous but taking my time and waiting for it to return each time I spooked it I eventually got almost (but not quite) close enough to take a decent photo with my phone.
Its body is about 5 cm long and mostly jet-black. However it has a bright, solid white or blue-white band about 1 cm long behind the fat part of it's body along the long "tail section".
I'm showing the two best photos below, for the darker one I lowered the brightness of the photo on my phone before taking it so that the band wouldn't be saturated but it is still extremely bright. It may in fact be slightly blue-hued or that could be an effect of the phone's camera.
Is it possible to identify this particular species of dragonfly?

update: A week later on August 7th I revisited the same pond and it's drangonfly stick and photographed what appears to be the same species, but this time it was perched at a different angle and I was able to photograph the "white forehead" more clearly. The first one is overexposed, so I set the exposure on my cellphone camera lower and took the second image. It's remarkable just how bright white these markings are in bright daylight!

@Alex's answer found a very close match with Pseudothemis jorina but as pointed out there that species is generally found in Southeast Asia, not Taiwan or Mainland China.
Pasting Pseudothemis jorina in the species search box in https://www.inaturalist.org/observations (found in this answer to Identify this large, beige or pine cone-colored squareish beetle and/or the pine cone it's on?) it is recognized and the alternative name "Banded skimmer" is also displayed. I show a screen shot of the map of reported sightings below, and it confirms that the range is SE Asia from northern Laos to Singapore. This is not likely the right species, but it seems close.
I remembered another site for Taiwanese insects that was cited in this answer to Identify this insect with a big “face” pattern on its brown fuzzy wings. The site is in Chinese and I can't read it, but I could use google to search the main page http://gaga.biodiv.tw/ for Pseudothemis and we may have a winner!
黃紉蜻蜓 (Huáng rèn dragonfly) Pseudothemis zonata (Burmeister, 1839 )!
inaturalist.org calls this a "Pied Skimmer" and shows sightings from Myanmar in the west to Davao in the southern Philippines up to to South Korea and southern Japan, and even a reported sighting in northern California!
Like Pseudothemis jorina, this species is also reported to have a "white forehead" (per Google translate). I can almost see it in one of the images in the question, I'll be walking past that pond again today so I'll see if one is there and if it has this feature.
I notices in the second image below that there is also a slight bluish hue to the white band on the lower dragonfly. This could also be a photographic artifact and not real, but it's worth noting at least.

The closest match I can find is Pseudothemis jorina:

It's very similar to your pictures in regards of body shape and the light distinct band, although I'm not sure it would normally be found in Taiwan. It's more common further south like Thailand and Malaysia.

Yes I see what you mean, this looks quite close! More images here; but I also see what you mean that it seems a long way from home https://www.inaturalist.org/taxa/149689-Pseudothemis-jorina (I think I'm going to have to get a real camera very soon)

aha! in one of my other species identification questions I've also had links to  http://gaga.biodiv.tw how about this one? http://gaga.biodiv.tw/new23/s3-64.htm

@uhoh Yeah, that looks even closer and also have the black wingtips. I think you have found it, make that an answer.

Oh for Biology SE it's difficult for me to write answers; in this case I'd appreciate it if you just incorporate this into your answer if you don't mind, it's the same genus after all, I just searched the gaga.biodiv.tw site for Pseudothemis. Thanks!

@uhoh I think that you should write an answer and get credit for your research, but I might do as you suggest if this isn't resolved otherwise.

I just checked and my answer to question ratio in Bio SE is 3/89 which seems a little low, so okay I'll write this up. Thank you for your encouragement!

I checked and my answer to question ratio in Bio SE is 3/89 which seems very low, so okay I've written up an answer. Have a look and please feel free to edit if it needs work. Thank you for your encouragement!

Looks like this species is Orthetrum triangulare commonly known as blue-tailed forest hawk.
It is an Asian fresh water dragon fly species.
As you mentioned that the dragonfly had a bluish hue, it became clear.

Since a similar type of this, called Orthetrum albistylum commonly known as black-tailed skimmer is found in Central and South Europe to China and Japan.
However it has got a black color.

Well this is an interesting situation, because these images look very much (but not exactly) some pics I took 20 minutes later at a different pond! https://i.stack.imgur.com/ldszK.jpg and https://i.stack.imgur.com/arDJx.jpg This one was much more approachable and I could get quite close. The band on the dragonfly in my original posted image looks much more abrupt and contrasty than your images or these I've put in this comment. I wonder if I should post them in the question instead of the one that's there, and then post that one separately? What do you think? Are both the same species?

I don't think this is right. The distinct white band in OPs pictures ends right after the second wing pair, quite different from this. Also, it has black tips on the end of the wings, while this has black markings slightly in front of the tips.

@uhoh are you sure the images which you have given in the comment section are of the same dragonfly which you had seen earlier?

@Alex yes but the op had mentioned about the blue color instead of black. That changed my answer

@Ojasvi no I think they are different, and the images in my comment are a better match to your answer than my question. Why don't I post those two as a new and separate question and you can copy/paste this answer there as well?

@uhoh I think my images do not match your pic in the comment. Since it is not much clear in the pics can you recall whether it's tail had a uniform color or had straps ?  I am talking about the one you have posted in the comment

I don't recall at all, the only thing I have is these and a few more photos very similar to them. The photos are taken from much closer to the insect than my eyes were, I definitely didn't see this level of detail until later when reviewing the photos.

And yes, you should make those two images into a new question!

@Ojasvi okay I'll get to it today, thanks!

@Ojasvi well not quite the same day, but I've finally gotten to it! I’ve now just asked: Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head

@uhoh Thanks for letting me know. However I think I agree with Andrew's answer

@Perhaps it's one of these? Identify these two big, beautiful dragonflies in Taiwan?

