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Difference Junk DNA and Pseudogenes
1-Are Pseudogenes and Junk DNA both Non-Coding DNA or they are different entity? How much Pseudogenes & Junk DNA do we have respectively?
2-I read that Non-Coding DNA has functions, my question is-since we have 98.5% NON-CODING DNA, how much of them has been found to be functional?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done some research on your own before asking questions here — in particular you will find answers to both your questions on this site by searching for "non-coding DNA" and "junk DNA". For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

The ENCODE consortium classifies human and mouse genome elements to try to answer your second question.
Work by ENCODE suggested up to 80% of the genome is functional in some way. In other words, by that upper-bound measurement, there is apparently more to DNA's role in biology than just encoding genes — there's a lot going on under the hood.

Case for Abundant Functional Genomic Elements.
Genome-wide biochemical studies, including recent reports from ENCODE, have revealed pervasive activity over an unexpectedly large fraction of the genome, including noncoding and nonconserved regions and repeat elements (58–60). Such results greatly increase upper bound estimates of candidate functional sequences (Fig. 2 and Fig. S2). Many human genomic regions previously assumed to be nonfunctional have recently been found to be teeming with biochemical activity, including portions of repeat elements, which can be bound by transcription factors and transcribed (79, 80), and are thought to sometimes be exapted into novel regulatory regions (81–84). Outside the 1.5% of the genome covered by protein-coding sequence, 11% of the genome is associated with motifs in transcription factor-bound regions or high-resolution DNase footprints in one or more cell types (Fig. 2), indicative of direct contact by regulatory proteins. Transcription factor occupancy and nucleosome-resolution DNase hypersensitivity maps overlap greatly and each cover approximately 15% of the genome. In aggregate, histone modifications associated with promoters or enhancers mark ∼20% of the genome, whereas a third of the genome is marked by modifications associated with transcriptional elongation. Over half of the genome has at least one repressive histone mark. In agreement with prior findings of pervasive transcription (85, 86), ENCODE maps of polyadenylated and total RNA cover in total more than 75% of the genome. [emph. added]

However, people outside the ENCODE consortium have criticised this research with strong language, such as in this article by noted critic Dan Graur:

Actually, the ENCODE authors could have chosen any of a number of arbitrary percentages as “functional,” and … they did! In their scientific publications, ENCODE promoted the idea that 80% of the human genome was functional. The scientific commentators followed, and proclaimed that at least 80% of the genome is “active and needed” (Kolata 2012). Subsequently, one of the lead authors of ENCODE admitted that the press conference mislead people by claiming that 80% of our genome was “essential and useful.” He put that number at 40% (Gregory 2012), although another lead author reduced the fraction of the genome that is devoted to function to merely 20% (Hall 2012). Interestingly, even when a lead author of ENCODE reduced the functional genomic fraction to 20%, he continued to insist that the term “junk DNA” needs “to be totally expunged from the lexicon,” inventing a new arithmetic according to which 20% > 80%. In its synopsis of the year 2012, the journal Nature adopted the more modest estimate, and summarized the findings of ENCODE by stating that “at least 20% of the genome can influence gene expression” (Van Noorden 2012). Science stuck to its maximalist guns, and its summary of 2012 repeated the claim that the “functional portion” of the human genome equals 80% (Anonymous 2012). Unfortunately, neither 80% nor 20% are based on actual evidence.

Other critics, including Sean Eddy, focus a great deal on what is called the C-value paradox: Given a genome of a certain size, if it was all functional — or a lot of it functional, as the ENCODE consortium has claimed — then it would all be under evolutionary pressure, i.e., you'd expect certain mutation rates to occur, but they don't. Evolutionary biology would say about 5-10% is functional, I believe, based on how much selection takes place and where. So those critics would say (and have had indeed said) a lot of negative things about results reported by ENCODE.
I suspect that the true answer, if there is one, depends on what one defines as functional and as evolutionarily conserved, by what means you measure it, and what the balance is between functionality and conservation. You pick your definitions and processes, and you accept the compromises and limitations that go along with those choices.
Caveat: I am a contributing author to ENCODE papers released in Nature in 2012.

thnk u very much,I m a layman bro.u said 80% of the genome is functional in some way, does it include 98.5% NON-CODING as well? or its just 80% of Coding portion of DNA?
Am I right to say There are many types of Non-Coding DNA, Junk DNA and Pseudogenes are two of them? (plz pardon my amateurish queries)

is it findings of ENCODE that Junk DNA is functional? I heard that there is no Evolutionary Biologist in their Project, is it true?

ENCODE found that a lot of the genome was transcribed, that in no way proves it is all functional.


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Are MacAdam ellipses theoretically predictable?
MacAdam ellipses were found as a fit to experimental results on color matching by human observers. Multiple color spaces attempting to make euclidean distances more perceptually uniform, like CIELAB and CIELUV, are based on these experimental data too.
But what about theoretical side of the color distance question? Is current color vision theory able to predict sizes and orientations of these ellipses? If not, what are the obstacles?

So, are you basically asking if there is a biological explanation (supported by a mathematical model) for the size and position of these ellipses and reason for their occurrence? There is a formula for the ellipses. See here (section 3.4).

@WYSIWYG yes, I'm interested in a biological explanation and calculation — something like, starting from biochemistry (for phototransduction), through neuroscience (or whatever branch of biology studies this), to a prediction of whether a pair of spectral distributions of irradiance of the cones would be distinguishable. The formulas given in your link are from the empirically-based color spaces like CIELAB, which is not what I'm looking for.

source: Stack Exchange

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

sort: votes


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Why are red blood cells not attacked by NK cells?
All cells containing a nucleus present MHC-I, while some specialized cells present MHC-II in addition to that. Since erythrocytes lack any MHC why do natural killer cells not attack them?
It is my understanding that any cell which starts presenting foreign peptides on MHC-I will undergo apoptosis after Th finds them, or if they stop presenting anything at all, they will be eliminated by the NKs.
So what mechanism prevents erythrocytes from being destroyed by the immune system?

Too bad the duplicate has an answer, such as it is, only in a comment under one of the three "Answers".

I'm voting to reopen. The linked question is not a duplicate and doesn't have a suitable answer for this specific question.

The question states, not quite correctly, that "if they stop presenting anything at all, they will be eliminated by the NKs".  In fact, simply not having MHC is not enough to trigger destruction by NK cells.
NKs have a two-part trigger. Part 1 is an activator; part 2 is a suppressor. When the activator is present, and the suppressor is not present, then NK cells will destroy the target.
The suppressor is typically MHC class I, which is present on almost all normal cells. That means that NK cells will not destroy normal cells. There are many different activators, but most normal cells have at least one of the activators also present. That means that NKs are normally primed to destroy, but refrain from destruction because they also sense the suppressor.
With that explanation, it should be clear why RBC are not destroyed by NK cells. Even though they lack the suppressor, they also lack any activators. Since there are no activating signals, the NKs don't need to be also suppressed, so the lack of MHC doesn't lead to an attack.
Sample references:

Two-signal requirement for activation and effector function of natural killer cell response to allogeneic tumor cells
Controlling NK Cell Responses: Integration of Signals for Activation and Inhibition

It's also possible that RBC further protect themselves by showing a "marker of self" on their surface (Role of CD47 as a Marker of
Self on Red Blood Cells) but that doesn't change the important point about NKs mode of activation.

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


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The role of voltage-gated ion channels in chemical synapses
I am trying to understand the mechanisms underlying action potential generation on
the cellular level.
Typically, there is an emphasis on voltage-dependent permeability changes of Potassium (K+) and Sodium (Na+) channels which lead to the respective changes of the membrane potential.
Also typically, synapses in the brain are chemical synapses (in contrast to the smaller fraction of electrical synapses, e.g. in the hippocampus, which make use of gap junctions for signal transmission).
My confusion is now this: Chemical synapses depend on neurotransmitters to trigger permeability changes. The canonical explanation of action potentials is with reference to voltage-gated channels -- how do these two things go together?

Have you learned about what neurotransmitters bind to?

Yes, so I think to understand that they bind to the receptors/ion channels on the neuron's membrane - but then again, it is the NT binding and not the voltage-changes which affect these channels permeability?

Yes. Those are called ligand-gated channels.

I understand that, but if an AP is dependent on ligand-gated channels, I still don't see how voltage-gate channels fit into the picture

When you learn about voltage gated channels and APs, you probably started with resting conditions and then with some depolarization of undescribed origin: it could be by an experimenter or it just "happens". Next you learn about ligand gated channels, which it turns out provide that initial "kick".

I see, thanks! So what you are saying is that the change in membrane potential which "kicks off" the VGICs is in a first step induced by the ionotropic/metabotropic channels?


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Proteomics data Vs Transcriptomics data?
I want to use either of Proteomics or Transcriptomics data for integrating it into my kinetic model. Before proceeding, I want to know what are the advantages of using either of them so that I could make an informed decision on it!
Many studies have shown that the best we can do is integrating both transcriptomics and proteomics data with our kinetic model, but I've some time constraints and have to proceed with only one of those.
My effort and findings: I've found from discussions with researchers that gathering transcriptomics data has an amplification step which increases the chance of finding a particular one whereas gathering proteomics data has no such step but has fragmentation and then rejoining which creates many problems(such as splice variants etc) and thus leads to a loss of data. But a PostDoc told me that even after the loss of that data, I'll get more information from Proteomics data.
I want to know such type of points and want to know if these are valid or not!

This is a broad question. Moreover, you should put in some research effort from your side before asking.

I've updated it @WYSIWYG

By research effort, I mean you should read thoroughly about different transcriptomics and proteomics techniques to know about their advantages and limitations (including the technical issues, cost etc). The answer to your question would be an essay and not a precise paragraph. Therefore your question is not suitable for a stackexchange format.

