text:
Why are telomeres needed to allow DNA replication at the ends of linear chromosomes?
I’m reading Molecular Biology of the Cell by Alberts et. Al and at one point the authors mention the following:

We saw earlier that synthesis of the lagging strand at a replication
fork must occur discontinuously through a backstitching mechanism that
produces short DNA fragments. This mechanism encounters a special
problem when the replication fork reaches an end of a linear
chromosome. The final RNA primer synthesized on the lagging-strand
template cannot be replaced by DNA because there is no 3ʹ-OH end
available for the repair polymerase. Without a mechanism to deal with
this problem, DNA would be lost from the ends of all chromosomes each
time a cell divides [emphasis mine].

They use this explanation as a motivation for why telomeres are needed. But I don’t quite understand it. Below is a diagram that they show earlier. It seems to me like the process shown can just as easily be done at the ends of chromosomes. In particular, if we imagine that the left-most primer has no DNA following it, it seems to me like polymerase can just do what it normally does to replicate the DNA until the end is reached. Where’s the problem?

How is the 3’ end of the orange strand replicated?

@canadianer I see. But what is meant by "there is no 3ʹ-OH end available for the repair polymerase"?

It means that DNA polymerase only extends existing chains and doesn’t create new chains de novo. In other words, it needs a primer.

@canadianer right but why is there no 3’-OH end available?

This just means that because the final part of the 'reading' is in the 3'-OH to 5'-OH direction (R to L in the orange lagging strand), the last available component for synthesis of an RNA primer by the DNA primase is from that latter 5'-OH towards the 3'-OH end of the strand.  So, the final 3'-OH component of that strand cannot be synthesised: there is no 5'-OH component to its right in the diagram. Telomeres perform other functions; nature is fantastically efficient. The whole thing is an immensely beautiful wave (interference) dynamic in 3-D, wrapped around the tetrahedral form of histones.

@jeremiah but why can another primer not be added right at the 3'-OH end (at the rightmost end of the lagging strand template)?

This video: https://www.youtube.com/watch?v=2NS0jBPurWQ answered my question

The final 3'-OH component cannot be 'read' due to the absence of a further 5'-OH to its right: the requisite directional sense for the initiation of a further primer is absent. I'm glad you found the video -- that's the point.

And yes, the video clarifies it all very nicely.  The key information is the absence of the 3'-OH at the correct end of the Okazaki fragment (right in the video), to prime further DNA synthesis.  So, thank you for that: I'm a wanderer too.


text:
T-Cell Receptor Receptor-Associated Immune Receptor Activation Motifs (ITAMs) Inconsistency
In reading the information associated with the cytoplasmic machinery of the T-Cell Receptor (TCR), the one tyrosine motif that is consistently mentioned is the receptor-associated immune receptor activation motifs (ITAMs). All sources I can find on the motif says the sequence is YxxL/Ix(6-8)YxxL/I [1]. However, in the CD3ζ chain of the TCR in homo-sapiens, this sequence is not present according to separate protein structure and sequence sources [2,3]. It is only the TCRβ chain that has this sequence motif in it [4]. The importance of the ITAM seems to be it is the binding location of the protein ZAP-70 (which stands for Zeta-chain-associated protein kinase 70), therefore given the name it is canonically associated with just the zeta chain not the TCRβ chain, what is the ITAM truly then?
The sequence seems to be conserved in murine TCR sequences [5], however, many of the articles being written are not specifically talking about murine TCR structures.
Is this an oversight in regard to the lack of clarity in the writing of the papers describing the involvement of ITAMs in TCR signaling or what is the source of the disagreement between the ITAM sequence and what is seen with the protein structure?

source: Stack Exchange

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

sort: votes


text:
Can the coding strand for an RNA act as the template for another?
Can the same strand of DNA act as a sense strand and an antisense strand at two different occasions of transcription and result in two different proteins?

Welcome to SE Biology. Please finish the [Tour] to learn more about how this site works. Could you clarify please. Are you only interested in total or partial usage of both strands for synthesizing proteins (partial being just overlap between the ends of ORFs with the opposite directionality, which is quite common in bacteria). And do you require that the two proteins to use the same reading frame (which I suspect would lead to frequent stop codons) or different ones? (And thanks for using sense and anti-sense, my own preferred terms.)

Yes, the DNA strand that is usually the sense strand, coding for the mRNA and protein sequence can also become the antisense strand if transcription happens in the reverse direction. This phenomenon called antisense transcription is a relatively recent discovery has been discovered to be quite pervasive in all types of organisms by sequencing all the transcripts in the cell, a method called transcriptomics.
Although the antisense transcript is usually a short non-coding RNA which plays regulatory roles influencing the stability of the sense transcript by it's complementary binding, in rare cases it can form a protein if it has the required site to initiate translation (ribosome bidding site) and the codons to make a protein.
Source - Pelechano, Vicent, and Lars M. Steinmetz. "Gene regulation by antisense transcription." Nature Reviews Genetics 14.12 (2013): 880-893.
Wikipedia - Antisense RNA
These old papers from 1994 talk about antisense proteins -
Do "antisense proteins" exist? J protein chem, 1994
Antisense overlapping open reading frames in genes from bacteria to humans Nucleic acids research, 1994

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


text:
Are all genes capable of being switched on or off?
Are all genes capable of being switched on or off or only some genes? Are there some genes that permanently do not have the functionality that enables them to be switched on or off?
Everything I have found in response to this question seems to assume that ALL genes are capable of being switched on or off.
When I have searched for the answer to this question all I find are explanations about how things like epigenetics, gene regulation and expression work. I understand at the basic level how these things work and that there are different ways by which they are accomplished.
I realize the answer may be "as far as we know" or "we don't know" or "it's complicated" and that's fine and definitely understandable.

Welcome to SE Biology. This is a question and answer site where we hope the Q&A will be of general benefit. For that reason we try to ensure that questions are unambiguous, editing if necessary. Hence two requests for clarification. 1. Are you taking about bacterial or eukaryotic cells? 2. By “switching off” do you mean specifically prevent transcription of a gene, excluding general effects of starvation of metabolites?

Eukaryotic. I expect "prevent transcription" is the appropriate clarification but preventing something is different than lacking the functionality for something. With regards to my question either would have the same effective result - a gene where regulation is not possible.

I cannot think of a mechanism that would entirely prevent a gene from being regulated. For example, consider mechanisms like histone modification: there is very little about the sequence of a single underlying gene that can itself cause or prevent histone modification, yet those changes regulate the expression of associated genes. However, you can really only provide evidence in science for things that happen; providing evidence that things do not happen is often questionable. If you have some example gene and you'd like to say "this gene is not regulated", the best you can ever get to is "I haven't yet found a circumstance in which this gene is regulated by any manipulation I know of".
In practice, there are some genes that are not typically "switched on/off" and always expressed at fairly constant rates, we call these housekeeping genes. For many of these, the consequence of 'switching them off' would be death of the cell. However, I would not consider that these genes are "not capable" of being regulated, rather, I would say that they are specifically regulated to be always active, and that there is very strong evolutionary pressure for this to occur. To show that I mean by this, consider some quoted lines from Wikipedia:

The housekeeping gene expression levels are fine-tuned to meet the metabolic requirements in various tissues. Biochemical studies on transcription initiation of the housekeeping gene promoters have been difficult, partly due to the less-characterized promoter motifs and transcription initiation process.

Little is known about how the dispersed transcription initiation of housekeeping gene is established. There are transcription factors that are specifically enriched on and regulate housekeeping gene promoters.[12][13] Furthermore, housekeeping promoters are regulated by housekeeping enhancers but not developmentally regulated enhancers.[14]

In summary, steady activity is carefully controlled, and difficult to study. Comparatively, if a gene has very different expression in different environments, you can follow an iterative process to look at cells in each environment and see what is different: if you find another protein is phosphorylated or otherwise modified, or has also changed expression, you might be looking at a transcription factor involved in your gene of interest. On the other hand, if something never changes, where do you start? Trickier problem for an experimentalist.

Thank you very much for your comprehensive answer. I do appreciate you taking the time to provide links, quotes and your thoughts.


text:
Copy number deletion and high expression
I have a region that has significant CNV loss. But the expression for the genes in those regions is high compared to the expression found in the samples that don't have the regions lost. How can this happen?

Welcome. Please provide some more details 1) organism, 2) sample size, 3) how significant is the CNV loss, 4) how big is the region of CNV loss, 5) how did you identify CNV loss, 6) how did you assess whether the gene expression was less, 7) how much less was the gene expression. All of these are important if you want a good answer. Thanks.