@uhoh Thanks! You seem to have a great interest in dragonflies!! :)

I grew up in a cold climate with limited flora and fauna. I've been living here a long time now but I'm always seeing something I've never seen before; it's very exciting for me :-)


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kcat in uncompetitive enzyme inhibition
Why doesn't $k_\text{cat}$ change in uncompetitive inhibition, given the fact that uncompetitive inhibition lowers the enzyme–substrate complex efficiency (which is the reason for lowering of $V_\text{max}$ as well)?
Source of information: https://youtu.be/0ZiCqwtFMTs

Welcome to the Biology community! Aside from grammar and punctuation fixes, your question needs attention to the following issues: 1. Please mention the source of the information (kcat remaining unchanged in uncompetitive inhibition) and the context in which it was given. 2. 'enzyme–substrate work efficiency' is not a well defined term in biology. Can you word it better? Please edit your question to incorporate these changes. Thanks.

The source: https://youtu.be/0ZiCqwtFMTs

Enzyme- substrate complex.

Please add these changes to the question itself (comments might not be read by everyone).

Sorry, and thankyou

Short answer
It all depends on how you look at $k_\text{cat}$ and enzyme concentrations

Long answer
The effect of an uncompetitive inhibitor on $k_\text{cat}$ can be interpreted in two ways.
Interpretation 1:
This is followed in the lecture series mentioned in the question.
See the video https://youtu.be/rNBEUGYu034 from 7:37 to 11:01 minutes. The instructor says:
... the turnover number basically describes the ability of that active site to actually transform the substrate molecules into the product molecules per unit time. Now because when the inhibitor is not bound to that particular enzyme-substrate complex, the active site's ability or efficiency to change that substrate to the product doesn't actually change, we see that the $k_\text{cat}$ value in uncompetitive inhibition also doesn't actually change...
Mathematically, $k_\text{cat}=\frac{V_\text{max}}{[\ce{E}]}$ (where $[\ce{E}]$ is the concentration of enzyme, excluding that which has been inactivated by inhibitor). Now, uncompetitive inhibition reduces both $V_\text{max}$ and $[\ce{E}]$ by the same factor. Thus $k_\text{cat}$ remains unchanged.
Interpretation 2:
Some people do things differently. They regard $k_\text{cat}$ as $\frac{V_\text{max}}{[\ce{E}]}$, where $[\ce{E}]$ is the total concentration of enzyme in the mixture (including inactivated forms). In this treatment, the uncompetitive inhibitor reduces $V_\text{max}$ but $[\ce{E}]$ stays the same. Thus $k_\text{cat}$ is reduced.
Qualitatively, the enzyme in the mixture is now a combination of active and inactivated forms, and thus has lower "efficiency" overall, i.e. lower $k_\text{cat}$.

Thanks for the answer.


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How does noradrenaline result in rise of systolic blood pressure even when the cardiac output is decreasing?
Systolic blood pressure[SBP] depends on the cardiac output. When Nor adrenaline is given there is vasoconstriction due to alpha-1 action on blood vessel, vasoconstriction results in increased total peripheral resistance and thus increases the diastolic blood pressure. The beta-1 action [increase in cardiac output] on heart by Nor adrenaline is counteracted by the reflex bradycardia  resulting in decreased cardiac output. Given the fact that SBP depends on cardiac output and the cardiac output is decreasing, why is there a rise in SBP on administering nor adrenaline?

Vascoconstriction, research it maybe?

Your question involves comparing an observed response to administration of noradrenaline/norepinephrine, which causes vasoconstriction thereby increasing the BP (during both systole & diastole,) to the hemodynamic/pharmacodynamic response of the cardiovascular system as a whole, which is decreased cardiac output & decreased cardiac work.  This is similar to asking why opening a finite water tank eventually slows down even though the pressure increases when you turn on the faucet.

Welcome to Biology.SE! This might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and very difficult to verify by a non-expert. This is a good example of how to format references. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!


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Why does the sandalwood tree produce a fragrant oil?
Why do sandal trees produce fragrant oil? Is there any purpose for it? Is it to make it unpalatable for other herbivorous animals? If so, why do humans find the fragrance pleasing?

Probably the same reasons as lavender, sage, vanilla, lemontree, jasmin, thyme, and other plants used for extracts. They generally protects the plant and aromatic effect is a coincidental side effect for our species. Catnip is an odd example of aromatic side fx.


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Genotypes without Recombination
When given that the parent generation's genotypes are linked traits, how do you determine the genotypes of the F1 generation when no recombination has occurred.  For example, given the parents BbNn and bbnn what would be the expected genotypes of the F1 generation to be?
My current understanding is to follow Meiosis and separate the homologous pairs into Bb Nn and bb nn. Then, because no crossover is occurring, my guess would be that the daughter genotypes are BbNn and bbnn.  However, in reality, the answer should be Bbnn and bbNn.  Am I doing something wrong?  How would I draw the related chromosomes?

My current understanding is to follow Meiosis and separate the
homologous pairs into Bb Nn and bb nn.

No.  If the alleles are linked, then you either have one chromosome with BN, and the other with bn, or you have one chromosome with Bn, and the other with bN.  From this information alone, you can't know which.  Your answer assumes the first situation is how the alleles are linked, the given answer assumes the second.

So.  Just to make sure I'm following, the link could either be BN and bn or Bn and bN but it is impossible to know which.  Thus, either answer would be correct?  If not, how you would you know which way the linking is taking place?
Note:  I am studying from the following practice set if you would like to see the original question text:  https://ocw.mit.edu/courses/biology/7-01sc-fundamentals-of-biology-fall-2011/genetics/linkage-and-recombination-genetic-maps/MIT7_01SCF11_3.2sol1.pdf

It's impossible to know which given only what you posted.  If there's more information, that would change things.

@hhghh You can often figure out the gametic phase of BbNn parent from genotypes of its parents. Sure enough, this information is included in the link you provided. By omitting it in your question you have rendered your question unanswerable.

Ah.  Okay.  Could you elaborate more on how you would do that?  I'm not 100% sure I understand.  Sorry.  So the parents of BbNn are BBnn and bbNN.  From this, how would you determine how linking is taking place?