I sure did put efforts before posting it here. Now, I have written my points in the form of an answer. I tried pasting a table in markdown but was unable to do that. So, I posted in simple bulleted format. Please check it and add suggestions. Thanks! @WYSIWYG

This is what I found from doing some research. Comments are welcome at any point!

Capture percentage for data gathering:

Transcriptomics Data: There's an amplification step in Transcriptomics data gathering methods. Hence, it's possible to capture almost the totality of the Transcriptome using those methods(scRNA seq methods, Nanopore tech, Spatial transcriptomics, etc)
Proteomics Data: There's no amplification step in Proteomics data gathering methods. Those methods have fragmentation and a rejoining step which leads to a loss of the data.

Scalability of methods:

Transcriptomics Data: Scalable methods available
Proteomics Data: Less scalable methods for protein studies

Reference availability:

Transcriptomics Data: Fully annotated references available on consortiums such as ensembl biomart, etc
Proteomics Data: Universal and Comprehensive Human Proteome reference is still in question and because of the incomplete and inaccurate references, much of the newly generated data is being rendered useless

Uniformity

Transcriptomics Data: Lots of publications on pipelines, and their benchmarking available
Proteomics Data: Lack of uniformity across labs/research groups and lack of related literature lead to differences in protein fragmentation and solubilization and differences in algorithms to run analyses

Technical Bias

Transcriptomics Data: Many methods available to tackle cell-bias, noise in data, and batch effects, so as to capture maximum biological variability
Proteomics Data: Cell-wide Mass spectrometry has a bias towards the identification of peptides with higher concentration or contamination from other experiments

Please give your views @WYSIWYG


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What type of snake is this?

We came across this snake when were on a hike in a typical dense forest in the Philippines. . Been wondering if this snake is venomous or not.

Where did you see this?  There are many countries with many "dense forests".

Definitely venomous. It's a viper but you should tell the exact geographical location for correct identification.

My guess is that it is a juvenile temple pit viper (Tropidolaemus subannulatus).

It's in Asia. Thanks for the info!

@Jay Asia is a huge continent with diverse ecosystems. Can you be more precise with the geographical location?

It's in the Philippines.

Can you please [edit] your question to include all the necessary information?

It is a green tree python (Morelia viridis)

I think that's accurate. A young one, perhaps 10 months old.

Green tree pythons are limited to Australia: https://animaldiversity.org/accounts/Morelia_viridis/

Please add some references to support your answer. I guess your answer is also incorrect. The snake looks very much like a viper. Can you add some explanation on why you think it is a green tree python?

Thank you. I would agree. This one is close to a viper.


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What is this tiny, transparent creature found in my home?

Found these in my bathroom, everything was literally crawling with them - there were thousands of those on walls, sink, bathtub... I have all surfaces were sprayed with chlorine spray and with bug repellent afterwards. Still these creatures came back same day, although in smaller numbers.
There's not many features I can use to describe this creature aside from:

Size: very tiny, below 1mm; (black strands are beard hair)
They are pale-yellowish and semi-transparent as it's seen on photos provided
Rather slow and they walk aimlessly on all kinds of surfaces
They seem to be coming from cupboard under the sink, where it's warm, moist, dark and there's access to sewage piping shaft

I'm aware photos could be much better, but they were taken with smartphone combined with a lens from a flashlight to enable macrophotography. Not a best tool for that purpose though.
EDIT: Added circles around creature. Please ignore zoom cursor on first image.


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What causes cellular differentiation?
Each cell in our body contains identical dna. And, yet some cells become liver cells, some become brain cells etc. How this happens , when all of them has same dna? Is it because of epigenetic control of gene expression?

This is a very broad question. Please start reading a textbook on this topic.

You can start with Wikipedia's cellular differentiation article.


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Is this a roach or a beetle?

I'm pretty sure it's a beetle due to the lines on it's back/rear but I'm not positive and if I'm wrong I need to take action quickly. Thanks in advance :)

Welcome to Biology.SE! Have you tried searching for similar images or compared your insect with pictures of cockroaches? It is expected that you will demonstrate that you have done some research on your own before asking questions here — for example try: https://bugguide.net/.  For information on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

Please add where and when the creature was found. This is expected for species-id questions.

@tyersome The OPs insect is not an Anobiidae, as your comment suggests. For one, the pronotum and head angle is completely off.

@fileunderwater: Great I learned something!

This is a click beetle (Elateridae), so not a cockroach. This is most easily seen by the long pointed corners/angles at the posterior part of the pronotum, which is part of the “click” mechanism they use to flip themselves when they land of their back, or to startle predators.


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What kind of worm is this in my food? (Tuna sandwich from canned tuna)

Can I have some assistance identifying this worm which was in a tuna salad sandwich I purchased from a local co-op in Minneapolis MN?

Looks like a maggot (fly larvae) of some sort — see for example the following image:

That particular image is of a common green bottle fly maggot, which has a distribution consistent with your posted location.


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What kind of spider?
I’d much appreciate help figuring out what kind of spider this is. I’m in Western Washington, in the northern suburbs of Seattle. Its outside, on the eaves of the house. Particularly wondering if a yellow sac spider.

Interesting!  The size, shape and posture, as well as the visible patterning on the body, are all reminiscent of Dolomedes tenebrosus, the common terrestrial fishing spider here in the east.  However, there are a couple of odd things here:
1.  Dolomedes is a genus only found (as far as I know) in the eastern half of the US,
2.  The abdominal color pattern is a bit off from what I would expect (dark flank marks at the front of the abdomen, especially), and
3.  That looks like an egg sac the spider is sitting on top of, as if it was guarding, but fishing spiders (as far as I know) do not make egg sacs like that - they make ball-shaped egg sacs which they carry around with them using their fangs to hold them.
The thing is, nothing else rings a bell with me - the only other large wandering hunter that would be anything like that in the Pacific NW, that I know of, is the Giant Crab Spider Olios giganteus, which doesn't look much like that, although it does make a silken retreat/egg sac protection.
I confess that I am stumped, although I can confidently say that it is not a Yellow Sac Spider.
However, I can suggest two good options for identification:
the Burke Museum: https://www.burkemuseum.org/collections-and-research/biology/arachnology-and-entomology/contact-form
and Bug Guide: https://bugguide.net/node/view/6/bgimage
both of which can often do identifications from photos alone (although with spiders, this can sometimes be tricky).
Good luck!

This is not a Cheiracanthium (a yellow sac spider) as those are fairly homogenously-colored with no discernable markings or speckles.
This is a Running Crab Spider of genus Philodromus. Here is a picture of Philodromus Spectabilis from Washington state:

(Source: https://inaturalist.org/observations/140737985 identified by two arachnologists )
The crab-like stance places this in the crab and running-crab superfamily Thomisoidea and the fact that the second legs are its longest legs separates this from the normal crab spiders, placing this is the Philodromidae (running crab spiders) as regular crab spiders have their front-most legs longest.
There are no Giant Crab spider (Olios sp) this far north in the US.
There are other genera of running crab spiders in Washington, but they are distinguished by a darker cardiac mark and/or significantly different leg proportions.
It is not always possible to identify spiders to species level with photos, but P. Spectabilis is a close match. There are over a dozen species of Philodromus found in Washington state.


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Is there any biosafety level scale for plant pathogens?
Biosafety levels commonly defined on basis of human/animal pathogens, but what would be the biosafety levels for plant pathogens?

Plant pathogens are not a health hazard to the experimenters. However, they can pose health hazards to plants and cause damage to ecosystem. There are plant biosafety levels: BL1-P up to BL4-P (also sometimes abbreviated as BSL-1P and so on). The four levels have an increasing order of stringency of containment. Containment of plant pathogens (also seeds and pollen) is the primary concern, not exposure to them.
From NIH guidelines:

For research involving plants, four biosafety levels (BL1-P through
  BL4-P) are described in Appendix L, Physical and Biological
  Containment for Recombinant or Synthetic Nucleic Acid Molecule
  Research Involving Plants.  BL1-P is designed to provide a moderate
  level of containment for experiments for which there is convincing
  biological evidence that precludes the possibility of survival,
  transfer, or dissemination of recombinant or synthetic nucleic acid
  molecules into the environment, or in which there is no recognizable
  and predictable risk to the environment in the event of accidental
  release.  BL2-P is designed to provide a greater level of containment
  for experiments involving plants and certain associated organisms in
  which there is a recognized possibility of survival, transmission, or
  dissemination of recombinant or synthetic nucleic acid molecule
  containing organisms, but the consequence of such an inadvertent
  release has a predictably minimal biological impact.  BL3-P and BL4-P
  describe additional containment conditions for research with plants
  and certain pathogens and other organisms that require special
  containment because of their recognized potential for significant
  detrimental impact on managed or natural ecosystems.  BL1-P relies
  upon accepted scientific practices for conducting research in most
  ordinary greenhouse or growth chamber facilities and incorporates
  accepted procedures for good pest control and cultural practices.
  BL1-P facilities and procedures provide a modified and protected
  environment for the propagation of plants and microorganisms
  associated with the plants and a degree of containment that adequately
  controls the potential for release of biologically viable plants,
  plant parts, and microorganisms associated with them.  BL2-P and BL3-P
  rely upon accepted scientific practices for conducting research in
  greenhouses with organisms infecting or infesting plants in a manner
  that minimizes or prevents inadvertent contamination of plants within
  or surrounding the greenhouse.  BL4-P describes facilities and
  practices known to provide containment of certain exotic plant
  pathogens

Section III-D-5-a. BL3-P (Plants) or BL2-P + biological containment is recommended for
  experiments involving most exotic (see Section V-M†, Footnotes and
  References of Sections I-IV) infectious agents with recognized
  potential for serious detrimental impact on managed or natural
  ecosystems when recombinant or synthetic nucleic acid molecule
  techniques are associated with whole plants.