Yes, I think we need to look into chromatin states as well. Thank you for the link and the pointer to the previous question.

@user438383
I can answer some of these questions but I am not sure we can resolve this because these are computational results. I was looking at the underlying biology.


text:
Do we know the genome contains all the information necessary for embryonic development?
Since high school biology I've assumed that all information necessary for creating an organism is found in its genome.  As Nature's Scitable site says:

Deoxyribonucleic acid, more commonly known as DNA, is a complex molecule that contains all of the information necessary to build and maintain an organism.

However, I've been reading Sean Carroll's "Endless Forms Most Beautiful" and here is one passage that illustrates the question in the title.

Ultimately, the beginning of spatial information in the embryo often traces back to asymmetrically distributed molecules deposited in the egg during its production in the ovary that initiate the formation of the two main axes of the embryo (so the egg did come before the chicken).

Dr. Carroll seems to be saying that the information determining whether genetic switches are on or off ultimately does not come from the embryo's genome, but rather comes from other molecules provided by the mother.  So, my question is whether we know these molecules responsible for initializing the switches that regulate gene expression can be traced back to something in the mother's genome?  If we don't know these molecules trace back to the mother's genome, then is there some other reason we think the genome "contains all of the information necessary to build and maintain an organism"?

Comments are not for extended discussion; this conversation has been moved to chat.

The second quote is about stochastically determining which side is the "head" and which is the "tail", effectively, which occurs by positive feedback of an existing gradient. This is not really a matter of information stored in the sense that we think of information stored in DNA bases or bits on magnetic tape, the passage seems to be referring to information in the sense of a reduction in uncertainty about the state of the universe. The way a developing embryo chooses where the head is going to be is like dumping a bag of M&Ms on the table and having the head develop wherever the highest concentration of yellow M&Ms are. If you expect them to be uniformly distributed, you'd be correct statistically, but for any one iteration there will be a non-uniformity that determines what happens next: that's information, reduction in statistical uncertainty. If you, via the power of a thought experiment cousin of Maxwell's demon, were to scramble the positions of molecules in the egg cell, that would change where the "head" develops.
Yet, all of this is guided by proteins that are created and function according to the "instructions" in DNA. DNA doesn't have information about where in the future there will randomly be a concentration of yellow M&Ms, but it does have the information to synthesize proteins that react to concentrations of yellow M&Ms, causing a positive feedback loop that further concentrates them on a particular axis.
For embryonic development, these yellow M&Ms are mRNA transcripts, and at least in drosophila, these initial transcripts are indeed made in the egg cell, not post-fertilization (see https://en.wikipedia.org/wiki/Drosophila_embryogenesis#Anterior-posterior_axis_patterning_in_Drosophila). It's possible to introduce a mutation to a fly that will only affect her offspring, by interfering with transcription of these mRNAs. More generally, maternal effects are observed when the egg cell or developing environment has some influence on the offspring.
However, all those influences are coded in the DNA of the next generation, too, so it also seems reasonable to say that the genome contains all the information necessary. Containing all needed information to do X is not the same as being able to do X. To turn DNA into RNA transcripts, and to turn transcripts into proteins, requires more than information, it requires machinery. We can say the information to build those machines is also in the DNA.
Honorable mention to mitochondrial DNA, which comes entirely from the egg cell.
Generally, I think learning about biology from these grand pronouncements like "all information is in DNA" is a bad way to learn biology. Biology is not mathematics, we do not operate in the certainty of proof. Learn how things actually work, first, rather than trying to prove or disprove "truths". These statements are meant to capture wonder and convey the basic order of things, they are not dogma (even if someone regretfully calls it that).

Nice answer! Reminds me of the last line of Gunga Din. Mitochondrial DNA does deserve an honorable mention. :)

Also, and feel free to delete this, but I always thought of Watson as something of an imposter, a feeling that solidified on listening to him speak a few times at Cold Spring Harbor, and we’re chiseled in stone with his racist views.

Thanks, great answer, and your answer does illustrate why scientists tend to think all the information is ultimately stored in the DNA.  From what you say, the asymmetric concentration appears to be as informative as a coin flip.  The head formation has to start somewhere, and there has to be a concentration to get things started, but the concentration's placement is randomly distributed, so there is no specific instruction identifying a particular location where the head has to form.  I'm acquiring some books on epigenetics to see if all developmental instructions are indeed encoded in DNA.

I also just found this question https://biology.stackexchange.com/questions/30645/do-changes-in-an-organisms-cell-modify-the-genetic-information-it-uses-for-repr?rq=1, which says mutations in the gametes are heritable.  Which would be one example of heritable information that is not encoded in the DNA.  I can ask a separate question about this to see if it falsifies the statement that "all information is in the DNA".

@yters Though "epigentic" is quite broad, most of what is described as epigenetics still involves DNA, it's just outside the traditional ACGT bases. I do not understand why you think heritable mutations in gametes would not involve DNA. I don't think "all information is in the DNA" is a statement you should bother falsifying, rather, you should think about and understand what someone meant to convey by making that statement.

@BryanKrause there is a subtle distinction in my question that I'm having trouble getting across.  It can be both true that the mechanisms of transmitting epigenetic information is encoded in DNA, i.e. proteins, while the information itself may not track back to specific instructions encoded in the DNA.  I'm having trouble asking my question in the right way to get the answer.  Think of this analogy.  When I type a Word document, the document is dependent on the Word source code that generates the Word program.  However, the information in the document cannot be traced back to the source code.

@yters Part of the problem might be that you are not expressing a question of interest to biology. Most biologists only really care to understand how the biology works - there's enough stuff going on there to spend many lifetimes on figuring it out and it isn't necessary to apply it to some greater truth for it to be interesting.

It might be worth thinking about a plant...many plants are of indeterminate size. They grow according to their environment. The instructions for that growth are all encoded in their DNA, but there is a lot of external "information" that will determine the plant's final morphology. For example, if it's receiving a lot of shade early on, some plants will attempt to grow very tall very quickly to escape the shade, at the expense of growing wider. That's "information" in the universe uncertainty/entropy sense; it's not information in the sense of the first quote in your post.

Let us continue this discussion in chat.

In your Word document example, all of the environmental conditions: sunlight, soil contents, neighboring plants and any signals they release, damage from predators, these are all like the keys you strike while you have Word open, but the way that those inputs are rendered into the plant shape you see today is all in Word's source code, and to generate another plant that follows the same rules given the same external input, all you have to do is copy the Word source code.

@BryanKrause - so many attempts to teach/answer. Hence why you’re a better [person] than I am, Gunga Din.

First of all, concerning the theory of epigenetics and the concept of epigenetic modification of 'gene expression' -- or of the data encoded in DNA in the form of its base sequence and structural conformation --, it is important to realise that all the enzymes implicated in such epigenetic processes must themselves be encoded in DNA and produced through the mechanisms of transcription and translation, all of the enzymes and proteins associated with which processes, transcription factors and so on, and including histones themselves, must also be thus encoded.
Putting aside such contention about what is inevitably the self-controlling function of DNA transcription however, the conception of a genome constituted primarily by the DNA molecules comprising cell nuclear chromatin is a theoretical construct permitting a broad understanding and its more-or-less consistent experimental verification of the phenomena of heredity and of the relation between the old-fashioned ideas of the phenotype and genotype.
The derivative notion that DNA contains all the information necessary for the growth of organisms is only the imputation of the prevailing paradigm of causality to that relation: thus that the form of DNA 'causes' the intricacies of growth to occur -- and this is no doubt useful in an empirical context, particularly one in which the genome embodied in or by DNA is to be manipulated towards some end.
However, it might be helpful at times to consider the scenario from a different philosophical perspective, to put the horse before the cart as it were, and to imagine that the dynamic and evolving structure of DNA is rather a reflection, at what we define as the cellular level, of the singular process of life, growth and attendant evolutionary transition -- correspondingly understood as an orderly process -- conceived in its more essential sense, than its cause; therefore to view DNA as a theoretical instrument for describing fairly precisely and in an analytically consistent way in physico-chemical terms this singular process, notwithstanding significant gaps in the capacity for that theory generally to account for the entirety of that instrument: for example, to account for the function of non-coding DNA (which must inevitably require a revision and expansion of the philosophical perspective itself).
Clearly there is far more to this process of life and evolutionary growth than can be accounted for by the view of DNA as it currently stands in orthodox cellular biology, even if it is also true that there is no conceivable aspect of that process which will not be reflected -- which will not have its manifestation -- at some level, however subtle, of that dynamic structure and conformation of DNA.