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Can elephants smell when they have water in their trunks?
For humans, humans cannot smell when they have water stuck in their noses. However, I am wondering if elephants can smell scents when they have water in their trunks, as they are designed to hold water.

Yes they can, as the G protein-coupled olfactory receptors detect presence of molecules and no receptors exist that are inhibited by competitive binding of water molecules.
Both you and an elephant can smell (with) water in the nose! Just try it! I am sure you can smell a difference between pure water and water with a tiny drop of perfume in it if you aspirate it though your nose!

But can elephants inhale while holding water in their trunks? That is the question; because airflow through the nose is necessary for olfaction. E.g., humans can't smell well when they have a blocked nose, people who have had their larynx removed can't smell well because they no longer breathe through their nose (see https://www.cancerresearchuk.org/about-cancer/laryngeal-cancer/living-with/stoma/life), etc.

When you say 'humans can not smell when they have water trapped in their noses', I believe you mean the loss of the sense of scent caused due to nasal congestion, which is due to inflammation, blocking the scent receptors in the nasal cavity (any mechanical blockage preventing odours from reaching the olfactory nerves can cause a loss of sense of smell. This blockage can be due to inflammatory processes like simple infections causing mucus plugs or nasal polyps(1)). Since the basic structure of the respiratory tract is similar in mammals, mucous plugs reduce scent sensitivity in elephants as well.
Olfaction occurs when odourants bind to specific sites on olfactory receptors located in the nasal cavity. They get into the nasal cavity when you breathe or sniff the air.

Molecules of odourants passing through the superior nasal concha of the nasal passages dissolve in the mucus that lines the superior portion of the cavity and are detected by olfactory receptors on the dendrites of the olfactory sensory neurons. This mucus acts as a solvent for odour molecules, flows constantly, and is replaced approximately every ten minutes.
...(2)

(Thanks to @Adhish for the above point.)
If the water itself has a scent, then, as @KaPy3141 pointed out, it can be distinguished because it is in contact with the olfactory receptors. Scent of anything else outside cannot be determined, because they do not reach the receptors.
Elephant lungs are attached directly to the diaphragm and chest wall, allowing them to create much greater "vacuum pressure" for sucking water through their long trunks, while drinking.(3) To open its mouth to breathe would cause the loss of the low pressure and the water column would expelled. So the water column must first be transferred to the mouth, then swallowed before breathing can recommence.(4) Thus, as far as respiration is concerned, they cannot breathe when the trunk contains a column of water, and, as a result, odourants cannot enter the nasal cavity, and elephants cannot smell in this case.
1-https://www.ncbi.nlm.nih.gov/books/NBK482152/
2-https://en.wikipedia.org/wiki/Olfaction
3-https://www.elephant.se/elephant_lungs.php?open=Elephant%20anatomy
4-https://www.quora.com/How-do-elephants-breathe-when-drinking-water

I am not familiar with elephant nasal anatomy, but this answer definitely needs corrections regarding human nasal anatomy and physiology. E.g., (a) mucus, far from being a barrier to olfaction, is ESSENTIAL for chemicals to dissolve and reach the olfactory epithelium. (b) Not everything in the nose is in contact with the olfactory epithelium, which is a localised structure far up in the roof of the nasal cavity. For a review of these topics, see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131780/

Also, the Quora website cannot be considered a reliable source of scientific knowledge. Most of their answers are opinion-based and do not cite any sources.

I agree with your opinion regarding Quora, but the lines I picked were from a well detailed, clear answer. I was looking for a logical explanation of a known fact, and Quora seemed to have it - so I used it. 'Most' of Quora is junk, not all. If there are still things that are not clarified yet, I would humbly delete the lines I borrowed, but that would just make the answer difficult to digest.

+1 for the edits. Also, I just came across this book (which can be previewed for free on Google): https://books.google.co.in/books?id=A3GFYySwY1cC. It talks of the vomeronasal organ, which has a role in olfaction in the elephant, particularly where pheromones are concerned. I'd recommend it, I found the text on pp 411–412 quite interesting.

Humans are not designed to have water inside their nose, so water doesn't get stuck there very naturally. Neither humans nor elephants can inhale new scents if they have their nose blocked by water or otherwise, but the olfactory cavity will still transmit some information to the brain even if the nasal passage is obstructed.
There isn't a lot of research on the subject online.

Oops, I accidentally clicked downvote and can't undo it now.

I think I'll be able to undo it if you make any edit, even if it's just a comma. You could also edit it to include information about the vomeronasal organ, a parallel olfaction system in the elephant (see https://books.google.co.in/books?id=A3GFYySwY1cC). And sorry for the mistaken click again.

oh it's ok. no worries.


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Truncated ORF3a protein of SARS-CoV2! Why? How does it formed?
Across the world so far, we have three truncated ORF3a proteins in SARS-CoV2 in India only.
Can you illuminate me how does a protein (here accessory protein of SARS-COV2) generally get such nonsense mutations and what happens to such proteins in protein-protein interactions?

Your question couldn't be answered using just suggestions: we need proofs. In this study (from which I've quoted the sentence below) authors suggest an implication for inflammation response in patient.

Among the mutations, the ORF3a-Type-3 and ORF3a-Type-4 mutations are restricted to only the Indian patients based in Ahmedabad so far it is identified. These mutations (Q to H, D to Y, S to L) are located near TRAF, ion channel, and caveolin binding domains respectively, suggesting that Type-3 and Type-4 might have effect on NLRP3 inflammasome activation. This unique non-synonymous mutations might affect the virulence of the virus and this needs a special attention from pathogenesis perspective by the medical scientists


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Why are the other bases not used for RNA capping and tailing?
Why does the addition of a 5' cap and that of a 3' tail involve guanine and adenine respectively? Why aren't any of the other two bases added to an mRNA to protect its ends or act as a signal to transport it to the cytoplasm?