†Section V-M.  In accordance with accepted scientific and regulatory practices of the discipline of plant pathology, an exotic plant pathogen (e.g., virus, bacteria, or fungus) is one that is unknown to occur within the U.S. (see Section V-G, Footnotes and References of Sections I-IV).  Determination of whether a pathogen has a potential for serious detrimental impact on managed (agricultural, forest, grassland) or natural ecosystems should be made by the Principal Investigator and the Institutional Biosafety Committee, in consultation with scientists knowledgeable of plant diseases, crops, and ecosystems in the geographic area of the research.

These descriptions refer to plant experiments in greenhouses. When working with plant pathogens in a lab (in vitro culture or on whole plants in incubators), similar guidelines should be followed.


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Reptiles are a paraphyletic group because?
Here is a question I am trying to find the answer to

Reptiles are a paraphyletic group because... ?
A) They include worm lizards, which have no limbs
B) The group doesn’t include birds
C) The group doesn’t include mammals
D) Not all of them have three- chambered hearts

I’m a bit confused about the reasoning. I know a paraphyletic group does not have all of its descendants so if birds were to be included it would become monophyletic. So is B the answer? Could anyone help explain it better?

I think the question's phrasing is a little wobbly, which make it a little hard to understand. But I think you understood what your teacher was expecting. I agree with you, answer is B.

I think the question's phrasing is arguably a little wobbly, typically as to the nature of what someone would mean by the term "reptile". But I think you understood what your teacher was expecting. I agree with you, answer is B.
Reptilia is a clade (clade = monophyletic group) that encompasses all species that we traditionally classify as reptiles + all birds. Hence, our traditional definition of reptile makes up for a paraphyletic group as birds aren't included.
Related post: If dinosaurs could have feathers, would they still be reptiles?

To me it seems "Reptiles are a paraphyletic group because the group doesn’t include birds" is fine and not the least "wobbly", assuming Reptiles != Reptilia.


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Can Green color give Rest to Eyes?
Is it correct that Green color gives rest to our eyes compare to other colors?

I think "eye-soothing" effect of green plants is more of a psychological/ neuro-psychological effect than directly a rest on eye.

Theoretically any light of visible spectrum (and their mixtures, including white light) will cause our rod and cone cells to work. none will make the rod and cone cells to "rest".

In a quick search I found some blog posts claiming that some scientists believe that green gives rest to the retina, because green is in the mid range of the visual spectrum and therefore "easiest" to detect.. Of course these posts didn't cite any sources for that. So, I couldn't track down the supposed research..

@Rk003 not sure, if you're talking to me, but as I said: I couldn't find a reliable source for that claim and therefore don't believe it.

Similar question and answer is  here

In our eyes, the dioptric difference between the dispersion of red versus blue light is approximately 2D.

Remembering that the human eye's peak spectral sensitivity lies at 550 nm (green), the human retina is deliberately placed such that it is in between the dispersion of white light, i.e., between red and blue. This optimizes the best level of focus specifically for its peak spectral sensitivity. The pupil and the nucleus of the lens also help to minimize chromatic aberration.
In short, the eye is constructed such that it is easiest to focus on green light, which is in the middle of the visible spectrum and has the strongest receptors.


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What are these little bugs?
I recently found at least 50 of these little bugs roaming around my window  sills indoors in my bedroom right behind the head of my bed. I can’t seem to find what they are. I’d love tips on what they are or how to get rid of them. They’re extremely small probably no larger than 1 mm. I tried vacuuming them away but I still see plenty of them.

Welcome to Bio-SE! Where is your window sill located? We require a where and when component to all species-ID questions. A size estimate and slightly better pictures would also be useful.

Related: Help identify this mite?, Bug Identification: Tiny Bugs, Tiny white very hard cell bug! Please help to identify!

These are very likely mites (notice their small size and 8 legs). Based on their size, appearance, and abundance, I'd guess they're bird mites (family Macronyssidae). Since they're near your window, I assume you either have a bird nest outside your window or frequent bird visitors to your window.

 Credit: user Aewills on bugguide.com
you can find existing posts about bird mites on Bio.Stackexchange below:

Help identify this mite?
Bug Identification: Tiny Bugs
Tiny white very hard cell bug! Please help to identify!


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What would the ploidy of a multinucleate cell be?
If we have a haploid organism, and it undergoes karyokinesis without cytokinesis, would the organism be considered haploid or diploid?

Ploidy is generally defined in terms of the number of chromosomes in the nucleus, rather than the number of chromosomes in the cell.
Some examples in support of this:
- A paramecium has a diploid micronucleus and polyploid macronucleus
- Muscle cells are generally considered diploid even though they have multiple nuclei
- The additional chromosomes in mitochondria and chloroplasts are not considered to make cells polyploid, even if the organelle itself may be polyploid.
Thus, I would assess a cell such as you describe to be haploid, albeit with two nuclei.

This was very helpful, thank you so much!


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Protein inhibitory process
I usually find substances that activates proteins, like ApoA-I, but I don't find substances that inhibit it.
So in an experimental design, could I consider the absence of a drug that directly acts on the increase of a protein could be considered an inhibitory process?

Your question is not very clear. Can you please rephrase it and add some relevant background?

There are many inhibitors of protein function. Inhibitors are more common, in fact.

No, absence of an stimulating substance is not appropriate to consider as inhibition.
To see why, consider a situation where there are two such substances, substance A and substance B, which can both stimulate protein P (many such relations exist).  If you add only substance B, then protein P will be stimulated. Since P is being stimulated in this case, it would thus not be reasonable to describe the protein being inhibited by the lack of substance A.


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How do carbon 13:12 ratios confirm the biological origin of oldest microfossils?
I was reading this article about how Schopf and Valley’s findings in 2017 confirmed that the 3.5 billion–year-old microfossils found in the Apex chert of Western Australia are indeed remnants of living organisms, as opposed to abiotic geological structures. The most detailed part of the article’s explanation is:

Using SIMS, Valley’s team was able to tease apart the carbon-12 from the carbon-13 within each fossil and measure the ratio of the two compared to a known carbon isotope standard and a fossil-less section of the rock in which they were found.
“The differences in carbon isotope ratios correlate with their shapes,” Valley says. “If they’re not biological there is no reason for such a correlation. Their C-13-to-C-12 ratios are characteristic of biology and metabolic function.”

Can someone explain this in more detail? In particular, why should this ratio be different in biological carbon samples, compared to abiotic carbon samples?

Via: https://en.wikipedia.org/wiki/Carbon-13#Uses_in_science

Due to differential uptake in plants as well as marine carbonates of 13C, it is possible to use these isotopic signatures in earth science. Biological processes preferentially take up the lower mass isotope through kinetic fractionation.

Via: https://en.wikipedia.org/wiki/Kinetic_fractionation

All organisms preferentially use lighter isotopic species, because "energy costs" are lower, resulting in a significant fractionation between the substrate (heavier) and the biologically mediated product (lighter). As an example, photosynthesis preferentially takes up the light isotope of carbon 12C during assimilation of an atmospheric CO2 molecule. This kinetic isotope fractionation explains why plant material (and thus fossil fuels, which are derived from plants) is typically depleted in 13C by 25 per mil (2.5 per cent) relative to most inorganic carbon on Earth.

The second Wikipedia article points out that kinetic fractionation also occurs in at least some known non-biological processes. So why is this being used as evidence of life?

Non-biological processes referred to in the Wiki article appear to discuss oxygen and hydrogen, not carbon. However, I have not read the paper you're referencing. My guess would be that selective uptake of lighter carbon isotopes is evidence of carbon-based life, and that there are other indicators to corroborate that conclusion.


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Where does the carbon in new spring leaves of a deciduous tree come from?
When a leafless deciduous tree 'comes to life' in the spring and puts forth new leaves, where does the mass for these leaves come from? The tree has no leaves to make use of photosynthesis to get the carbon it needs to grow these leaves, so where does the carbon come from: has it been stored in the root system over winter just for this purpose? And if so, has enough been stored for the tree to produce most if not all of its new leaf growth for this season, or only enough to get a few leaves out that will 'take over' the task of providing carbon fixation (making sugars) via photosynthesis to grow the remaining new leaves?
It has been suggested in the comments that the new leaf buds were grown at the end of the previous season. It would seem to me that this strategy for new growth in the spring would be fraught with all sort of dangers from 'winter kill', so these buds would not remain viable come the next spring. So, are the sugars needed for new spring growth coming from the roots or last seasons leaf buds?

Possible duplicate: https://biology.stackexchange.com/questions/1041/how-does-a-plant-grow-before-photosynthesis-is-possible The first answer might be a bit unclear that it is not only talking about seedlings but everything written there applies to wintering trees as well. Though there still may be an additional question here to be answered as far as the precise storage mechanism.

@BryanKrause Thanks for the link. The first answer seems to say that the carbon for new growth comes from stored sugars. Was this sugar supply 'stored' in the plant's roots? Was it stored there to be ready for its new spring growth? How much mass are we talking about, i.e., enough to grow all new leaves for that season, or just enough to get a few leaves out that will take over through photosynthesis?

Leaf buds are usually prepared the preceding summer/autumn.

I think you could edit your question to add what you've learned and clarify what you'd still like to know. I'm not a plant guy so I'm uncertain if some of your questions are too broad across the diversity of deciduous trees. SE questions are supposed to be individual questions rather than multiple but think yours are probably related enough to be part of one question.

@user1136 Answers are not supposed to be posted in comments.