It’s nice that you gave an answer, but one of the top expectations on this site is that answers are supported by reliable sources. Please provide some support for your answer(even though it’s good, helpful, and a perspective as opposed to an actual answer.)

@anongoodnurse  The intention was only to proffer a reasoned response to a question which cannot really be answered in the ordinary sense, not the least because the terms are ill-defined -- 'information', 'build an organism'. Eventually, the only way to address confusion about the relation between the chemical structure of the genome and the phenomenon of living organisms, of dynamic life itself, is to adopt a view capable of putting the theoretical construct of DNA as the basis of the genome in its proper philosophical perspective. The logic of a perspective must be able to support itself.

I am only informing you about site culture, which is meant to be helpful. You have no upvotes; I hope that changes. This type of answer may be perfect on a different site. That says something about the site and about the answer. It doesn’t answer the question, that’s all. On this site, answers must do that.

The main remit of the Stack Exchange network is to exist as a repository of knowledge and solutions to problems. Whilst a fresh perspective on the underlying philosophy of an approach can be healthy and sometimes very necessary, it's not what we do here.

As you wish. The question had remained unanswered for 5 days, which should tell you something about the sort of response required -- which is one that attempts to reframe it in terms more likely to address the philosophical confusion implicit in that question itself. Perhaps I should have been more succinct: 'We' do not KNOW that DNA, considered as a 'molecule', contains ALL the 'information' etc., nor CAN we know that. At the same time, we do not NEED to know that in any meaningful empirical context. Also, the first paragraph of the answer DOES address the contention about epigenetics.

Your reasoning is appreciated, as is your willingness to help the OP. On this site, the answer is not philosophical, it’s empirical. It’s also(to me) just too broad and the OP too argumentative to bother answering the question.

Here's an example of missing information.  When scientists inserted the fly's eyeless gene into a mouse, it created mouse eye cells, not fly eye cells.  So, the gene had enough information to signal "create eye cells", but did not have the information to specify the kind of eye cell.  In the context of my question, this is an example where the eyeless gene has insufficient information to create an eye.

@yters It's also an example of the limitations of the term 'information' in such contexts; as pointed out in the answer you cite, this sort of example clearly illustrates the experimental impossibility of validating your argument in the way you suggest, which is not to say that the idea itself that there is more to the elaboration of living organisms than the physicochemical form of DNA construed as the substrate of the genome is incorrect.Consider the case in which sensory 'information' is conveyed to mechanisms of epigenetic modification of 'gene ' expression. While the origin of this data..

...while the origin of this data is exterior to the cell and even the body, it becomes 'information' relevant to the organism only within it; moreover, all the pathways of this transmission and transition of such data to epigenetic function -- including the constituents of sensory organs themselves: cilia in the nose, tension of the stapedius muscle and so on -- directly implicate enzymes and peptides, including transcription factors etc, whose production is eventually encoded as some form of 'information' within the cell, primarily in the structure of DNA, but also importantly within...

...within the whole cellular and cell nuclear context of that DNA, conceived in its dynamic entirety; meaning that this inevitably includes such information as the relation between chromosomes, and between DNA constituents of cell nuclei and of mitochondria, in cells adjacent and distant, considered at a quantum mechanical level

...considered at a quantum mechanical level. A real can of conceptual worms, especially in the empirical terms of attempting to relate specific pieces of DNA explicitly to crude phenotypical features. It is however a subject worthy of deeper contemplation than is likely pertinent to experimental scenarios; which is what ordinarily leads to some expansion or revision of 'philosophical perspective'. Good luck with that; it can get pretty scary sometimes.

What I don't understanding is why the term "information" is considered confusing in this discussion.  Information, in my programming mind, is the bits encoding instructions on how to bring about a certain result.  Take Windows, for example.  The code for Windows contains all the instructions necessary to instantiate the operating system within a particular hardware context.  However, the code does not contain all the instructions necessary to create the hardware context.  Likewise with an organism's genome...

Likewise with an organism's genome, the question is whether it is the same sort of situation.  Obviously, within the context of a cell and the womb, the genome has enough information to instantiate a particular creature.  But, is the information sufficient to create the cell and womb?  Let's imagine we have the perfect scientist, with skill and knowledge way beyond current human limits.  Can this scientist, with full knowledge of biochemistry, look at a genome and use the instructions encoded there to make the creature, womb and all?  If not, then there is further information...

If not, then there is further information necessary for the generation of the creature that is encoded elsewhere than the genome.  This has practical implications.  My prior naive understanding of genetics was that all DNA was in a sense "interchangeable".  Every genome contained a complete set of instructions to generate a creature.  Which also means that different instruction sets could be mixed and matched (at least by our perfect scientist) and generate new creatures....

and generate new creatures.  For example, our perfect scientist could graft in the wing instruction set from a bat into the genome of a walrus, and with suitable adjustments to the genome code taking into account the new environment, could produce a flying bat walrus.  On the other hand, if the genomic information is incomplete, and epigenetic information is also necessary for creation of the bat wing, then no matter what DNA from the bat genome is spliced into the walrus genome, our scientist will never be able to attach bat wings to a walrus....

bat wings to a walrus.  In a more practical context, human characteristics may not be fully reducible to the genome, and so no matter how much knowledge we gain about manipulation of the genome, we may never be able to, say, give everyone a perfect IQ, exquisite physical beauty, nor extremely long life.  Such human traits may be hereditary, but not encoded in the genome, but encoded in some other fashion...

encoded in some other fashion. That bioengineering human perfection is possible through manipulation of the genome I believe is a huge assumption of the modern biotechnology enterprise, one which no one appears to apply much of a critical eye.  Going back to my question, this sense of information as the instruction set which gives full control over all aspects of a creature seems plain to me, and I'm curious why we are confident this complete instruction set is contained within the genome.

@jeremiah I've rewritten my question with a specific example.  Hopefully this is clearer what I am asking.

@yters Quite right: more generally, sensory 'information' is modifying the existence of an organism at all times through what amount to 'epigenetic' means. However, in order to respond to this 'nurture' side of things. the state of the organism must already be open -- primed -- to respond to it; it must be able to 'hear' the data as it were, and this is the function of the dynamic condition of the DNA/genome at any moment. You must ask yourself WHY you are asking this sort of question and the answer to that is philosophical: thus the form of my answer, which as is evident is not welcome here.

All philosophical inquiry, into truth, eventually reduces to a single question: is all of this beautiful intricate reality accidental, or is it ordered? Here it is critical to concede that if universal reality is ONE INDIVISIBLE UNITY, one 'quantum field', one 'substance' etc., then it must be one or the other, totally and entirely accidental, OR totally and entirely ordered by a singular universal CAUSE. Real understanding, wisdom, flows only from the latter if the assumption of universal unity is accepted as self-evidently true. The prevailing paradigm in the sciences is based on the former.

@jeremiah I'm asking because what I was taught about DNA does not seem to be correct based on what I now know about science.  Yes, there may be some sort of teleological cause behind it all, which does seem the much more plausible explanation.  I have a lot of experience programming, and my MSc was in evolutionary algorithms, and evolutionary algorithms cannot produce anything like the intricately arranged structures we see in animals, nor the sort of code that programmers can write!


text:
Order of iNaturalist taxon levels
Purpose
I want to take a collection of iNaturalist observations and build a tree diagram of the taxonomic levels that occur in that sample.
Background
Most of us have seen diagrams like this

or like this

that illustrate some of the taxonomic ranks that biologists assign organisms into.
I am looking at the data export options for iNaturalist and I see that there are more possibilities than conveyed in these simple diagrams. I am also unfamiliar with precisely what these added levels are telling us. I could ignore these additional levels, but I would rather not if they are biologically meaningful. I have tabulated these export variable options in the order that I am guessing they belong in, alongside the similar names mentioned on wikipedia.

iNaturalist
Wikipedia

taxon_kingdom_name
Kingdom

taxon_phylum_name
Phylum

taxon_subphylum_name
Subphylum

taxon_superclass_name

taxon_class_name
Class

taxon_subclass_name
Subclass

taxon_superorder_name

taxon_order_name
Order

taxon_suborder_name
Suborder

taxon_superfamily_name

taxon_family_name
Family

taxon_subfamily_name
Subfamily

taxon_supertribe_name

taxon_tribe_name
Tribe

taxon_subtribe_name
Subtribe

taxon_genus_name
Genus

taxon_genushybrid_name

taxon_species_name
Species

taxon_hybrid_name

taxon_subspecies_name
Subspecies

taxon_variety_name
Variety

taxon_form_name
Form

Questions

Is there a total order on the iNaturalist taxon levels? If not, what are the exceptions?
Do I have the taxonomic levels in the right order in my table?