Although I can see why you posed your question in the way you did, it is actually two separate questions. The problem with this is you have received an answer that I regard as a reasonable speculation about the polyadenylation, but not about capping. And as @KaPy3141 makes clear, you should realize that answers to questions of this sort are most often only opinions, and the answer may well be “we don’t know” or “perhaps just chance”.

Yeah, I understood that after reading the answer @KayPy3141 wrote. And, I could make sense of the speculation about polyadenylation alone, not about capping. I was just wondering if there was any explanation to each of the processes. As you said, turns out it may be just chance.

I usually try to alert students to all the possibilities of this sort of thing: chance, some structural feature of the molecule that makes it “better”, or its easier to make because the precursors or enzymes are already there or it involves fewer synthetic steps than alternatives. There’s a common tendency to assume it must do the job better, and answers of that sort tend to get accepted uncritically.

As others have pointed out, any answer to this is speculative, there is no reason why it would be impossible to use some other bases. It might be helpful to point out that there ARE alternative 5' caps that are occasionally used in living cells, based on coenzyme A, NAD, FAD, and others, see for example: https://pubmed.ncbi.nlm.nih.gov/27383794/

As David correctly pointed out, my listed theoretical 'reasons' are purely speculative and come closer to a collection of facts that seem interesting for someone who asks the OPs question. In this context it's hard to not fall in the category of the "chicken-egg problem". In the end, all reasons are pseudo-reasons describing phenomena by other phenomena that cannot be explained and will lead to "because it is like that" after some iterations of "why?".

I don't think definite answers exist but I can think of theoretical reasons:

First, Poly A tail can efficiently be synthesized because ATP is the
most readily available nTP, being the main energy source.

More to the mechanism, but this is no explanation to the evolution:
The termination sequence 'TTTATT' on the DNA template and 'AAUAAA'on the RNA is the start of poly-adenylation. But this falls in the 'chicken-egg problem' category.

As a bioinformatician, I happen to know, that 3'UTR is highest in A-content of the 3 genomic contexts and the 5'UTR is highest in G-content of the 3 contexts, so possibly these post-transcriptional modifications further strengthen the compositional differences of the contexts.

For the poly-A tail it might also be relevant to mention that G or C sequences have higher propensities towards structure due to amount of hydrogen-bonds.

I hope there were some helpful pieces of information.


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Why do wild lizards often tap with their front leg?
I have a lot of wild lizards (possibly Podarcis muralis) in my garden, and I have noticed some of their behavior I'd like to understand:

whenever they are in 'still' position on any surface, they are quite often 'beating' with one of their front legs on the surface

in some cases they put the tail of the mate in the mouth

What is this behavior? Some kind of communication?

It would help to specify the species of lizard. If you don't know, can you provide some description, images or location?

Looking on various pictures on the internet I believe it might be something like Podarcis Muralis

I found a paper(1) about the 'tail in the mouth' behaviour in the whiptail lizard, Cnemidophorus ocellifer:

Every time that the female moved, the male followed her. During these periods, he often maintained physical contact, covering her hind legs and base of tail region . The male also performed a series of tongue-flicks on the female's back during this activity. During the observation, the female twice executed a sequence of two or three sinuous, figure-eight movements, which were confined to a small area, and after which, the female moved away. After each movement, the male remained motionless for a few moments and then resumed following her while foraging. After 45 minutes and nearly 15 m from their initial positions, the pair entered in dense underbrush, where we could not continue to observe them. While we observed the pair, there was no agonistic encounter between the accompanying male and other males for access or copula with the female.

The paper continues to explain this behaviour as simply a mating strategy:

Two conditional mating strategies have been described for teiid males (Zaldívar-Rae & Drummond 2007).  1) In consensual copulations,
the male courts the female, slowly circling her for several minutes,
then straddling her and copulating; this strategy is often performed
by a male companion, and thus is linked to accompaniment.  2)
Opportunistic copulations are not preceded by courtship, and are
characterized by a male chasing and holding a foraging female, and not
accompanying her after copulation (Zaldívar-Rae & Drummond 2007).

The 'taping the surface they are on' seems like an attempt to induce vibrations, which is a method of communication.(2)

Some chameleon species communicate with one another by vibrating the substrate that they are standing on, such as a tree branch or leaf. Animals that use vibrational communication exhibit unique adaptations in morphology (i.e., body form) that enable them to detect vibration and use it in communication. These include unique adaptations in ear and jaw morphology that give the animal direct contact with the surface they are standing on, and enable them to detect subtle vibrations. Lizards that live on substrates that can be easily moved (such as thin tree branches or leaves) are probably more likely to use vibrational communication than lizards that live on substrates that do not transmit vibrations as easily, such as the ground or thick tree trunks.

1- https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1676-06032011000400031#:~:text=The%20most%20commonly%20reported%20mating,Bull%202000%2C%20Ribeiro%20et%20al.
2- https://en.wikipedia.org/wiki/Lizard_communication


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What is the fate of the typical tree?
Walking through the local established broadleaf forests dominated by oak and tulip poplar (Eastern U.S.), it is common to find patches of young tree saplings, say 10-20 oak or tulip poplar saplings growing in close proximity. The obvious restriction on living space means that probably at most one of these trees will make it to maturity. In fact, judging by the apparent lack of mid-aged trees of these types in the woods, it seems very possible that none of these trees will last much longer. I'm curious: at what point and how would these trees die? The answer might also help me take better care of trees I've planted in my yard.
I can easily speculate about some causes:

Competition for water/nutrients in the soil
Not enough sunlight
Animal predators
Pathogens

But these suggestions don't answer the how or the when. And it's not clear which accounts the biggest impact. Clearly, the above factors didn't prevent the trees from growing in the first place. And the first suggestion (competition for nutrients) puts a limit on their growth but doesn't say per se why a plant would die.