While I can't provide references to actual studies, simple observation suggests that it must be stored in the roots, at least in part.  That observation is the existence of maple syrup (and other tree syrups, such as birch: https://practicalselfreliance.com/trees-species-tap-syrup/ In the spring, before leaves start to grow, sugar-rich sap rises from the roots, and can be collected by tapping the tree.


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Is there a maximum testosterone limit, or is it more accurate to say use?
I am constantly amazed at how we cannot differentiate between male and female.
The International Olympic committee sets the target testosterone at 5 nmol per deciliter with active androgen receptors.
What are active androgen receptors? Do they count sex hormone binding globulin (SHBG) bound Testosterone, especially in the brain? If I was serious about asking someone who would I ask ?

Whatever is the exact definition of the threshold that the Olympic committee sets, it's going to be relatively arbitrary and unfair to some people.
When it comes down to it, biology is generally messy and blurry, and that includes matters of sex and gender.  Thus, even if most people cluster in a fairly straightforward manner into male and female, there are all sorts of things like androgen insensitivity syndrome that can end up causing a person's normal body state to be judged as too extreme for their gender.
In the end, there is no simple line that can be drawn simply because the biology of gender permits many different ways for naturally occurring variations to form a continuum across any given metric that one might wish to establish.


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Why is the variance of the Wright-Fisher model not equal p(1-p)/(2N)?
I was looking at the properties of the Binomial probability distribution and it says that the variance is np(1-p). In population genetics, n = 2N. So I would expect to see that the variance is 2Np(1-p).
But when looking at the Wright-Fisher model, I often see that the variance is $p(1-p)/(2N)$ (see this presentation page 6).
How to derive the variance of the Wright-Fisher model to get this variance from $Prob\{X=i\}=\frac{n!}{i!(n-i)!}p^i(1-p)^{n-i}$?

The binomial variance $2N p (1-p)$ is for the number of individuals $n'$ carrying the allele in the next generation. The frequency of the allele in the next generation is $p'=n'/(2N)$, so its variance is $$\text{Var}[p'] = \text{Var}[n'/(2N)] = \text{Var}[n']/(2N)^2 = p(1-p)/(2N).$$

This is because $Var[n'] = 2Npq$ which is the variance of the binomial model $(2Np(1-p))$ Right? Because $n'$ is also coming from a binomial sampling

@M.Beausoleil: yes, exactly.


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What is the total mass of leaves on an 'average' mid-latitude deciduous tree?
I know that this is a broad question as there are a very large number of different species of tree with all manner of profiles, height, leaf sizes, etc. My ultimate goal is to estimate the total mass of leaves that fall each autumn in both the Northern and Southern Hemispheres, separately. It seems appropriate to ask for a single tree to start with, hence this question. If there is a better way to get to the final 'ultimate' answer, feel free to post it.

You might have better luck asking how much leaf litter falls on a unit area of forested ground on average, I suspect that at least has estimates. Per tree will never give anything reliable due to the wide varieties and sizes of trees.

There's a big difference between the mass of the leaves on the tree, and the mass when they fall and dry out.  Anecdotally, I'd guesstimate that the leaves from my large maple tree that I rake up in fall (when they're quite dry) weigh a couple of kg or so - say maybe 5-20 kg if you count the ones that blow into the neighbors' yards.


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Difference between Premature Atrial Contraction and Atrial Fibrillation
what is the difference between Premature Atrial Contraction and Atrial Fibrillation. I know that both have irregular heart beat but have normal QRS complex. Both have abnormal or absence P waves but a normal T waves.
Can PAC be considered as an isolated event? and AFib be considered as chronic event?

Atrial Fibrillation is a dysrhythmia while PAC is an early depolarization coming from the atria. An occasional PAC can be normal for some people. In that case their heart rhythm would be a sinus arrhythmia instead of a normal sinus rhythm.
In AF, the atrias don’t contract/pump at all, but they quiver/twitch due to the many simultaneous ectopic foci that are being discharged from random cells; similar concept to Ventricular Fibrillation. Due to the atrias not fully depolarizing, you won’t see any P waves on the EKG. If/when an electrical discharge reaches the AV node, it goes through the normal electrical condition system from there, forming a narrow QRS complex. AF is the only irregularly irregular rhythm, meaning that the QRS complexes have no regularity at all, and have no pattern to their irregularity.
Video example of AF.
Rhythm Strip

As for PACs, the atrias depolarize earlier than expected creating what looks like an early beat. The next beat though will be later than expected. The pacemaker cells “reset”, returning to their pattern after this early beat.

Both AF and PACs can be acute or chronic depending on the person.

i see~ thanks for the response!

another question, so does it mean you cannot have PAC in two consecutive peaks right? because otherwise clinically how would you know the atria depolarized earlier or just because the patient's heart rate is increasing

You can have what’s called a run of PACs(PJCs and PVCs as well). Remember that what is seen on the EKG is the electrical activity, not the actual contractions. On the cardiac monitor the HR will increase a bit. There is a debate on whether to count premature beats as part of the heart rate or not. You can tell if someone has a premature beat by feeling the pulse, but to know the type of premature beat, you’ll need an EKG. Clinically, premature beats are not an immediate life threat because they can be caused by something as simple as stress. A run of PVCs (aka run of V Tach) is dangerous.

I hope this answered your question, as I was a bit confused about the second part.

Not quite haha. So you know there are bigeminy and trigeminy for PVC, because you can have consecutive premature ventricular contraction. But my question can you have consecutive "premature atrial contraction"? Because wouldn't it be difficult to distinguish a consecutive PAC and an increased heart rate?

Yes you can have bigeminy/trigeminy PACs, but I don’t understand your point on increased heart rate. Any time you have a premature beat, your heart rate on the cardiac monitor will increase by a couple of beats because the monitor calculates approximately how many beats per minute your heart will beat based on how often it senses electrical activity. This is not clinically important as you might be thinking it is. You can always manually calculate the pulse rate or use a 6 second strip to calculate the heart rate accurately.

With irregular rhythms, it’s more important to know the range of the heart rate rather than the actual number. For example, Atria fibrillation will always have different numbers displayed on the monitor, but as if the range of it is in the 70-85 range, then you know it’s a stable rhythm (if the patient normally has AF).


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Is there any biological basis for the commonplace "eyes popping out" cartoon?
We might all be familiar with images like these below:

I see this clearly "works" in a cartoon context. It makes a point. That "eyeballs" hanging outside belong to the individual and can be shown next to him and not in the floor or so. But, is there any biological basis for this? Is something like this ever possible? Probably the answer is no, as the (optic) nerve connecting the brain with the "eyeball" surely cannot be extended like that. Would the eyeball actually hold its shape?
PS: for the sensitive among the crowd (including myself), please do not post gore-like pictures to show what actually happens. If want to provide some visuals, diagrams might suffice.

I once saw a guy in "Ripley's believe it or not" who could pop his eyes out to some extent (not till the optic nerve is visible).

Also, see this guy. What extent of eye popping are you asking about? Usually, in cartoons eye popping is associated with an extremely delightful visual stimulus. Are you asking if such a thing happens in real life?

@WYSIWYG "What extent of eye popping are you asking about?" Well, that's probably an important part of the answer. If this is ever possible to any extent, or if actually it doesn't work that way at all. E.g. optic nerve cannot be extended and so can ever be visible.


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Insertional inactivation using pBR322
I have questions regarding "selection using insertional inactivation".
In a typical DNA recombination experiment using plasmid pBR322 where a new gene in inserted in the place of tet gene, it is said that entities with the recombinant plasmid can be selected by growing all the bacteria in two different medium: one with tetracycline and one with ampicillin.
I know that pBR322 contains two genes that make it resistant to both tetracycline and ampicillin, and also that the newly created plasmid will only be resistant to ampicillin, since its tet gene is no longer functional.
So in the plate with tetracycline, only entities with the original plasmid will grow. In the plate with ampicillin, however, entities with the original plasmid and the modified plasmid will grow.
How can this be a selection when two different types of entities are growing in one plate?
Am I misunderstanding the meaning of "selection" in this case?
My explanation above seems very immature, so it would be great if someone can provide me with deeper understanding.

Yes. I concur with canadianer.  As currently described, replica plating is the way to go.  IF: you had a drug that killed bacteria resistant to tetracycline, THEN: you could use that as a selection.

The ampicillin plate is selecting for bacteria transformed with the plasmid, either the original or recombinant, whereas the tetracycline plate is selecting only for bacteria transformed with the original plasmid. Since you are only interested in the recombinant plasmid, you need to do some form of replica plating and compare the two plates to infer which colonies contain the recombinant plasmid (those which grow on ampicillin but not on tetracycline).


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Why was the evolution of large, slowly reproducing organisms preferred?
One of the very basic facts that Darwin pointed out was about the life span of organisms. Organisms with smaller lifespan reproduce quickly and hence variations are produced faster. This helps in faster evolution.
One of the main goals of living organisms is to reproduce, this fact being the backbone of neo-Darwinism.
For organisms with longer life span, say humans, the amount of time required for new generations to come up, as well as the energy requirement is high, much higher if compared to bacteria. Then why did evolution of complexity arise if bacterial life forms could survive in harsh conditions and reproduce and mutate faster?

Successful lineages survive. That doesn't mean they are restricted to minimally long generation times. All that is required is that they compete sufficiently in the struggle for life. Sure, they may adapt slower, show lesser variation, require more energy for sustenance, etc. But it works as an evolutionary strategy, and large animals not being extinct are a testament to this. I don't see the difficulty of the question, sorry! Additionally, there are advantages that come with size.