Wikipedia has another table with some more of these levels: https://en.wikipedia.org/wiki/Taxonomic_rank#Terminations_of_names

I am not interested in software recommendations along the lines of "just put your data in <software_name> and it will figure it out". I have software solutions. I want a conceptual understanding of the (possibly partial or total) order.

I'll just point out that these rank-based definitions are highly problematic and not really consistent with current thinking (despite their prevalence on the web). https://biology.stackexchange.com/questions/55457/why-is-traditional-rank-based-taxomomy-considered-by-some-as-logically-inconsist

Too echo what @kmm says, these other middle/intervening levels of the hierarchy exist precisely because it doesn't quite work to build a hierarchy like this. When you want to refer to some relevant group, you sometimes have to come up with a new name for it.

This may be a better question for the iNaturalist forums.

I believe this is the correct order, based on this question:

kingdom
phylum
subphylum
superclass
class
subclass
infraclass
subterclass
superorder
order
suborder
infraorder
parvorder
zoosection
zoosubsection
superfamily
epifamily
family
subfamily
supertribe
tribe
subtribe
genus
genushybrid
subgenus
section
subsection
complex
species
hybrid
subspecies
variety
form
infrahybrid

Note that the hybrid ranks, biologically, break the otherwise strict hierarchy.
This FAQ may also be helpful.


text:
What is the name of this species of bird?
I've enjoyed watching this pair of birds build a nest in my patio light.  One bird now appears to be in residence, and the red bird seems to come and go.  I think they might be mates?  These photos are taken in Mesa, AZ, in the USA.

And here's the red bird:

The birds are pretty small.  I'd say maybe 4-5 inches from beak to tail.  As I said, this nesting behavior started about a week ago.
Can anyone help me identify these birds so I can learn more about them?

Check out the Cornell Lab of Ornithology app Merlin (https://merlin.allaboutbirds.org/) it has a super easy to use and intuitive way to help you ID birds in your yard. You put in the approx size, colors, location, and it gives suggestions with pics and info. Very fun!

Thank you @selene, that app looks fantastic.  I wasn't sure what to put for what the bird was doing so I selected "On a fence or wire" as closest and it listed the house finch as the second search result.  I'll definitely be keeping this in my back pocket.

great! It's pretty forgiving on the location I think so I'm glad it still gave you what you needed :D

Also check out the iNaturalist app. It is for any recent evidence of life, including observing birds.

House Finches Haemorhous mexicanus (pair).

These birds are mainly permanent residents throughout their range;
some northern and eastern birds migrate south. Their breeding habitat
is urban and suburban areas across North America, as well as various
semi-open areas in the west from southern Canada to the Mexican state
of Oaxaca; the population in central Chiapas may be descended from
escaped cage birds.
They primarily eat grains, seeds and berries, being voracious
consumers of weed seeds such as nettle and dandelion; included are
incidental small insects such as aphids. They are frequent visitors to
bird feeders throughout the year, particularly if stocked with
sunflower or nyjer seed.

Copyright unknown, via eu.gosanangelo.com 2022, fair usage
The female is the least colourful of the pair, here seen less fluffed-up:

Paul Lauenstein (mis-named in this case), via Sharonfoc.org, 2022 fair usage.

Looks like a match to me, thank you!  The birds in your first photo seem a bit portlier than mine.  :)   I'll wait a bit before accepting as per convention.


text:
How does non-cell autonomous work - how can a mutant cell make other non-mutant cells exhibit a mutant phenotype?
I am reading a journal paper, and I have coming across the following statement:

Furthermore, although late-born neurons that take up exogenous Dcc
fail to settle in the superficial layer of the dorsal horn, other
non-electroporated late-born neurons exhibit no apparent aberrant
migration. Thus, Dcc appears to function in a cell autonomous manner.

I am not sure, in the context of the paper, what is meant by "cell autonomous". I have come across this definition, where it is said that cell autonomous means: "A genetic trait in multicellular organisms in which only genotypically mutant cells exhibit the mutant phenotype. Conversely, a nonautonomous trait is one in which genotypically mutant cells cause other cells (regardless of their genotype) to exhibit a mutant phenotype."
I am assuming that cell autonomous in the context of this paper is that neurons that took up exogenous Dcc had migration defects, while neurons that didn't take exogenous Dcc migrated properly.
One thing that I am wondering is, in the context of non-cell autonomous, how can a mutant cell make other non-mutant cells exhibit a mutant phenotype? Any insights are appreciated.

This is one of those cases of biology terminology that really makes me groan, because although it can be a useful designation, the word choice is just... not excellent.
Cells interact with each other all the time, particularly in a multicellular organism: it's absolutely essential that they do. That means that one cell type can influence the behavior of another cell type.
When you describe some mutation as "cell-autonomous", you're basically saying that the phenotype is just dependent on the cell where the mutation is expressed. For an example off the top of my head, a mutation in a pigment-producing enzyme causing albinism is almost certainly going to be cell-autonomous: if you introduced the mutation in only the pigment-producing cells, you'd get exactly the same result as if the entire organism had the mutation. You could understand what is going on if you just cultured some of those cells in a dish and compared those with and without the mutation. You don't need the whole organism to understand what's going on, just the autonomous cells in a dish.
You ask about non-autonomous, though. Again, I think it's easier to use some example. Searching Google scholar for "non cell autonomous" one of the first results is this paper:
Di Giorgio, F. P., Carrasco, M. A., Siao, M. C., Maniatis, T., & Eggan, K. (2007). Non–cell autonomous effect of glia on motor neurons in an embryonic stem cell–based ALS model. Nature neuroscience, 10(5), 608-614.
They're looking at mechanisms of amyotrophic lateral sclerosis (ALS). ALS is a neurodegenerative disorder: the overall phenotype is that neurons die. However, this paper isn't about neurons, it's about glia. When you co-culture neurons and glia, you're looking at the neurons for the phenotype (do the neurons die?), but it's the glia where the genetic manipulation matters. This particular paper is about SOD1, which is involved in protection from oxidative stress.
Back to your paper, this is talking about neuronal guidance cues that are important in the developing nervous system. Simplifying a bit, typically neurons express some collection of receptors for various guidance cues, and other cell types present these cues on their cell surface or excrete soluble molecules. Growing neurites then follow the concentration gradients (either in an attractant or repellant fashion) to get where they belong. Dcc is also called the netrin receptor. The authors describe mutations in Dcc as being cell autonomous for neuronal migration, because you only need the mutation in the neurons to see the phenotype. This makes sense mechanistically because it's a receptor expressed by the neurons themselves.
However, if you had a gene of interest involved in netrin-1 synthesis or expression, that would possibly demonstrate a cell non-autonomous phenotype: it doesn't matter if you interfere with netrin-1 expression in the neurons themselves; as long as their receptor and signaling pathway is intact, they'll navigate just fine. However, if you put normal, unmutated neurons into a nervous system where all the other cells fail to express netrin-1, even those wild-type neurons won't know where to go. The phenotype: failed migration, is occurring in a different cell type than the ones that need to be genetically altered for the organism to show the phenotype.


text:
Why do bacteria denitrify?
Denitrification is the microbial respiration in anoxic condition. If the process is complete we have :
$$2 \text{NO}_3^{-} + 10 \text{e}^{-} +12\text{H}^+ \rightarrow \text{N}_2 + 6 \text{H}_2\text{O}$$
In this series of reactions, nitrate and hydrogen are transformed into nitrogen and water with bacteria's energy. All the elements are given back to the environment. So why do bacteria denitrify? What do they take for themselves in this process?

The same thing they get from aerobic respiration, just less of it.

Need water? Need to lower pH? Remove excess nitrogen to something relatively inert?  These questions might serve to hypothesize about the 'biological function' that this chemical reaction serves in the metabolism of an organism.

nitrate is energy you can even use it to make explosives so it contains a lot of energy for bacterial growth.

Welcome to SE Biology. One of the things we ask people who ask questions to do is to research their question themselves before posting, and tell us what they found and how it was insufficient for their purposes. One obvious resource is WIkipedia which gave me the answer. Did you try that and understand the page? You say that this process uses energy — but that is not correct. Have you learned about energy generation in living organisms?

I said 'lower pH' above, but rather it would be 'raise the pH'. I meant lower the hydronium concentration rather than lower the pH.

On the topic of energy, "Denitrifying bacteria use denitrification to generate ATP." is suggestive.