I think this is really too big to answer, since a lot depends on the kind of tree, the climate, ecosystem, and more.  E.g. in my local (Sierra Nevada) forests, lots of small conifers sprout where there's open space and enough (but not too much) water.  As they grow, the weaker get crowded and die.  The dead trees may be fuel for a fire, or cut for firewood by a human like me.  The survivors may grow for centuries, unless killed by fire or toppled by winds.

@jamesqf We could narrow question down by considering my own locality: broadleaf forests in the Eastern U.S. and more specifically "peak" trees growing in already established forest. Here, oak and tulip poplar seem to be the main ones; I seem to find many mature trees and many very small saplings, but virtually nothing in between. You're suggesting competition for space as the main limiting factor?

In the future, please [edit] that narrowing into your question — comments are both ephemeral and often overlooked so they should not be used to convey information essential to understanding the question. ——— Please also consider taking the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

This is a great question.
Without going into too much detail, there is a series of studies done in northeastern US temperate forests (specifically at Great Mountain Forest in Connecticut, USA) on the growth, survival, and dispersal of canopy trees. In this particular community, light appears to be the primary limiting factor. Seedlings and saplings in low-light environments (i.e. stuck under the canopies of mature trees) grow slowly and have poor carbon balance, which makes them susceptible to mortality (probably from pathogens, although the proximal cause of death of seedlings and saplings is rarely known). Early successional tree species (in GMF, white ash/red maple/red and white oak) grow especially slowly, and hence are more likely to die, in low-light conditions; late successional (hemlock and beech) grow slowly even in high light, but are tolerant of slow growth, so are likely to survive until the adult tree above them dies and falls down.
The exact answer to "at what point do these trees die" is a little tricky, but here's a figure from Kobe et al. showing estimated survival probability for different species as a function of light availability (the assumption is of independent mortality probabilities, given light availability, at each time step, so there is no particular stage at which individuals die in the model).

Kobe, Richard K., Stephen W. Pacala, John A. Silander Jr, and Charles D. Canham. “Juvenile Tree Survivorship as a Component of Shade Tolerance.” Ecological Applications 5, no. 2 (1995): 517–532.
Pacala, Stephen W., Charles D. Canham, John Saponara, John A. Silander Jr, Richard K. Kobe, and Eric Ribbens. “Forest Models Defined by Field Measurements: Estimation, Error Analysis and Dynamics.” Ecological Monographs 66, no. 1 (1996): 1–43.
Pacala, Stephen W., Charles D. Canham, and John A. Silander Jr. “Forest Models Defined by Field Measurements: I. The Design of a Northeastern Forest Simulator.” Canadian Journal of Forest Research 23, no. 10 (1993): 1980–1988.
Pacala, Stephen W., Charles D. Canham, John A. Silander Jr, and Richard K. Kobe. “Sapling Growth as a Function of Resources in a North Temperate Forest.” Canadian Journal of Forest Research 24, no. 11 (1994): 2172–2183.

Interesting; I have seen sugar maple seedlings dominate the low light understory in a mature woods. And red maples die after a few years in a modest light woods; Although both are maples they have different light requirements as shown in the graph.

also see https://www.jstor.org/stable/3450004 (red oak/red maple/tulip tree experiments)


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Convert fasta to ascii?
Is there an algorithm or tool to convert a fasta sequence file (such as the file linked below) into an ascii file for the purpose of gene synthesis?
https://www.rcsb.org/fasta/entry/6EQJ
To the best of my knowledge, the fasta file contains the entire sequence of a protein, in which case there must be a way to convert it to a standard ascii formatted sequence, but I havent been able to find any tools to do so.

Why would gene synthesis require ascii format?

What do you mean with ascii? FASTA is plain text.

FASTA files are just text files, so you can open them up in your favorite text editor to see what they look like. The file you linked has a single entry. The first line begins with > and contains information about the sequence, delimited by | characters – the accession number, chain info, gene name, species, etc. Subsequent lines are just the protein sequence using the standard 20-letter alphabet for amino acids, or the nucleotide sequence from 5'-3' using ACTG. There can be multiple entries in a file, delineated by one or more blank lines.
If for whatever reason your instrument or vendor won't accept FASTA files, a very simple low-throughput solution is to just delete the first line of single-entry files, or delete any lines beginning with > for multiple-entry files. If you have many files to process, this can be automated using Unix/Linux command line tools or a scripting language like Python or Perl.


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Disprove mitochondrial eve is 6500 years old
Some creationists, such as Roger Liebi, actively exploit this article:
A high observed substitution rate in the human mitochondrial DNA control region (published in Nature Genetics, April 1997).
This study directly measured  the mitochondrial DNA mutations rate across 327 generational events (mother-daughter, grandmother-granddaughter, and siblings) and calculated it to be 20x greater than values previously estimated by evolutionary models.
It gives the age of mitochondrial Eve to be 6500 years, which is surprisingly similar to the biblical (Jewish calendar) date.
I am looking for the best way to disprove this position.
Since 1997, has this article been disproved?
What is the best way to disprove this estimate?

It's not much use to argue with creationists who didn't get to their positions from science in the first place. https://biology.stackexchange.com/questions/7184/what-is-a-mitochondrial-eve-and-y-chromosomal-adam may help you.

Thanks for the answer, i also would like to have an info about normal article where the mitochondrial DNA mutation speed is properly empirically measured, means, like in this article but normally, with big base and not "not 10 mutations on 300 events"

If you feel you want to try - its an experience you might learn from, 'Giving up' is not always the right advice.  acheological evidence that is not DNA based... https://www.nature.com/articles/1601646 radiocarbon dating was the most common evidence before 2000.  I do agree with the others that there are alt explanations for all this data tho...  I really do think this a valid question and downvoting it is unfriendly and it doesn't invite the spirit of enquery which is the basis for all the best science.

Yes, people do not read carefully the question and downvote, do not recognize the question is valid and different from mentioned above.
And please do not mention the radiocarbon dating, it is also strongly attacked by creationists, and unfortionately, this attack is fair, because date can easy become old for a young sample, what have fewer isotopes for some reason for example some fish, etc.
I d still like to have study like that, but normal and have a clear mDNA mutation rate, and it would be very, very strange, if the first possible m-Eva would be realy 6500 years old dated...