This is a good, but very broad (and complex^^) question. Bacteria and humans are worlds apart (and both complex in their own way). If you mainly meant complexity of a single organism, the link S Pr gave should give a good overview, this wiki article mentions a couple of mechansims that can affect complexity. I'd recommend you to focus on complexity in a specific trait (like size), since otherwise a proper answer might not even fit in a textbook.

Related: If evolution is not about increased complexity, why does so much complexity evolve?

The simple answer is that the evolution of large, slowly reproducing organisms is not preferred: it is simply not selected against.
The key mistake in your thinking is this statement:

One of the main goals of living organisms is to reproduce

Most living organisms have no such goal, they simply take actions that have, historically, led to the continuation of their lineage.
In a complex world, there are many different strategies that can lead to survival and propagation of an organism, and cooperation between cells is one of them.  Even simple bacteria often form large multicellular aggregates, which can provide physical advantages for their members over dissociated individuals, such as resistance to physical damage and formation of protected microclimates. The inside of your body is another such protected microclimate. So multicellularity can be quite advantageous.
As for limiting reproduction: remember that the closest competitors every new organism has are its own relatives, who occupy the same space and compete for the same resources.  Even bacteria will often limit their reproduction when resources are limited. Reproduction also takes significant resources. A faster reproduction then, is also not necessarily advantageous for long-term survival.
Bottom line: neither large nor small, fast nor slow is preferred.  Instead, the study of evolution predicts that we will see what we do see: a multiplicity of forms and strategies adapted for different niches in the ecosystem formed by their interactions with other species and the external environment.

Also, we could easily argue that the large & slowly reproducing life forms are not PREFERRED, they just manage to survive.  There are many more rabbits & mice than elephants & whales, they're outnumbered by insects, which are vastly outnumbered by microorganisms.


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How can a drink contain 1.8 kcal energy while 0 g fat/carbs/protein?
How is it possible that the Red Bull Zero contains 0 gramms of fat, carbs and protein, but it still has 1.8 kcal of "energy".
I always thought that the human body can gain energy only from 3 kinds of nutrients: fat, carbs and protein. Is there a 4th kind? Or they just display an energy value that's not accessible to the body?

This is slightly off-topic, since it's very unlikely to be related to your question - but yes, humans can gain energy from many more things than just sugar, fat and protein; it's just that those three are dominant in the food we eat. One example would be alcohol (ethanol); we can also process polyols and organic acids. Even fiber, which is often considered empty (and useful, mind) filler can be partially digested for about 2 kcal/g - so a single gram of fiber would be enough for that energy value (while being both a carbohydrate and a (poly)sacharide, it's usually listed separately).

@Luaan Exactly, I wanted to mention ethanol too. It was a big surprise to me and I actually had asked a question to find out how is it possible.

@Luaan I thought that alcohol is a carbohydrate.

@CrouchingKitten Nope. It does have carbon, oxygen and hydrogen atoms in the molecule, but that doesn't mean it's a carbohydrate, just like fats aren't. Especially in food context, "carbohydrate" essentially means "sugar", usually including some non-sweet saccharides like cellulose (in your photo, that would be in "Kohlenhydrate" but not under "davon Zucker"). Really, alcohol is closer to fats than carbohydrates, but even that isn't really all that useful. It's not commonly included in either group.

@Luaan Thanks. So this means that the body can't convert it to glucose? So the only way the brain can make use of alcohol is if it's first converted to fat, and then to ketons?

@CrouchingKitten The body does convert it to fats (if you're well fed), but I don't think there's any specifics dealing with the brain - after all, ethanol goes through the blood-brain barrier with no trouble. It has long been thought that ethanol doesn't cause the well known CNS symptoms on its own - it's the intermediate products of ethanol metabolism that do, probably mostly acetaldehyde. Assuming this is true, ethanol must be metabolised in the brain (and thus provide energy, as outlined in Tomáš's link), since acetaldehyde doesn't cross the blood-brain barrier.

@CrouchingKitten I doubt anyone would recommend it as a food source for the brain, unlike sugars and ketons, though; for obvious reasons :)

The list of ingredients on the can mentions "Zuckerkulör," which is caramel colour, which can have 2 kcal/g, according to one producer.
Next, there is "Citronensäure," which is citric acid, which can, as other organic acids, have 2-3 kcal/g, according to this source.
There is also taurine, which is an amino acid-like compound, so it could, like proteins, have 4 kcal/g, but is, according to Taurine Metabolism in Man (Journal of Nutrition), poorly metabolized and probably has less than 0.2 kcal/g.
It is sometimes allowed, at least by U.S. Food and Drug Administration, to round the amounts of macronutrients (carbs, proteins, fats) smaller than 0.5 g per serving to zero, which is what they obviously did in this case, but they decided to keep the summary of calorie values of all ingredients exact.
It is usually said that only 3 types of nutrients contain energy: carbohydrates, proteins and fats.
Digestible carbohydrates (sugars and starch) provide 4 kcal/g. Undigestible, but fermentable, carbohydrates, such as soluble dietary fiber, sugar alcohols or polyols (maltitol, mannitol, sorbitol, xylitol, isomalt) and organic acids (citric, acetic acid, etc.), can provide 2 kcal/g of energy in average. On the other hand, some carbohydrates (such as "Sucralose" from the ingredient list) are neither digestible nor fermentable, so they do not provide any calories.
The "fourth" nutrient that can provide energy (7 kcal/g) is alcohol (ethanol), but is not considered a nutrient by some authors.
According to Food Label Accuracy of Common Snack Foods
 article (Obesity, 2014), the calories on the food labels should represent usable calories (metabolizable energy):

Of note, it is important to distinguish that food label calories
  actually represent metabolizable energy, which is total caloric
  content minus calories that are presumably not absorbed by the body
  and excreted as waste.

This article says that ~95% of ingested taurine is excreted. KEGG also says that taurine is not converted into any energy molecule in humans.

Could it be Zuckerkulör (caramel colour)? It's just caramelized sugar.

@AkselA -- answer should be edited to include your comment as that is almost certainly the answer. If not then it is that plus some of the other ingredients -- Aromen e.g. or anything else that constitutes a fraction of a caloric intake as, total, they only need to add up to <2 Calories.

This reminds me of a "zero calorie" recipe I once saw which involved ten squirts of cooking oil. Somebody had calculated the calorie count of one squirt, rounded to zero, and then multiplied that by ten...

@AkselA There's very little caramel colour and, also, I'm not sure it has much energy in it: it's essentially already been partially burnt.

@DavidRicherby: I don't think there's much energy in a couple of drops of caramel colour either, but then again we are only looking for a very small amount of energy.

@AkselA Oh, good point. I'd not noticed the actual numbers. Since the question is, essentially, "How is there more energy than I expected?", I didn't stop to think that "more than I expected" could still be "almost none."

@GeoffreyBrent Reminds me of how TicTacs have 0g of sugar per serving (1 mint), while they're probably mostly made of sugar.

@WYSIWYG, I checked that article and it really seems it is not taurine that provides calories.

@AkselA, it's quite likely that it is caramel colour and citric acid that provide calories.

@DavidRicherby: Why do you think all the sugar in the caramel is burnt? Ingredient design is an art nowadays. Listing sugar as an ingredient is actively avoided nowadays. Burning just 1% of the sugar and labeling the whole as "caramel colour" would be a sneaky way to put sugar in the recipe without explicitly listing it as such. And it's certainly a whole lot cheaper than putting in honey (another common "non-sugar" ingredient)

@MSalters 1kcal of sugar is a tiny tiny amount and not really detectable as sweet in a volume like this, so what you describe probably doesn't apply here.


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Do Traits Have to be Adaptive in Order to Survive?
I'm reading Michael Pollan's book 'How to Change Your Mind', which is largely about psychedelic mushrooms. In discussing the biology of the mushrooms, he writes:
'Even if psilocybin in mushrooms began as 'an accident of a metabolic pathway', the fact that it wasn't discarded during the course of the species' evolution suggests it must have offered some benefit.'
I'm wondering if this is actually true. In general, I'm wondering if it is true that traits that do not confer advantage will eventually be weeded out.
Being ignorant of the finer points of evolution/natural selection, I can make arguments both ways. On the one hand, it seems that the intense competition would make investing any resources at all in a trait that was not beneficial a totally losing proposition. Therefore no traits that weren't positively adaptive would survive. On the other hand, there seem to be all kinds of traits that are 'neutral' in fitness terms but which survive anyway. E.g. coccyx, male nipples, appendix, whale legs, etc.
I am not talking about information encoded in the genome, which can be present but not expressed. I am talking about phenotypes, i.e. traits that get expressed in interactions with the environment, such as the psilocybin chemicals in these mushrooms. (Though I suppose unexpressed genetic info could never be selected for or against by natural selection by definition.)
So to put a very fine point on my question: Is it possible/likely that psilocybin mushrooms produce a chemical that happens to engender hallucinations, not because doing so is adaptive, but just incidentally? So that this property would be something like the redness of blood, i.e. not adaptive in itself but just a matter of happenstance?

Possible duplicate of Why do some bad traits evolve, and good ones don't?

Good question. And good analysis. I have little to add! I'll simply provide my own list of thoughts to complement your ideas, which are not mutually exclusive.

The fact that it wasn't discarded during the course of the species'
  evolution suggests it must have offered some benefit.