Notice that the reverse process, biological nitrogen fixation, requires lots of energy.


text:
How does a (stem) cell keep track of its own 'specialization'?
If I understand correctly, as stem cells divide, they become more and more specialized. The very first (fertilized) cell still can divide into every other cell in the body, but as they divide further, each cell can divide only into a smaller subset of different cell types.
However, it seems that (other than gametes) each cell contains the full genome, an identical copy of the entire DNA. So if the DNA does not get altered as cells specialize, how does a cell keep track of which parts of that DNA it is supposed to read - and how does it tell its daughter cells to change their specialization when it divides?

This is the age-old question.  Since DNA encodes all the data for growth and differentiation of cells, and since every cell; contains essentially the same complement of DNA, how does each cell differentiate from others?  In the usual answer, reference is made to transcription factors and epigenetic factors etc., but since these must also be encoded in DNA itself, the essential question remains.  Eventually reason demands some sort of deterministic approach and a corresponding mechanism. One might propose  -- and I know that this site is averse to such conjecture --...

.. one might propose a wave dynamic in which not only is DNA itself, its structure and chemical constituents -- its entire substance, in common with the rest of reality-- the function of a fundamental 'wave interference effect', but both its mechanisms of replication and transcription conform to the progressive aspect of such an oscillatory wave principle. An incremental advance in the property of wave recurrence both within the pattern of transcription itself and in its cell-to-cell aspect would permit both features of the phenomenon of cell differentiation: that each cell derives its own...

.. each cell derives its own characteristic and definitive set of both basic and more-or-less specialised proteins and that successive cells in contiguous relation to each other derive proteins which differ slightly in conformation and definitive identity as this wave effect progresses incrementally from cell-to-cell; this latter aspect in particular implicating the requisite production of transcription factors etc. commonly encoded in all DNA. Clearly such an idea requires some substantial modification of what is eventually the philosophical approach to scientific inquiry, of its paradigm.

The process of "specialization" is usually referred to in biology as "differentiation".
Largely, differentiation is a function of expression of transcription factors; these proteins determine which proteins are synthesized in a given cell by either promoting or suppressing transcription. Transcription factors can also influence the transcription of transcription factors themselves. Simplifying things a bit, imagine you have a "muscle cell" transcription factor, we'll call it "MCTF", that is only expressed in muscle cells. MCTF binds to DNA and causes transcription of muscle-related genes, including MCTF itself. It also causes transcription of not-a-neuron transcription factor ("NNTF"); NNTF binds to DNA and prevents transcription of neuron-related genes.
Epigenetic modification including DNA methylation and histone modification can also silence sections of the genome to make cell fate a bit more concrete and less likely to revert.

Thanks! So is the emergence of a new transcription factor that specializes the cell based on some probabilistic process? Like if an "arm cell transcription factor" is present on each division a cell will produce with some probability a "hand cell transcription factor"? Or how are new transcription factors introduced into daughter cells that weren't present in the parent cell?

@matthias_buehlmann That's quite complicated and too much to talk about in a single SE answer, I feel. A textbook on developmental biology would be a good place to start. Very generally, in early embryonic development there are some push-and-pull stochastic relationships, where certain molecules might signal "head" or "front" and others "tail" or "back"; "head" makes more "head" and suppresses "tail"; "tail" does vice-versa. What starts out unstable very quickly reaches an equilibrium where "head" and "tail" are clearly separate. Something similar happens at local scales, as well.

@matthias_buehlmann https://en.wikipedia.org/wiki/Cell_fate_determination is another place to start reading.

Transcription factors usually initiate the cellular changes, but it's mostly the chromatin state of the nucleus that maintains the state of a cell and stops it from changing back and forth.
Embryonic stem cells start out with open chromatin ('open' means 'accessible'). This means low DNA methylation and overall epigenetic modifications that enable transcription. This can be interpreted as "a cell with full potential", since many regions on the DNA are available for transcription.
The further a cell differentiates, the more DNA regions assume a closed chromatin state, meaning higher DNA methylation and repressive epigenetic marks that lead to DNA condensation. It's as if the 'potential' decreases, since huge regions on the DNA become 'locked up'. These huge regions on the DNA are partitioned into 'TADs' (Topologically Associating Domains) and their epigenetic state can be determined by ATAC-Seq
See this review for reading about chromatin state and stem cells.
As mentioned by Bryan, specific transcription factors are unique to a cell type. Some transcription factors bind to multiple promoter regions and initiate a complex differentiation program that orchestrates cellular/biochemical/morphological changes needed to fulfill specialized function.
The promoters involved in cell differentiation can be in a 'poised' (aka 'bivalent') state, meaning that they got both transciption -inducing (H3K27me3) and -repressing (H3K4me3) epigenetic marks, so it's as if these promoters are "ready and waiting" for a signal to decide whether to transcribe or lock up a DNA-region. And once a DNA region is locked up, the cell knows that it has lost some potential and "knows" what cell type it is. Lesch & Page 2014
Such poised promoters are not just present in embryos, but also in adult tissues, like mesenchymal stem/stromal cells (MSCs) in the bone marrow. The RUNX2 Promoter is poised and is waiting for signals to turn the MSC into an osteoblast (or chondrocyte or adipocyte). Wu et al 2017


text:
Photolysis of water
Photolysis of water releases $\text{O}_2$, $\text{H}^+$ ions and $\text{e}^-$.
$\text{Mn}$ in the $\text{O}_2$ evolving complex also produces $\text{e}^-$.
What provides $\text{e}^-$ to P680:$\text{Mn}$ and water?

Can you clarify your sources and where this information derives from? Even though this is related to fundamental biochemistry that every undergraduate learns, it's still good for us to understand what your materials are.

Consider this diagram from Wikipedia.


text:
Could a bearded woman ever become pregnant?
I am referring to woman who are facing Hirsutism. So I gone through Hirsutism, there is no mention of pregnancy. So could a bearded woman ever become pregnant ?

Did you research this much before posting? A quick google shows a lot of results.

Welcome J to the community and please make sure you do a thorough search prior to posting, with that, two noteworthy items:
1- Your title is misleading. It could be modified by adding Hirsutism. "Bearded woman" may cause confusion.
2- Referring to the wiki page you mentioned:
Diagnosis of patients includes assessment of ovulation and ovarian ultrasound as well as 17α-hydroxyprogesterone. (DHEA-S) levels >700 μg/dL is indicative of adrenal gland dysfunction.
This means that the reproductive system may not have much to do with facial hair growth. The diagnosis will cover its prevalence.

Yes.
There is a famous Mexican family that suffers from hypertrichosis and female members of that family have given birth to children. The BBC has an article about them here

Aceves has three daughters, all of whom have been born with hypertrichosis. His eldest, Karla, is now in her early 20s.

"It's harder for the women because it's less socially acceptable for a woman to be very hairy," says Eva Aridjis. "Most of the women have been abandoned by the non-hairy partners that fathered their children. But for the men, they are actually considered virile and tend to have a lot of girlfriends...

After giving birth to a baby, she was abandoned by the child's father.


text:
Should soundscape ecology be a component of STEM education?
I'd like to see soundscape ecology be included in STEM education. I realize there is so much to teach and so little time, but think that primary and secondary students would be highly motivated and interested to learn about this topic and its importance to us all. A basic lesson including definition and examples of soundscapes from different realms (aerial, terrestrial, freshwater, marine, subterranean, etc.). Especially classes like biology that include "lab" components, it does not cost much to get a simple hydrophone and microphone and dat recorder and bring kids out to the field to listen and then show them how to look at acoustic data. It might be an exceptional way to integrate physics, biology, geography, and societal concepts into one lesson plan. Does anyone know of schools incorporating this? Example of some basic info (a bit too specialized): https://youtu.be/NplXdD616WM,  https://fieldnotes.nationalgeographic.org/expedition/listeningtofish, http://www.fishecology.org/soniferous/Listening%20to%20fish%20children's%20book%20final%20wlinks.pdf

What's the question - should it, or is it?

The FishSounds project (https://fishsounds.net) just got a grant to produce classroom and lab materials for marine acoustic and soundscape education. Material should become available within the next year. We hadn't considered tracking which organizations or schools are using the material, but likely could (and I can see the benefit of the resulting dataset)

These sorts of opinion questions are frowned upon across the SE network; I know a bunch of you are interested in starting a new SE site, but I highly recommend immersing yourselves in what rules the site has found to work well for curated Q&A here and not bypassing them by upvoting every post by a fellow Area51 contributor - you're doing your colleagues a disservice.