If the age of Mitochondrial Eve actually is consistent with the Biblical account, then so what? That doesn't prove that there was a flood or that some shepherd led his people across a river. Even a broken clock is right sometimes.

Quick science lesson, if you use a much smaller sample size and get a drastically different answer,  statistically you are far more likely to be the one who is wrong.

You don't need to disprove it with the same paper, you can just ask them where the thousands of skulls and bones dated previous to 10-20k years ago, which are obviously human come from, and why they don't cite modern papers and resort to a single old one? what about flint tools and 400k year old wooden spears? like the yew speak tip of 37cm found in teh sea, dating from 400k years and others from germany dated 300k from neanderthalis.

Estimating the age of the so-called "mitochondrial Eve" (i.e. the most recent common ancestor, MRCA, regarding mtDNA) is a very complex issue, exactly for the difficulty in correctly estimating the mutation rate.
So, it is not so easy to disprove the estimate, but at the same time there aren't particular reasons to choose that (and not the several other available estimates) as the correct one.
I point you to three papers that discuss the issues of estimating mtDNA mutation rates and my be of interest for you:

Estimation of Past Demographic Parameters From the Distribution of Pairwise Differences When the Mutation Rates Vary Among Sites: Application to Human Mitochondrial DNA
Pattern of Nucleotide Substitution and Rate Heterogeneity in the Hypervariable Regions I and II of Human mtDNA
Hypervariable Sites in the mtDNA Control Region Are Mutational Hotspots

It will also be an interesting exercise for you to collect from these papers (and the several references therein) all the different estimates of mtDNA mutation rates (and thus of age of the mitochondrial Eve) and you will realize how reliable the 6500 years (without confidence intervals) would be!
Finally, the literature I provide is well established, but also a bit old (but still more recent than the 1997 paper). You might want to see more recent literature.

Additionally it's very very important to realize that a "biblical Eve" as in "first woman" (a nonsense concept in biology) has nothing to do with "mitochondrial Eve".

I’m afraid that referring to papers is not an answer. Also the verb is “disprove” — the noun “proof” exists in English, but no noun “disproof”. Also note that appropriate questions for SE Biology regarding a paper like this are 1) whether the results are reliable or repeatable? 2) If so, how can they be interpreted? There is no need to even consider interpretations based on religious superstition. The general evidence for the dateline of evolution is supported by a mass of diverse evidence and is not in question.


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Will a nucleic acid sequence deduced from a protein sequence be expressed from a plasmid?
I have a fasta file containing the amino acid sequence of glycogenin-1: https://www.rcsb.org/fasta/entry/6EQJ
I want to create a plasmid that produces glycogenin-1.
Is it possible to use the glycogenin-1 amino acid sequence to produce said plasmid? Or would one need the nucleic acid sequence to do so?

Companies like Origene sell pre-made plasmids in a variety of backbones, with or without epitope tags, for a relatively small amount of money. For example, human glycogenin-1 for US$420.

Thanks @MattDMo.  However I don’t need to purchase a plasmid, I need to make one.  If I had the nucleic acid sequence I would just use that, but all I have is the amino acid sequence, so I need to know if I can use the amino acid sequence to make the plasmid.

You just need to reverse-translate the protein sequence (e.g. on the free online IDT codon optimization tool) and include it in a common plasmid backbone. Basically in order to answer we need to know exactly what you are trying to build.

What happened to the answer to this question and the comments on that answer?  Someone decided to just delete it?

@user1454024 The answer was deleted by the author. Users with high enough reputation (like me) can still see it and the comments, though, and I have two responses. First, you don't need to optimize the codons like you suggested, because once the transcription machinery is in place on the open reading frame, it skips ahead 3 bases (1 codon) at a time. So, unless you expressly design the plasmid to have two overlapping ORFs, you don't need to worry about that. Second, the nucleic acid sequence of your protein is available online, so you don't have to reverse-engineer your protein sequence. [...]

[...] The sequence is accession number NM_001184720.

The NM sequence is for the wild-type protein, not the Tyr->Phe mutant that you have, if that makes any difference.

I lack the knowledge to fully answer your question but I can give some potentially useful pieces of information:

In theory you can easily in-silico reverse translate a peptide
sequence to an unambiguous nucleotide sequence using the GMOs
optimized codon usage. I can share a Python script for that.

Also you could easily search for the 'real' nucleotide sequence in
databases. For example use 'Blast' to find the gene of your peptide
sequence.

But attention! There are known cases of codon-optimized sequences
causing bad protein folding or even (paradoxically) worse expression
levels than the native sequence.

There is software that helps with the design of plasmids, also in
light of use of unique restriction sights, helping to decide which of
your restriction enzymes are applicable.


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Help in understanding a sentence about TCR-MHC interaction and immune synapse formation

T-cell co-stimulatory and co-inhibitory molecules (collectively named co-signaling molecules) play a crucial role in regulating T-cell activation, subset differentiation, effector function and survival. Following recognition of cognate peptide-MHC complexes on antigen-presenting cells by the T-cell receptor, co-signaling receptors co-localize with T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

I'm not sure I understand the second sentence. The language is a little confusing to me. Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR? Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?
Here's my paraphrase of this sentence:

Following recognition of a cognate peptide-MHC complex on an antigen-presenting cell by a T-cell receptor, co-signaling receptors co-localize with (other) T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

Is it correct?

Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR?

Yes. Other TCRs bind other MHC/antigen complexes and they all cluster together, forming an immunological synapse.

Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?

No. TCR:MHC bind 1:1.
Your final paraphrase is correct.


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The blood pressure when blood comes out of body
Is there any certain amount of pressure difference between our blood pressure and barometric pressure when blood of our body begins to come out?