This statement is speculative. The key word here is suggests. i can think of several speculative scenarios, of course the list is by no means exhaustive:

Traits that are not adaptive can still exist in the organism as vestigial traits. This can be because the trait was recently useful but no more, over evolutionary time scales, and not enough time has passed for the trait to be lost.
The trait may also be floating, i.e. has not been selected against, and acts as a neutral trait. It therefore remains as a phenotype. Traits are theoretically unlikely to float for very long periods of time, as I will describe later.
Some traits can very indirectly affect other traits. In practice it is often difficult to completely describe or understand which traits are a result, or cause, of other traits.
Many traits can also be byproducts of other useful traits. With nipples it might have something to do with early exposure to hormones; developing a way to bypass male nipple formation could be difficult and costly. With psylocibin, it may be a side-effect of a particularly useful biochemistry to the fungus, perhaps metabolic, that is completely unrelated to its neuroactivity in humans. It may be that a biochemical pathway might form psychoactive intermediates or products that are difficult to remove or metabolize, and find themselves in the mushroom co-incidentally.
The trait may simply be very useful, but we don't understand why it is useful. Humans often overlook this possibility; for instance, I assume you have not considered that psylocibin may have unknown effects on non-human or even non-vertebrate life.
I am not an expert but filamentous fungi sometimes/often have very complicated sexual reproductive strategies. Psylocibin may be maintained through sexual selection, rather than natural selection. This is probably far fetched, but hey- we're speculating about our ignorance.
Lastly, but very importantly, all organisms face pressure to survive and replicate. It is expensive to maintain useless features and traits, or to produce excesses, or to overdevelop or harbor chemistry that is not doing anything. Natural selection is ever-active in limiting in which traits are maintained within a population. This I think is the most convincing argument; the principle of economy. This argument fares well in all discussions on biology; life is difficult, and the costs of survival are very important to consider, always. It is expensive to store or maintain constituent chemicals, even if they are not toxic, nor if they have no use for the survival of fungi. It is more economical, and less costly, to lose such traits; selection will favor fungi that save or spend this energy elsewhere. This is a very important point, and I think it is the most salient to understand the quote you provide.

I think it would also be a good idea to study the number of times psylocibin arose. If it occurred ('was invented') multiple times independently, it must have had some functionality for the organism, like wings, or vision. If it occurred only once, one can ask whether the majority of descendant strains has lost it, or whether they maintain the trait. That could also shed some light on whether it is maintained through positive selection. Lastly, psylocibin may be a chemical that allows to explore a very specialist niche of the ecosystem. If few descendant strains contain it, that can mean it is still selected for, though only by fungi that rely on it as a strategy. This would also mean that psilocybin-less fungi would have found no need to maintain it, and may point to the occurrence of negative selection. Hope that makes sense.
Mandatory reading for you on relaxed selection.
tl;dr yes, psylocibin may be maintained by happenstance, though likelier via positive selection, at least in specialist fungi

Also, a trait may be adaptive in some circumstances, but maladaptive in others.  For instance, the sickle cell anemia gene, which protects against malaria (if there is just one copy) but causes serious health problems with two copies, and/or if you live where malaria is not present: https://www.sciencedaily.com/releases/2011/04/110428123931.htm

S Pr lists a number of reasons that might allow non-adaptive traits to spread. One other that's probably important in some populations is "allelic surfing".
If you imagine a smallish population that suddenly expands (say, starlings in the Americas, or humans in the past few thousand years), the original genes are going to expand no matter what - even useless, or mildly harmful, genes will be carried along on the overall success of the rest of the organism. The most obvious example of this is the founder effect, where populations can carry along irrelevant or harmful effects simply because there were very few founders, and some happened to have red hair or Tay-Sachs Disease; but more subtle effects can be seen whenever populations expand.

Several studies have found strikingly different allele frequencies between continents. This has been mainly interpreted as being due to local adaptation. However, demographic factors can generate similar patterns. Namely, allelic surfing during a population range expansion may increase the frequency of alleles in newly colonised areas. ...  We therefore conclude that most of the observed large allele frequency differences between continents result from demography rather than from positive selection.

--Large Allele Frequency Differences between Human Continental Groups are more Likely to have Occurred by Drift During range Expansions than by Selection

... remember that it isn't actually the gene that has the advantage, it is the person who has that gene. Usually the two are linked but not always. ... The difference is that the genes weren't the advantage, the situation was. The frontier people's genes were just in the right place at the right time and so were spread more widely.

--Gene Surfing: The Surprising Genetic Advantage of Being on the Frontier


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Which animals don't have pheromones?
Which animals are known to not have pheromones besides humans?
I can't find any research on this. There are examples of every class that uses pheromones. However nobody seems to answer conclusively that any particular species is not likely to have pheromones.

I'd guess none. If any chemical factor used in an organism's metabolism is volatile, it could be easily released and trigger a response in a nearby organism. And that's essentially a pheromone. Even bacteria do it.

Ok, does it get more complex if we limit it to sex pheromones?

Possibly. Approximately half of all animal species (including hammerhead sharks) can reproduce asexually, so it's possible they have less need for sex pheromones. But I'd say it would probably be difficult to show that an animal doesn't use any pheromones since there's often thousands of substances released by the animal that could plausibly trigger a response (and how would you test them all?).

But were there any that were extensively studied and none were found, as in humans?

I can't say with certainty. Someone else will have to weigh in on that one

Like for humans, this is not really an answerable question. Even for humans, the absence of pheromones is controversial. Failure to identify a single compound suggests pheromones are not as potent in humans as in certain animals, but cannot rule out their absence entirely.

Is it likely that all animals besides humans have pheromones? Is there a strong reason that there would be exceptions?


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How many different species have existed on Earth?
NOTE: Someone else asked this same question a few years back, but it was incorrectly marked as a duplicate and so the question may not have been answered satisfactorily. I'm asking it again, in hopes of getting a stronger answer (if there is one). Please do not mark as a duplicate; I really appreciate it!
(Original question: How many species have existed on earth?, incorrectly marked as a duplicate of: How many organisms have ever lived on Earth?)
QUESTION: How many species have ever existed on Earth, throughout the entirety of Earth's history? For clarity, I'm not asking about the number of individual organisms (answered in 2nd link above), nor about the number of living species estimated to exist today (also cited in an answer in the 2nd link above). All species, ever (never answered in any link, to my knowledge).

Species are not countable in time.

Not an answerable question.  The problem, besides the obvious one of lack of data (no one really knows how many species exist today, let alone in the distant past), is that the idea of species is a human construct,  For instance, are wolves & coyotes different species?  They have different names, but have interbred to produce the coywolf.  Or all the fossils of pre-humans that keep getting dug up: are they all really different species?  Then when you get into microorganisms and things like horizontal gene transfer, the species line gets pretty blurry...

I was only wondering if there was a ballpark figure, out of curiosity. I know there is no perfect way to answer the question, given the subjectivity of what constitutes a "species", and the incompleteness of the fossil record (and impossibility of many types of organisms being fossilized to begin with). I am not that strong in this particular branch of biology, so I posed the question. If there's no answer, there's no answer, and that's fine (once again, I wasn't sure since the previous asking of the question was shot down).

From Raup (1986).

Up to 4 billion species of plants and animals are estimated to have
  lived at some tlme m the geologic past (2), most of these in the last
  600 million years (Phanerozoic time). Yet there are only a few million
  species living today. Thus, extinction of species has been almost as
  common as origination.

I am not sure how exactly has it been estimated. Read the paper for more details.
In 1991, Raup comments:

Countless species of plants and animals have existed in the history of
  life on Earth. Estimates of the total progeny of evolution range from
  5 to 50 billion species. Yet, only an estimated 5 to 50 million
  species are alive today – a rather poor survival record. With, at the
  most, only one in every thousand species surviving, what happened to
  the others?

Mora et al. (2011) predict ~8.7 million extant eukaryotic species. So I would guess that there are >5 billion (extinct + existing) species on earth.
I guess there will be many more prokaryotes. We don't know anything about ancient prokaryotic species because there are no fossils records. I would say that it would be nearly impossible to estimate the number of prokaryotic species: even now we do not have a very reliable method of typing microbial species (people mostly rely on 16S rRNA sequencing). See What defines a microbial species?


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What is a flux control coefficient?
In metabolic control analysis, a number of coefficients are defined, including the flux control coefficients. How is this coefficient defined and what does it measure?

The flux control coefficient measures the relative change in the steady state pathway flux in response to a relative change in enzyme activity. Mathematically it is defined according to:
$C^J_{e_i} = \frac{dJ}{de_i} \frac{e_i}{J}$
Because enzyme activity is proportional to enzyme concentration, the flux control coefficient is often define with respect to the enzyme concentration, $e_i$.
This can be also expressed in log form:
$C^J_{e_i} = \frac{d\ln J}{d\ln e_i}$
It can also be expressed approximately as a ratio of percentage changes:
$C^J_{e_i}  = \frac{J\%}{e_i\%} $
This definition makes it easy to measure. For example, if the activity of a given enzyme is changed by a factor of 1.5 which results in a 1.25 fold change in the steady-state flux, then the value of the flux control coefficient is approximately 1.25/1.5 = 0.83. Because flux control coefficients are measured using relative changes, the coefficients are dimensionless.
Flux control coefficients are useful to gauge how much a given enzymatic reaction influences the flux in a pathway.
For further information I recommend the following paper:
Kacser, Henrik, James A. Burns, H. Kacser, and D. A. Fell. "The control of flux." (1995): 341-366.


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Will plants accumulate toxins from soil contaminated by toxic substances like paint thinner/lead paint?
After my grandfather died, demolition crews dumped garbage from the house onto his huge vegetable garden, including lead-painted windows, aluminum, asbestos tiles and more.  Much of it got burned in a few bonfires, which I assume released the toxins into the soil.
I've cleaned out every object I can see from that pile, but I'm wondering if the vegetables grown in that soil will be toxic?  It's been about three years since the demolition.
Also, to avoid the possible toxins from that area, we created a raised container garden using soil from a different location.  Yesterday, 3 Tablespoons of paint thinner mixed with water was dumped accidentally on one of the plants. We hosed it down, and it's still alive, but I'm thinking that the squash it will eventually produce is now toxic too, right?
Thanks in advance. We're new to gardening and really want to understand how this works.