God help education from hobby horse jockeys!


text:
Many viruses use pressure to pump viral DNA into host cells. Does that mean these viruses have a narrow acceptance of the genome size?
DNA viruses like bacteriophages and herpes viruses have rigid capsids. The viral DNA is densely packed inside, and the internal pressure is 1~2 orders of magnitude higher than the atmospheric pressure. When the capsids open, the viral DNA is pumped out by the pressure. Considering that DNA is not easily compressible like gas, a slight variation of its length will result in dramatic change in the pressure. As a result, if the DNA is slightly longer, it would be difficult to package it into the capsid during the assembly. If the DNA is slightly shorter, the pressure may be too low to pump the viral DNA out during the cell entry.

Please quote a source for these claims, as the idea of pressure within viral capsids is new to me at least. How is this supposed pressure generated and what form does it take? Are you saying that there is compressed air there? Are you aware that two orders of magnitude means “100s”?

Stress in the capsid is the dominant factor throughout early ejection, with the pull due to binding particles taking over at later stages.
https://www.sciencedirect.com/science/article/pii/S0006349506717428

There isn't enough data to give a clear answer to this question, but I can at least explain what I know.
First, it's not 100% certain that genome ejection of tailed phage and herpesviruses depends on stored pressure in the capsid. This is called the continuum mechanics model; but another possibility, the hydrodynamic model, suggests that the difference in osmotic pressure between the cytoplasm and outside environment allows water to flow through the capsid and tail into the the cell, dragging the DNA payload with it. Personally, I am skeptical of this second model because it doesn't seem to explain herpesvirus genome ejection, and it's not consistent with the lethality of R- and F-type pyocins, which are essentially just decapitated phage tails. But there is still some question as to how the genome gets fully out of the capsid.
Assuming that the continuum mechanics model is closest to correct, the nature of the pressure generated when DNA is loaded into the capsid by the packaging ATPases is not intuitive. From a 2013 review:

At this concentration, DNA is highly condensed, and much of the water that normally hydrates the DNA and its counterions must be removed in order to package a complete genome. Water removal during the packaging process occurs by reverse osmosis, the energy for which is derived from the activity of terminase.

Only about 10% of the energy stored in the packaged phage DNA is due to bending DNA more tightly than its persistence length. Most of the energy internal to the capsid is due to the dehydrated state of the DNA, which is reflected by internal osmotic pressures that reach tens of atmospheres.

...And from the herpesvirus paper linked above:

DNA can fill as much as 60% of the internal capsid volume, with the remaining volume fraction occupied by water molecules and small ions that freely diffuse through the capsid wall.

So, despite what we'd expect from our macro-scale experiences, the DNA IS compressible almost like a gas. Small differences in the length packaged won't change the final pressure dramatically.
Also, many of these viruses use a so-called "headfull" packaging method. The viral genome is copied continuously, with the end of one copy linked directly to the beginning of the next copy. The ATPase motor packs this continuous chain of genomes into the capsid until the pressure reaches a certain level, then the motor stops packaging and cuts the DNA chain into a piece inside and a piece outside.

When a threshold amount of DNA, representing
about 103% of the SPP1 genome, has been packaged (headful) a
sequence-independent DNA cleavage terminates the encapsida-
tion cycle (Fig. 1A).

So what will happen to a variant of the phage mentioned here, SPP1, if an insertion mutation increases the length of its genome by more than 3%? I don't know, but in my experience with capsid assembly, it's not uncommon for a small number of large capsids to be produced along with the normal capsids, so possibly large-genome mutants can get by until the structural proteins co-evolve to make the larger capsids the new genome requires. Alternately, even if individual virions no longer contain the whole genome, if multiple virions infect a single cell, all genes will be present in at least one copy, again giving the structural genes time to evolve.

That makes sense. If DNA is very stiff like water, the pressure will lose quickly as long as only a little DNA is spit out. So DNA must have an effective “bulk modulus” like gas, which enables the capsid to pump out the DNA continuously. Whether the pressure is due to compression, dehydration or Coulomb repulsion is insignificant.

The mechanisms that generate pressure inside the capsid are complex and nonlinear, so you can't really assign a "bulk modulus" to the whole thing. You could probably estimate a modulus for when capsid is 0-30% full, another for 40-55% and another for >60%, with intermediate values in between where no one mechanism is dominant. All the phage motors I know of can "switch gears" to package rapidly when there is low resistance, then package more slowly when resistance is high.


text:
What is the median concentration of spike antigen in COVID positive patients?
I am searching for the plasma spike concentration in COVID patients. The closest possible reference I found claims that spike was only detectable in 5 of 64 COVID-19 positive patients.
However, their spike assay is relatively insensitive with a LOD (limit of detection) of 70 pg spike protein/ml; multiple vaccine-related studies detected a spike concentration of around 1 pg/ml.
Are there better sources?


text:
Why does biomagnification of mercury occur more in large fish?
I love tuna so this question has been bugging me senselessly.
I am aware that larger fish tend to have more mercury concentration in their flesh than their prey, however, I don't understand how this can be possible.
I understand that there will be more mercury in the large fish than the small fish as it collects in the large fish over time, but why isn't it distributed across a much greater volume of animal tissue, therefore keeping the overall concentration the same?
The only thing I can think is that the larger fish have some reduced capability for excreting mercury. Whatever the reason, why don't we hear about it? Why is it always "bioaccumulation" this or "biomagnification" that?

Bioaccumulation occurs when organisms aren't able to excrete/eliminate/metabolize something as fast as they take it in. The specific circumstance of predators higher on the food chain accumulating even more is called biomagnification.
Every organism needs to eat more than it weighs to grow, as a simple consequence of conservation of energy. If you have a predator fish that eats smaller fish, it will have eaten far more than 10 kg worth of smaller fish by the time it grows to 10 kg in size. If it ate 100 kg worth of prey fish that each had 1 unit/kg of mercury and it can't excrete mercury effectively, it would now have 10 units/kg of mercury. The biggest fish eat prey that already experience the biomagnification effect in their own diets, taking the overall effect even further.

You hit the nail on the head! It didn't occur to me that the fish would have to eat substantially more than their body weight to grow (duh).

@JordanRegan This is also the same reason you get more food by eating the vegetables that an animal would otherwise eat than eating the animal itself.

[+1] Now I learnt the difference between "bioaccumulation" and "biomagnification".


text:
Human biology - liver regeneration after laprascopic segmentectomy
I am trying to understand to what extent human patients can regenerate liver mass after laprascopic segmentectomy: what part of liver will be regenerated and how fully.
My work with sources is not very good, but here is what I have found so far:
Michalopoulos, G. K., & DeFrances, M. (2005). Liver regeneration. Advances in biochemical engineering/biotechnology, 93, 101–134.:
"Following surgical resection of the two anterior hepatic lobes of rodents accounting for ~68% of liver tissue, the remaining lobes undergo compensatory hyperplasia restoring the liver to its original presurgical mass"

However, the article notes that:
"..PHx model doesn't apply to most common clinical scenarios.. patients who must regenerate liver mass after hepatic surgery often have cirrhosis, hepatic viral infection, steatosis.."
From this question (If the liver can regenerate why can alcohol abuse permanently damage it?) I gathered that only healthy hepatic tissue in liver can regenerate: the epithelial tissue.
Cytotoxic drugs like alcohol lead to steatosis and cirrhosis. Cirrhosis is the substitution of epithelial tissue by connective tissue. This connective tissue not only can't regenerate: it doesn't perform hepatic functions.
Assuming that the patient has otherwise healthy liver tissue, if a laprascopic resection of liver segment Sg3 has been performed, what part of the liver will be regenerated?

Thank you in advance, and I would be happy to edit/update my question with more info.

The healthy human liver has remarkable ability to regenerate in only a few months after resection.
In a study of 98 healthy donors who underwent left lobectomy donation, Chen and colleagues found that donors started with a mean liver volume of 1154 cm³, had an average of 276 cm³ removed, and then had an average liver volume of 1065 cm³ 6 months later (2006. PMID 17100722). Thus, on average, 68% of the donated liver volume had regenerated in those 6 months.
In my research, I was unable to find a systematic study of the location or direction of regeneration. Although hyperplasia appears to be the mechanism of regeneration (Marongiu et al 2017. PMCID 5352916), intuitively, we should suspect that the remaining liver will increase in volume rather than the removed lobe suddenly re-spouting somehow like a salamander's tail.
This set of 3 CT scans from a study by Esschert and colleagues provides anecdotal evidence for this intuition (2009. PMCID 2710489):

Figure 1 from Esschert et al 2009 showing post-operative liver regeneration after 3 months, available here.
In addition to the return of liver volume, donors also have no evidence of decreased liver function at least as long as 5 years post-operatively (Murad et al 2016. 27144969).
The above studies do not appear to delineate whether surgeries were performed open or laparoscopically, but I suspect that any effect of the less invasive laparoscopic procedure would only improve regeneration.
As an interesting aside, even after performing as many as 4 separate resections for patients with recurring hepatocellular carcinoma, Yamaguchi and colleagues found continued high rates of liver regeneration (over 90%) (Yamaguchi et al 2018. PMID 29947985).