Blood pressure is the pressure above barometric pressure.  When you pump up a blood pressure cuff, or a tire for that matter, you don't have a gauge with a line at 760 torr / mmHg; you're measuring the pressure relative to the air in the room.
Note that blood pressure is only 16% of normal atmospheric pressure.  Imagine what your blood pressure would be if you were the victim of explosive decompression in outer space!


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How is the cell membrane protective?
Generally in biology books, it is written that the cell membrane is selectively permeable and that it has a protective function, as in here
It says that the cell membrane protects the cell from its surroundings. However the selective permeability is only for the hydrophilic substances, and not for any foreign antigen which may be dangerous for a cell.
So how does this count as protective?
Also for hydrophilic substances, carrier proteins are present, ready to take the ionic substances inside the cell.
Hence my only question here is how is the cell membrane protective?

Not sure but by selectively allowing the non polar molecules, it helps maintaining the electrical charges and/or acid-base neutrality and thus aiding in protection of the cell?

carrier proteins don't let just anything in, that is why viruses need to have mechanisms to penetrate the membrane without a membrane the dna/rna could just float in and start changing things

You are right that the membrane doesn't stop everything.  Its main purpose is to separate the inside of the cell from the outside so that you can accumulate resources in it.  Your potassium ions, proteins, sugars, RNA (and DNA, behind another membrane) have to stay inside the cell because they can't dissolve through it.  There are indeed channels and transporters from some hydrophilic substances as you say, but they are usually very specific about what chemicals they will transport.*
The membrane is actually very delicate but it is reinforced by a cytoskeleton, and proteins are embedded in it to transmit force to features outside the membrane (such as desmosomes and hemidesmosomes connecting to other cells or extracellular matrix) so that the membrane itself is never put under strain.  Think of it like a thin plastic bag that can hold water because you put it inside a much stronger container - even though the stronger container is not waterproof.
Many harmful chemicals would not be harmful if they could not get into your cells, so you should not be surprised if they are often hydrophobic and dissolve freely through the membrane.  Some cells have other defense mechanisms (pumps to try to expel the toxins or enzymes to try to break them down), but ultimately any true toxin is defined as the one for which nothing works well enough.
Many pathogens have evolved methods of crossing the cell membrane.  Bacteriophages famously break a hole in the membrane with a special injection apparatus, while many human viruses fuse a cell membrane section they carry around themselves with the victim cell membrane, using proteins that have evolved the right hydrophobic features.  It is hard to defend against such things because our cellular membranes need to be able to fuse with themselves for purposes such as releasing vesicles of neurotransmitter.  The same "no true pathogen..." argument applies - we only get sick from the pathogens that can infect us.  If we lacked these protections, we would be even more vulnerable than we are.

Exceptions, perforins and granzymes, prove the rule:  they are meant to kill the cell affected.

A nice answer, but exceptions only prove a rule when there is no other evidence than the granting of the exception that the rule exists. Check this out on the Internet. So, they are just exceptions with explanations. Nothing to do with rules.

However this does not answer op's question that how cell membrane protects the cell? From your answer it seems that cell membrane is not protective.


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Why are children more active than adults?
I have observed that children are usually more active than adults. For example, in the morning they get up and start playing, they have their lunch and get up and start running, while as adults they are relatively lazy.
Why is this so or is it that my observations are somehow errenous?
Thank you.

Personally as an adult I don't find running around exciting. But adult people definitely would wake up early if that means they are having a resort trip that day or something. Also could be suitable for psy.SE.

Have you done any research into whether or not this is backed up by any scientific research, or if it's just your own observations?

@4galaxy7 my own observations. I made it clear in my question.

I know - but in Biology (and science in general), it's useful and expected to do some research into whether or not your observations are backed up by some kind of scientific research, or whether they are just anecdotal observations.

Thank you for your advice. It was just by observing and I've studied biology only when I was a kid.

@rus9384 nice viewpoint. Definitely plausible.

This is a great question!
As I see you are new and you have explained within the comments above that you haven't studied biology much I will keep the explanation short and sweet.
Young children have fatigue resistant muscles and they also recover faster from high intensity workouts when compared to adults. Children have also been found to use more aerobic respiration when compared to adults during high intensity workouts. This means the child will feel less fatigue and so can continue exercising for longer. As the muscles also recover faster, the child is able to get up and start exercising again much faster than the adult as they will still be recovering.
Aerobic fitness at the muscle level decreases however once the child reaches adulthood and this explains why children have more energy and can play/exercise for much longer. They experience less fatigue and recover faster.
I hope this answers your question.
References:
https://www.frontiersin.org/articles/10.3389/fphys.2018.00387/full

Fantastic answer, do you have any references for further reading? Thank you.

Could you please link the references. Thank you.

Hello, I have added a link to a study which looks at the metabolic and fatigue profiles of prepubertal children and well-trained adult endurance athletes. The study had some interesting findings. They found that the children recovered very quickly even faster than the well-trained adult endurance athletes. I hope this helps and is what you are looking for!

The reference also appeared to suggest they may have bigger lung-to-muscle-mass-ratio and good muscle aeration and circulation and heart characteristics as well as different muscle types.

Thanks for the additional info. I was hesitant in adding these points to my answer as Yasir Sadiq hasn't studied biology much and I didn't want to confuse him. This is also why I didn't go into depth in my answer about fatigue. I remember when I was new to biology and a lot of the answers that were too in depth took me a while to decipher and made learning difficult for me.

Thank you, :-)  .


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rapidly growing mold on flat surface
For an experiment I'm conducting, I need to grow mold on a 2 foot square piece of white fiberglass. I'm in Florida, with high heat and humility, so mold already grows easily. I've seen elsewhere that mold needs organic matter to feed on, to grow rapidly. Ironically, I've seen mold grow on the side of fiberglass motor-homes and showers with no present organic matter. Any suggestions on how to grow mold rapidly on my piece of fiberglass? I thought of locating fiberglass outside, in sun. I could mist it every hour or 2 to create more moisture. Maybe there is something I could rub/spray on the fiberglass sheet to encourage rapid growth? Any other suggestions about applying moisture, light, etc?