Was the paint thinner still clean (i.e. not mixed with actual paint)? Paint thinner itself is pretty volatile and will evaporate soon.

You could use other plants to extract harmful substances from the soil. There are plants which are called hyperaccumulators which absorb high amounts of contaminants from the soil.
Have a look at at Phytoremediation where the process of phytoextraction is described in detail.
Normally phyotextraction needs several generations of plants to be grown in order to be effective. Consequently you could just plant your vegetables as usual but take samples and test them for heavy metals or other contaminants of concern.


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Is it safe to feed the squirrels?
I hope this question fits here, I haven't found another community where it would fit.
Two years ago I was in a hotel in Sri Lanka (south-western coast) and in the hotel gardens there were a lot of squirrels. From what I could find out, they probably were Indian Palm Squirrels, but I don't know for sure. They were striped.
They were very tame and come to the hotel guests, hoping they would get something to eat. You could even touch some of them, so they are probably used to that.
We fed them some roasted peanuts (unsalted) and they were pretty happy about it, sometimes they also just took them by themselves =)
My question is, as I am about to visit the same hotel again this year, is it safe to do so? I know that they mainly eat nuts, fruits and insects, but our nuts were purchased in Germany (though propably imported from elsewhere anyway). Is there any danger for the squirrels or is it a terrible idea to feed those wild animals anyway or is it fine to do so, as long we don't cram them?

I request improvement by what did you mean by the term "feed". Did you mean "feeding" into their mouth by restraint force? Or you mean just leaving some foods, so just they eat that by themselves? In my village the squirrels ate (now drastically reduced) a lot of paddy grains (they removed the rice husks and ate the content). So i think leaving some paddy/rice grains isn't bad idea. Thats just my guess.

@David Its very true we generally shouldn't feed wild animals for multiple reasons; but I think the main hazard of feeding squirrel is to making them vulnerable to killing or entrapment. Otherwise  they seem to have some strong contact/ interaction with human, just as comparable to crows & house-sparrows.  it seems so many rural kids like to give food to the 3-striped squirrels. Also squirrels like to come on a routine basis on the places where paddy whole grains are packed or stored.

@AlwaysConfused: There is no force involved whatsoever =) They eat by themselves, come to humans by themselves. Some eat from the hand and when they have enough they leave. By "as long as we don't cram them" I wanted to indicate that I think it would be a bad idea to just give them too much.


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Surface perception
I'm looking for research studying:

How small and compressed together do particles of a surface need to be to be perceived as solid surface to human touch? E.g. sand still feels grainy. Has there been research on how much it varies between different areas of the body?
Same question, but for where the line of pain lies - walking on gravel can be painful, while walking on sand isn't.

Any pointers to relevant material much appreciated!

Both sensations are dependent on pressure (i.e. area over which a force is distributed). Remember that stepping on one nail is incredibly painful but lying on a bed of nails may not be.

1) Discerning between solid and granular
It is the distribution of the touch receptors in your skin that enables the distinction between solid and granular objects.

The ability to recognize two separate points applied simultaneously to
  the skin from a single point is called two point discrimination.
  Two point discrimination varies with location on body surface. It is
  about 2 mm on the finger tip and increases to over 40 mm on the back.
  (vcu.edu)

Image source: Annals of Neurology, CC licence
2) Touch vs pain
The sense of touch is enabled by touch receptors and pain by pain receptors (nociceptors). In general, pain receptors are activated by greater pressure than touch receptors. Walking on gravel (sharp-edged stones) likely applies greater force on a certain area of your skin than walking on rounded pieces of sand, so it will more likely cause pain.

Mechanoreceptive nociceptors have a high threshold for activation—they
  respond to mechanical stimulation that is so intense it might damage
  the tissue. (nobaproject.com)

More info:

Whole-Body Mapping of Spatial Acuity for Pain and Touch (Annals of Neurology, 2014)
Pain sensitivity and tactile spatial acuity are altered in healthy musicians as in chronic pain patients (Frontiers in Human Science, 2015)

This is exactly what I was looking for - thank you for the summary and references!


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Is there benefit of use of red light over dim white light when interacting with rodents in the dark phase?
I've come across some "percieved wisdom" that rats and mice do not "see" red visible light and so use of this wavelength will allow humans to interact with rats in their active nocturnal phase without affecting their circadian rhythms.  Having gone to read the evidence for myself of this I can see evidence that red visible light does indeed impact rodent circadian rhythm (Dauchy et al J Am Assoc Lab Anim Sci. 2015 Jan; 54(1): 40–50) so is not a "fix" to allow us to see without the rodent being impacted.  What I cannot see is if there is any "benefit" to use of red vs white light if it has to be used or whether it just has the same impact and the only negative is the human can see less!!!!  Can anyone help ?

I propably can answer this qustion. But still i need to be 100% sure, what are you exacly want to know. Your question is: Why does chronobiologiest use in experiment red part of visible spectrum, but not whole light spectrum (white light)? Am i correct?


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Partial muscle fibre contraction
I'm being taught that: a muscle fibre spans the entire length of the muscle, from the originating tendon to the inserting tendon.
The question is, can a muscle fibre contract only partially? Say, if the fibre is 1m long, can only the first 10cm contract without the rest contracting?
Additonally, to help me understand better:
When a neuron innervates a muscle fibre, does it do it only at one spot, or can a muscle fibre be innervated in several spots? Can several neurons innervate the same muscle fibre?


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Is it possible to breed neanderthals through selective breeding?
I've heard most non-subsaharan africans have neanderthal DNA with it being more prevalent in northern regions, that sometimes 1-4% of the DNA has neanderthal origins.
Speaking strictly scientifically, would it be possible through selective breeding to breed an individual where the majority of the DNA is neanderthal?

No, it is not. As you said only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences. The entire Neanderthal genome is not present in modern day humans, it is only a small set of sequences.

only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences More "more" than "less". A 2014 study Resurrecting Surviving Neandertal Lineages from Modern Human Genomes identified around 20% of the Neandertal genome out of just 665 modern humans; presumably a larger and more varied population would pull out more than 20%. Probably somewhat less than half the original genome, though.

I'm more than a little puzzled here, since numerous sources state that humans share about 96% of their genome with chimpanzees.  (Or 99% per this: https://www.sciencemag.org/news/2012/06/bonobos-join-chimps-closest-human-relatives )  It would seem that Neanderthals ought to share at least that much with modern humans, no?

Do apes and humans share 99% of DNA or 99% of genes? What is the difference? (particularly the answer by @rg255).  Summary, the Neanderthal genome in humans is alleles while the >99% similarity is in terms of DNA.

Selective breeding will select for genetics that are already present in your population, but won't introduce new DNA sequences that aren't carried by any of the population members. It would technically be possible if everyone carried a different 1-4% of the Neanderthal genome, since it would be possible to reconstruct the full Neanderthal genome by creative combinations of DNA that exists in the population. That's not the case, though, it will be a fairly consistent set of regions for which you can substitute Neanderthal DNA for homo sapien DNA and still have a functional human.
So no, this isn't possible - the complete genome of Neanderthals doesn't exist split among the human population, so it can't be refined to be complete through selective breeding.

I agree with the two previous posts, but they are a bit light on references / evidence, so I thought I'd throw my two cents in.
The answer it seems is most likely no. As others have alluded to, in order to 'breed' a Neanderthal selectively from modern humans, it would need to be the cases that the entire ~3.1Gb of the Neanderthal genome would need to be represented in modern humans.
Methods exist which are able to identify the specific segments in modern individuals which are derived from the Neanderthal admixture event. One recent example is IBDmix [1] from Josh Akey's group in Princeton. They inferred 110.98Gb in total across 2504 worldwide individuals from the 1000 genomes reference panel, which works out as an average at about 0.04 Gb per individual, or 1.3% on average across all individuals. There is a substantial amount of variation between population, with Africans having less Neanderthal ancestry than non-Africans.
However, when you collapse down the Neanderthal segments into non-overlapping regions, it turns out we can only identify 1.29 Gb of unique segments. This means that we have 1.29Gb / 3.1Gb = ~40% of the entire Neanderthal genome present in modern day humans. A similar, older study inferred a slightly smaller amount of 1.1Gb [2]. It is very unlikely this figure will change a large amount in the future.
This is why 'breeding' such an individual with 100% Neanderthal  DNA would be impossible; around 60% of that ancestry has been totally lost from modern humans, either through genetic drift or purifying selection.
References
[1]: Chen, Lu, et al. "Identifying and interpreting apparent Neanderthal ancestry in African individuals." Cell 180.4 (2020): 677-687.
[2]: Sankararaman, Sriram, et al. "The genomic landscape of Neanderthal ancestry in present-day humans." Nature 507.7492 (2014): 354-357.


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What species of mulberry is this?
I have several mulberry seedlings that have popped up in my garden.

What species (or hybrid-species) are they?
Details:

The location is Toronto, Ontario
The date is July 18th, 2019
I have several different kinds of cultivated and uncultivated mulberries in the surrounding area that could have been the parents. I would list their cultivars and species names, but to be honest, I don't have much faith in them (I think they might just taint our analysis/identification).