Thank you for your excellent answer, Ian! Great first post!


text:
Is there always a leaf(s) attatched to an auxillary bud?
I'm trying to create a 3D functional-structural plant model and I need to establish some axioms.
Is it guaranteed or extremely likely that where auxiliary bud forms there's a leaf(s) attached? That's what it appears to be from most of the images I saw. If so, what usually comes first, the leaf or the bud?
More generally, is there a rule about where a leaf is guaranteed to naturally grow? Perhaps suggest some literature on this. Thank you!


text:
Do *Ambystoma macrodactylum* predate on *ceuthophilinaens* like the one I observed?
I observed this Ambystoma macrodactylum within half of a meter of this Ceuthophilinaen under an old board. I can imagine salamanders eating cricket-like things, but this question is far outside my expertise. This page says that long-toed salamanders prey on small crustaceans, dipterans and tadpoles at the larval stage, but doesn't seem to discuss their terrestrial diet. Not much about predators on the putative prey's page.
Do Ambystoma macrodactylum predate on ceuthophilinaens like the one I observed?


text:
Why does the ecosystem of my house seem inverted?
My understanding of a typical ecosystem is that it is like a pyramid, with the mass of prey at the base and the apex predators at the peak.
However, the arthropod ecosystem in my house seems to be the inversion of this.  When I see critters, I mostly see spiders and centipedes, the apex predators.  Rarely do I see anything else.  This seems upside-down.  Shouldn't the apex predators of an ecosystem be relatively rare?

I’m curious why you think the apex predators should lay low. They’re apex predators. If anything should lay low, shouldn’t it be the prey? Also, there are different ways to remain undetected.

@anongoodnurse – I guess I'm thinking of something like a jaguar or panther which is very elusive.

Spiders that use webs are quite easy to spot for humans because they are stationary and they tend to be in the same places. The same isn't true for their preys which, for the record, need not be part of the ecosystem of your house: they can be some animals that are passing by.


text:
What are the implications for a small bird flying at high altitudes?
Are the aerodynamics of a bird flying at high altitude significantly different than a bird flying at low altitude? I would imagine a bird adapted for low, short flights (such as between bushes and trees) would have a difficult time flying at a higher elevation. What sort of air patterns are the wings of a high-flying bird adapted to mitigate or take advantage of? For instance, I imagine cross-breezes are strong and more frequent, meaning a bird with wings suited for low altitudes would have to flap much more to avoid being pushed around.
For this question I'm only really concerned with the aerodynamics. Obviously a high-flying bird will also be adapted for less oxygen in the air and flying for longer without needing to eat, but that's slightly out of the scope of this question.
Apologies if this is a repeated question, I couldn't find anything relevant here/elsewhere.

75% of earths total mass of air is below 11 kilometers and it is mainly birds with large wings that can reach this elevation of 10 km +.


text:
Is this a bedbug or something else?
Found it on my bedsheet close to my pillow. My boyfriend had a couple of welts a few weeks ago on his chest, but we can’t seem to find any other evidence on the mattress or around it.

Welcome Mel. Please take our [tour] and refer to the [help] for our guidelines as and when. Could you add some more detail such as what area of the world you might be in, if there was food involved nearby etc..

Does this answer your question? Insect identification - Is this a bedbug?


text:
Poison of the Japanese Tree Frog
The Japanese Tree Frog (Dryophytes japonica) (EN / JP) has a poison on its skin that can even make you loose your eyesight, if you touch your eyes, after touching{NOTE}. I found quite a couple of site stating that you must be careful with the poison of the frog. But I could not find any site that states what exactly that poison is.
{NOTE} Stated by

Wikipedia JP:

手で触る分には問題ないが、傷ついた手で触ったり、触った手で目や口を擦ったりすると、激しい痛みを感じ、目に入った場合は失明することもある。
(google translate:) There is no problem with touching it with your hands, but if you touch it with your injured hand or rub your eyes or mouth with your touched hand, you will feel severe pain, and if it gets into your eyes, you may lose your eyesight.

Japanese blog

触った手で目や鼻、口などの粘膜に触れると、最悪の場合失明する恐れがあります。
(google translate): In the worst case, you may lose your eyesight if you touch the mucous membranes of your eyes, nose, mouth, etc. with your hands.

And various other blogs, which don't necessarily add much value to this list

Question: What is the poison the Japanese tree frog uses on its skin?
If possible, please add a reference.
Why do I want to know this?
I'd ultimately like to know how dangerous it is to keep the frog around:

Can I eat vegetables the frog touched?
Do I need to boil the vegetables before eating?
Can I wash the poison away with water?
Do I perhaps not need to worry, because the poison evaporates very quickly?
What happens, if the frog touches my clothes from the inside and I take on these clothes?

I can only start answering these questions if I know what exactly the poison of the frog is.

Have you tried asking a zoology professor at your university? (presumably you are in Japan if these are your concerns).

Welcome to Biology.SE. Please [edit] in sources for your claim about these amphibians having a toxin that can cause blindness. A cursory check found no corroboration for this claim. Please see the [tour] and consult the [help] starting with [ask] for details about how to use this site.

@DKNguyen I'm not a student; so no prof here.

@DarkTrick I'm not assuming you are. I'm literally saying to find and e-mail a professor out of the blue and ask. I guess I should have said "your local university" rather than "your university".

@tyersome I added two sources. Sources on this are 1) generally in Japanese and 2) generally blog post-like sites. I'm aware that those are unreliable. If the frog has not the claimed poisonous effect, knowing that the information spread is a false claim, is also an important insight.


text:
What is the heredity model of the following heredity tree?
I have the following heredity tree:

and I need to decide which heredity model it fits the most, with the least number of assumptions, from the following models:

autosome dominant
autosome recessive
X-linked dominant
X-linked recessive
Y-linked
mitochondrial

I think the answer is autosome recessive because of the following analysis:

and the only assumption which is significant (the other assumptions are about the non-family members which are that they are carriers of the hilliness, it isn't said that the illness is rare, so in examining any model different assumptions about the out-of-family members are made) is the assumption on the last generation where there is two ill persons instead of one if we cross their parents alleles: AA, Aa, aA, aa, but we got 2 aa and AA, Aa, but that can be explained by little statistics in the family, so it is hardly even an assumption at all.
Then I've been told that it is a rare illness and that it autosome illness and not a linked one, its also said as a clue that there may be some Mendelic exceptions (known exceptions from the Mendel heredity models).
So In my understanding its more probable that the model with this data is autosome dominant with father genomic imprinting the following way":

As you can notice for the classic autosome dominant model the circled one should be black (ill) but they are not, so my assumption according to the clue that the ill alleles are imprinted in fathers (males) and expressed only when they inherited from mothers (females).
Till this part I would like you to check me did I any wrong in this analysis, but my major question that made me doubt my analysis is the following:
In addition to previous data, is is now given the the ill girl in the 4 generation (which is black circle on the image) got pregnant from one of two males:
male A: healthy male with both parent healthy and and Homozygous both.
male B: ill male with one parent Homozygous and the second parent Heterozygous
It is also given that no matter who is the father, the chances of getting an ill child are 50%.
From the previous analysis I decided that the heredity model is dominant autosome, so the first contradiction to that, that one of the parents of male B is Heterozygous, means he carries the ill allel and the healthy allel, but then in dominant model he has to be ill, but it said both parent are healthy.
The second thing that should correlate to the model is the chances computation. If the girl is Aa as was established by previous analysis then if the father is male A, i.e. his alleles are Aa (because he is ill with parents which are aa and Aa), then the chances for a ill child are 3/4 because the options are {(A_father, A_mother),(A_father, a), (a, A_mother), (a,a)} and if the father is male B then his alleles are aa because his parent are both aa, then the chances of an ill child are 1/2, so the total chances are (3/4 + 1/2) / 2 which is 5/8 which isn't 50%.
Or maybe this is wrong for male 1, because if the ill phenotype is delivered only by women (mothers) because of male genome imprinting, then for the option {(A_father, A_mother),(A_father, a), (a, A_mother), (a,a)} only two will make the child ill and not 3 : (A_father, A_mother) and (a, A_mother), then the calculation will be (1/2 + 1/2) / 2 which is 50% indeed, and for the parent of male B being Heterozygous but not ill can be explained by the assumption that he/she got the allel from his father.
Is it correct that the exception of genome imprinting is for the whole illness and not for some ancestry ?
I'm not sure if genome imprinting is a phenomena for the ill allele (the whole illness) or per concrete ancestry? (in the second option it will be that actually I do another assumption on the male B ancestry, that the imprinting is also as in the given ancestry tree).
But this make some sense' isn't it ?
It made me doubt because if the model was autosome recessive, then the computation would give me exactly 50% without thinking and explaining about the male's B Heterozygous parent (which then would be healthy just a carrier), but then the previous tree seem to be much more complicated because if you only look at the first generation in this model:
if the father is AA (A - healthy dominant allele, a - ill recessive allele) and the mother is aa, then they shouldn't have any ill children (because their cross is {Aa, Aa, Aa, Aa}), but they do, that's why I started to doubt is it dominant autosome as I concluded.