Hi Andrew, (great name) what type of mold is it?

I'm not sure of type of mold. I'm trying to replicate the mold growth which naturally occurs here in Florida, USA.  Could be a few species of fungi. Just trying to figure out how to grow dense mold quickly.

Mold is a general name for many species of Fungi, which are heterotroph so they need organic material to feed on. You can see them grow on fiberglass because many organic material can accumulate near or on fiberglass (skin cells, plants root hairs, microbes, oils) and become substrate for the mold.
If you want to grow a specific mold you should first identify it to find the best substrate for that species and not for other. If you simply want mold you can use some kind of starch on the fiberglass and keep it moist (not wet, wetness will give you also oomycetes and bacteria). No need to spray it every 2hrs. You can close the fiberglass with a box, dark box is better (bacteria grow best with light).
You can take (with mask and gloves) some mold and put it on your fiberglass to promote the growing of that mold.
Describing your mold or posting a picture can help to identify. If you see two different colors report both of them and location (center, periphery)

Thank you. What are some general examples of starches I can use to accelerate growth of mold, densely and quickly?

I use potato but any should work. Depending on the Fungi paper of cardobard can be more selective towards it


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Phantom Limb | Is that even possible?
I am fascinated by the fact that an amputee can control their robotic arm by thinking of the actions they would normally execute when the limb was present.
The mind sends signals to the nerve endings of the amputated limb, which gets picked up by the robotic sensor to perform actuation. Can we send similar signal if we assume we have additional limb (Say a third hand)?
E.g. A phantom hand attached to certain part of our body or is it bit of a stretch. Can we train our mind to control a Phantom hand we never had?

Hi @gfdsal. No, where are the nerve endings to this third limb? Non-existent right? (Also it is spelt Phantom)

@Andrew, I can ask the same thing for fhantom limb pain, where your feel pain at the part of the body that is already amputated. The pain lies not on the nerve ending but sent from the brain reference 1, reference 2

Not only can we, it has already been done with primates https://www.nature.com/articles/nn0799_583 behold the first 3 armed monkey.

@John, this is amazing! I reckon with the advent of assistive AI we shall be controlling exogenous limbs just by thinking of actuation!

@john Although the paper added does seem to prove another functioning limb could be added to a body. It is on rats, not primates.

@andrew, my bad wrong link, here is the correct one. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.208.6192&rep=rep1&type=pdf

@John - please don't answer the question in the comments.


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Constitutive Dark Skin vs Facultative Tanned Skin
Most can easily spot the difference between a tanned and dark person. But from my research, the only difference is in the size and concentration of melanin (Jablonski). But this continues to increase with sun exposure, so I was wondering what specific differences are there between people who tan or are naturally dark. Surely they are not the same color, so what is different?

note there are several forms of melanin.


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Horizontal gene transfer in a bacteria
I encountered an old examination question:

Which of the following is not required in Bacteria for horizontal gene transfers?

Infection 2. Translation 3. Transformation 4. Conjugation 5. Transduction

Clearly this is aimed at testing an understanding of horizontal gene transfer. So far I have tried to think about it in the following terms:
A horizontal gene transfer is defined as “obtaining DNA” which doesn‘t stem from the original cell line.
Transformation is the intake of DNA, Transduction is the transfer between two bacteria over a phage, conjugation is like sex (?) between two bacteria. All these would seem to be needed.
However, during Conjugation, a bacterium translates/produces new DNA, so translation would also seem to be needed.
In this case all five items listed would seem to be required. Is this correct?

I have edited your question to make it of more general relevance, focusing on the process of horizontal gene transfer. Your definition of horizontal gene transfer is fuzzy, and you need to find a text book that describes it in detail, checking against the five processes in the question. You only define three of them and your implicit assumption about translation is incorrect. You can edit your question after doing more work.

There's a difference between being technically correct and getting the correct answer on an exam. Yes, theoretically transcription and translation need to occur for the formation of a conjugation pillus, but it's a stretch. That's the only answer that isn't directly related to transfer or uptake of genetic material. If you really want to be technically correct, none of the answers are "required" since that specific word choice would imply they are necessary in every instance of HGT.

Horizontal gene transfer (HGT) is the transfer of genomic information between two already living cells. It is most known in Bacteria but happens also in Fungi (look for Ug99).
In bacteria the genetic information can come from the genome, a plasmid or from random dna or rna strains.
Transformation, Transduction and Conjugation are different kind of mechanisms. You should research them for better understanding.
I guess that by infection they mean infection by a bacteriophage which is a way of HGT.
Translation is the process of synthesize proteins from mRNA
This process is independent of HGT and therefore the right answer to the question.
As far as I know all the mechanisms needed for conjugation (the genomic material, pili and other cellular apparatus) are already present in the donor cell and therefore translation isn't needed. I belive you are confusing translation with transcription (creating RNA from DNA) but that isn't needed either as the plasmids containing the F-factor already exists.


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Diarrhea / constipation: why are they associated with failure of the large intestine (and not the small intestine) to reabsorb water?
When I see reference to diarrhea or constipation, it's almost always in reference to the under- or over-reabsorption of water, respectively, in the large intestine. However, if the large intestine plays a much smaller role in water reabsorption than the small intestine (80% vs 20%), why is the small intestine rarely implicated in these disorders? Is it because the small intestine usually doesn't malfunction in this way and malfunctions are much more common in the large intestine?

Suppose, small intestinal pathology occur, fat absorption won't take place, osmotic load will be delivered to colon and then osmotic diarrhoea occurs. Eg of such small intestinal pathology: celiac, Whipple, tropical sprue, chron, TB etc

Well, a lot of diarrhoeal diseases are because of small intestinal disorders too. (See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3621726 for a detailed discussion.) Something similar holds for constipation: https://www.msdmanuals.com/home/digestive-disorders/symptoms-of-digestive-disorders/constipation-in-adults.