Note: Here are some close-up photos of the plant in the bottom-right of the above photo:

https://i.stack.imgur.com/qi6dJ.jpg
https://i.stack.imgur.com/JlNh0.jpg
https://i.stack.imgur.com/rP2M8.jpg
https://i.stack.imgur.com/yWQGg.jpg
https://i.stack.imgur.com/vkH80.jpg
https://i.stack.imgur.com/ZJTx2.jpg

Even if we restrict ourselves to Morus rubra, the native species, versus Morus alba, the species introduced from China, and ignore possible hybrids, I think you may have to wait for the trees to be larger for an ID.  I found a relevant paper (Nepal, M.P., M.H. Mayfield, C.J. Ferguson. 2012. "Identification of eastern North American Morus (Moraceae): Taxonomic status of M. murrayana." Phytoneuron 2012-26: 1–6.) which contains the following paragraph:

Salient features for correct identification of M. alba and M. rubra
Morus rubra can be easily distinguished from M. alba using
  morphological characters of the leaf, bud, branch, bark and
  infructescence. Leaf characters present a challenge because of the
  tendency for leaves of juvenile shoots to converge in morphology among
  these species. Nearly all of the unique characteristics of M. rubra
  fail in juvenile leaves. Leaves of M. rubra (5–40 x 3–28 cm) are
  larger overall than those of M. alba (2–20 x 1.5–18 cm). In M. rubra
  leaves, the adaxial (upper) surface is rough and dull green (vs.
  smooth and lustrous) and the abaxial (lower) surface is usually
  densely hairy with erect trichomes evenly distributed (soft to the
  touch); the base is often cordate (heart-shaped); the apex is acute,
  acuminate to subcaudate; marginal teeth are often pointed; and the
  color of the main veins is more or less like the color of the lamina
  on the underside. Leaves of Morus alba are usually deep green and
  lustrous adaxially and have few hairs concentrated along the main
  veins on the abaxial surface; the base is rounded (vs. cordate); the
  apex is obtuse; the marginal teeth are fewer, relatively larger, and
  rounded; and the primary veins (underside) contrast more with the leaf
  surface than in M. rubra. The winter buds of M. rubra have bud scale
  margins with a darker (almost black) apical band, while in M. alba,
  the bud scale margins are uniformly brown. Morus rubra has grayish
  bark with flattened, thin plates that peel outwards in age. Morus alba
  bark has thick and solid ridges that are more of a reddish tan
  coloration. The orientation of branches in a mature M. rubra is
  somewhat planar (flat) and spreading like an umbrella. In M. alba the
  orientation of branches is more erect or spreading, and the plants
  appear more rounded or bushy as a result. The fruit of M. rubra is
  longer and narrowly cylindric, while in M. alba it is typically ovoid
  or ellipsoid.

This might be very useful for mature trees, but note the line "Leaf characters present a challenge because of the tendency for leaves of juvenile shoots to converge in morphology among these species. Nearly all of the unique characteristics of M. rubra fail in juvenile leaves."
There is also a recent, purely genetic analysis of the mulberries freely available at PLOS One but I don't think it's too helpful in this context other than it confirms that hybrids are common.
The Phytoneuron paper and a number of internet sites generally point to M. rubra being densely hairy on the underside of the leaves as one of the more important characters.  Your specimens appear glabrous, but the pictures though excellent may still not show tiny hairs well.  If we trust this character in the young plants then we would lean toward M. alba but as stated above, you may have to wait and see.


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Why squirrel behaviour varies greatly throughout India?
Common squirrels seen in India, probably Indian palm squirrels; seem to have drastic different behaviour. And all squirrels of a definite locality, behave in a very consistently same whay. That seems like  My drastic experiences at 3 localities were as follows.

On West Bengal (Howrah, Hooghly and Burdwan District): Squirrels seem to be incredibly timid. They always maintain a safe distance from human being. They sometimes consume human food leftover, or respond to cater; but the feeder person needs to be go away from the spot. They are also quite a bit picky eater, among human remains they mainly depend on paddy, some of them don't even touch grounnuts.
On Uttarpradesh Tourist spots, particularly Agra and Delhi, squirrels come too close to the tourists. Sometimes they take food directly from human hand. Some of them even follow the tourist population for foods. Some of these squirrels are very aggressive, however they are somewhat vulnerable because people easily touch them. They aren't very picky eaters, rather they are sort of gluttony... eats whatever the tourists feed them.
On Uttarakhand state, on many places (including the non-tourist) the squirrels come very closer to human being.  Not always for food, but they just come too close to human being. They aren't aggressive. They aren't very picky eaters. Though some are little bit timid; some are super easy to touch. They are super vulnerable.

I'm really surprised how the behaviour of these 3-striped squirrels vary throughout India and is consistent with locality. Learnt behaviour from parent/ peer squirrels? Epigenetic imprints? Genetic variability? Scarcity of foods? Its super surprising.

Scarcity of foods sounds like a convincing hypothesis. You could also argue that different squirrel types might prefer the food that tourists offer them. It could also be due to differences in hunting and pest control in different geographical regions.

Given that you're dealing with fairly smart mammals with a short lifespan and limited distance migration, it seems likely that you're dealing with strong local selection effects that are going to be reflected in all three layers:

Learned behaviors from observing other squirrels and their own interactions with humans.
Epigenetic effects tied to things like maternal stress
Differences in the frequency of genetic tendencies towards caution / aggression, etc.

Now, what would the source of those differences be? I don't know if anybody's studied these particular cases, but there's some pretty strong candidate hypotheses for a starting point:

In West Bengal, you're dealing with high-density non-touristy areas (especially Howrah, right on the edge of Kolkata). The squirrels there are likely in constant conflict with humans who do not want to be sharing their food, which will select strongly for aversion to humans.  Humans might well be poisoning them as a means of control too, which could explain the picky eating.
In tourist spots anywhere, the squirrels are probably getting fed well by humans either intentionally or accidentally (e.g., careless children), whcih will select strongly for attraction/aggression toward humans.  I'll bet you'd see this in Victoria Memorial too, for all that it's right next door to Howrah.
In Uttarakhand, which is a much lower density state than West Bengal (189/km^2 vs. 1029/km^2), you're probably seeing much more of the default state of interaction, without a strong selection in either direction.

Wow you know so much on Kolkata! I went Victoria Memorial probably only once at childhood and can only faintly remember about it.

@AlwaysConfused I have a family connection over there. :-)


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How DNA probe binds
I am studying about southern hybridization now and I've a doubt.After the DNA has been fragmented using restriction enzymes and obtained on nitrocellulose blot , it is still double stranded (the fragments) so how do single stranded probes bind to it ?

The double-stranded DNA fragments are fractionated by size during the agarose gel electrophoresis.  Prior to the so-called “blotting” step, the gel is briefly soaked in a solution of NaOH, which has a relatively high pH.  Under these conditions, double-stranded DNA will denature, or “melt” into two single strands.  This is the material that is “wicked” or “blotted” onto the nitrocellulose membrane in the presence of monovalent cations.
If the labeled probe DNA is also double-stranded then it is advisable to denture it as well prior to the hybridization step.  We used to use boiling hot water to denature the probes.


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How does a cell distinguish left from right?
Although the human body is mostly left-right symmetrical, it consistently has asymetries. The heart is consistently slightly to the left side of the body. The liver is consistently on the right side.
This is quite perplexing when we consider that the human body has developed from a single cell. It seems like a single cell is mostly left-right symmetrical. A single cell could be oriented any which way in the womb, and it is unclear how the developing body would "know" which way is left or right.
So, how is it that the body develops the clear assymetry. Can anyone explain this interesting phenomenon in layman's terms?

You are hitting nerve of many biophysics researchers here :) This phenomenon is called Symmetry Breaking is part of active research.

Developing symmetry is is just a matter of Homeotic genes creating axial patterning, genes that produce a chemical gradient across a cell or group of cells. This is how developing organisms orient individual cells, up, down, left, right, anterior, posterior, medial, lateral, are all just gradients of different chemicals, the cells can detect the difference in concentration one one side or the other to orient itself. Most of these start getting produced when the embryo is only around a few cells so there is not much room for ambiguity.  Later more homeotic genes are added to create gradients for things like segments and limbs. Note polarity is often exhibited in a single cell, even in single celled organisms, this is a chemical gradient that orients the inside of the cell, this can easily be turned into orientation of dividing cells.
As for why things move away form this symmetry that's easy, evolution can mostly only work with what it has, evolution is about good enough not perfection.  Often good enough creates a kluge, a rube goldberg type solution then descendants then get stuck with. The earliest vertebrate ancestor pikaia is completely symmetrical even down to the gut,  A fish is nearly perfectly symmetrical, with the only deviation being to increase the length of the gut without increasing the length of the fish, which would waste a lot of material The solution is to coil and pack the intestines instead of having a straight line. This does not just happen in vertebrates you can see these solutions again and again in mollusk, insects, and even echinoderms, keeping the body compact while making the gut longer means asymmetry. As Some organisms progressed further and further away form the "fish" body plan alteration would result in asymmetry. Lungs for instance force a big asymmetry because you are taking what was a simple one way path into two divided systems, blood now has to return to the heart twice before making a complete circuit. More energetic animals specialize even further abandoning or partitioning part of the circulatory system to close off these two parts entirely so they can have high pressure blood flow without exploding their lungs. Now asymmetry is not a bad thing limbs and sense organs stay symmetrical because there is a stronger evolutionary pressure to keep them symmetric, moving with asymmetric limbs wastes a lot of energy (try running with only one shoe on).

Image sources.

Sorry but I don't think this is right answer. It is not matter of 'just' Homeotic genes. There are lot of factors which plays important role in symmetry breaking even before these genes are expressed. One of the earliest symmetry breaking even is asymmetrical cell division (long before even tissues are formed). There are lots of hypothesis currently which explains this including maternal mRNA deposition, cilia rotation, external chemical gradient, uneven protein distribution etc.

This question could easily be construed as too broad if addressing every form of symmetry and asymmetry in biology. I was trying to restrict myself to the specific examples the OP gave. vertebrate symmetry and organ asymmetry.  If you want to address other occurrences feel free to create an answer.