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How does the brain activate retinal cones in darkness?
The activation of retinal cones by light is how vision is formed; yet there are other methods, such as mechanical one, for activating light, such as pressure photopsia/phosphenes. This occurs when ones rubs their eyes strong enough.
Yet even without light or mechanical pressure, at complete darkness, there can still be vision generated. I understand the underlying reason for this is the brain's necessity for stimuli; yet how do the cones activate in this scenario?

I don't know the answer to this, but a logical possibility is that it's not the cone "activating" but the brain simply amplifying the signal.

The fundamental sensory input to the sense of vision is through rods and cones in the retina, but these cells only constitutes the very first level of a large network of neurons, beginning with bipolar cells and ganglion cells in the retina itself, followed by interneurons in the brainstem, midbrain and finally the part of the cortex devoted to vision. Neural activity anywhere in this pathway will be interpreted as visual input by the brain, because it eventually stimulates the cells in the cortex associated with seeing. This is a very old realization in sensory physiology, known from the 1830'ties as Johannes Müller's law of the specific nerve energies, stating that neural activity in sensory fibers associated with a specific sensory organ will be perceived as sensory input of that organ itself. This is why pressing (lightly) on the eye will make you see light, because neurons in the retina are mechanically disturbed, which disturbs the membrane potential, which again may lead to the release of action potentials. The same is the case if you suffer a hard blow to the back of the head, where the visual cortex is located. That will make some of the neurons in the cortex fire action potentials, which you will perceive as seeing stars!
Back to your question, where does visual sensations come from in the total absence of light? The answer is the ubiquitous spontaneous activity in nerve cells. Simply by random fluctuations in membrane potentials, some nerve cells will fire now and then,. even in the absence of any input. And as we now know from Johs.Müller, this activity will be interpreted as vision. Adding to this is the fundamental feature of sensory systems known as lateral inhibition, where activity in one neuron suppresses activity in its neighbors. Lateral inhibition is essential for contrast enhancement and makes it possible for the brain to focus on particular parts of the sensory scene. In the absence of any real sensory inputs to the retina, there is also no lateral inhibition, which would otherwise suppress the spontaneous activity in the visual pathway.


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Ecology of the environment for the ruffed grouse
I live in a coastal New England town and while reading a local history I noticed frequent mention of the "partridge" as being a commonplace bird in the area. Now, however, this bird which is more specifically the ruffed grouse, Bonasa umbellus, is completely absent in our community and not to be seen at all. There are many turkeys, however. I am trying to understand what happened to them.
I read that apparently the critical ecological prerequisite for the grouse is "young stands of forest". For example, from one report: "Though grouse use all age classes of forests, they cannot do without thick stands of young forests 5 to 25 years old for cover, food, brood rearing and courting."
Our community used to be gentleman farming town and was mostly cleared for agriculture, except for a town forest, before 1950. Since that time it has evolved into quasi suburban town with a mix of conservation land, large 3 acre residential lots, and a few farms left over from the old days.
I don't quite understand how there could have been lots of grouse in the farming days, but none now. First of all, in the farming days, more or less the whole town was agricultural fields, so that hardly seems like grouse habitat. Secondly, how could grouse even exist in the pre-colonial times, because the habitat at that time would be primordial forest. When the first settlers came here in the 17th century the whole area was covered in 100 foot eastern pine trees, which were farmed for masts for the English navy.
So, should I presume that the grouse first came into the area when the farmers started cutting down all the trees, thus allowing "young stands" to arise; then the grouse population collapsed when most farming ceased in the 1950s?
If the grouse need "young stands", how do grouse even exist in areas without humans where no clear cutting occurs? I have read claims that "forest fires" clear areas naturally, but that is not the case in New England where it is too wet for forest fires to occur. For example, in Maine the ruffed grouse is abundant, but only in the "transitional zone" between unoccupied forest lands and abandoned agricultural lands where humans have cut down the trees and then left the land unoccupied. There are no "forest fires" to speak of in Maine, so the grouse apparently live only in areas modified by humans. However, this raises the question of how the grouse lived before there were farmers with axes.

It's "ruffed" not "ruffled". A common error. Ruffed is pronounced as a single syllable.

@MTA In New England they are actually ruffled grouse. They wear little lace Elizabethan collars around their neck. It's very cute.

When I am curious how things were with American birds back 200 years ago, I read Audubon.
https://www.audubon.org/birds-of-america/ruffed-grouse

Although these birds are particularly attached to the craggy sides of
mountains and hills, and the rocky borders of rivers and small
streams, thickly mantled with evergreen trees and small shrubs of the
same nature, they at times remove to low lands, and even enter the
thickest cane-brakes, where they also sometimes breed...
The charming groves which here and there contrast so beautifully with
the general dull appearance of those parts of Kentucky and Tennessee,
to which the name of Barrens is given, are sought by the Ruffed
Grouse. These groves afford them abundant food and security. The
gentle coolness that prevails in them during the summer heat is
agreeable and beneficial to these birds, and the closeness of their
undergrowth in other spots moderates the cold blasts of winter. There
this species breeds, and is at all times to be found.

Audubon goes on to note that ruffed grouse occurred everywhere in the US but most of all in the northeast.
There were always edge spaces - for example on hillsides where big trees lose their purchase and fall, or by water and in cane breaks as Audobon notes.  I think the barrens her describes had to do with the geology of Kentucky and Tennesee but there were no doubt equivalent open spaces for various reasons in the Northeast.  I can imagine that ruffed grouse did better when humans showed up and farmers increased edge spaces by clearing forests.
A question analogous to yours pertains to chimney swifts - how did those birds live before people put up chimneys?>  The answer is "probably not in such large numbers as they did after the chimneys went up".  So too the grouse and early farmers.
Chimneys and edge spaces are now both less common, as are swifts and grouse.  There are people who manage the forests they own for hunting, and increase edge spaces because deer and game birds like grouse like those best.
I am not so much for hunting, but I would like to put up a large chimney because I love the swifts!

Ok, but why are there zero grouse now? There should be some habitat somewhere.

Maybe they have just not found their way back yet.  You could help them.  https://www.purelypoultry.com/red-ruffed-grouse-hatching-eggs-p-1447.html


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Is CRISPR mediated RNA editing less specific and less efficient than DNA editing?
According to this diagram, the high efficiency and the high specificity of CRISPR lies in its reversible binding with the target DNA. The Cas protein unzips the target DNA and have the gRNA to base pair with it, forming a short R-loop. Because the formation of the R-loop doesn’t change the number of basepairs, there is minimal free energy change. If there is a mismatch, the R-loop formation is inhibited which facilitates the release of the Cas from the DNA.

However, RNA are single stranded and can basepair with the gRNA directly. As a result, the formation of dsRNA should be strongly exothermic even with one or a few mismatches. As a result, the Cas assembly will be trapped on the slightly mismatched target RNA, which will greatly reduce the efficiency of RNA editing and interfere with the functions of the target RNA (such as protein translation).


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Why DNA polymerases don't have helicase activity
RNA polymerases have intrinsic helicase ability, while DNA polymerases don't.
I am curious why DNA polymerases evolved in such a way that they lack the ability to unwind DNA.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Welcome to SE Biology. Please take the time to  finish reading the [Tour] and read the Help section on Asking Good Questions. Two things we require  of posters is clarity and evidence of previous research on the subject. You do not make it clear whether you are aware that there is a separate helicase involved in DNA replication and, if you are, whether you have thought about the differences between DNA-dependant DNA and RNA synthesis. Furthermore, evolution can lead to different solutions to the same problem, when asking why is fruitless.

@tyersome — I don't see how the referenced question is relevant to this one. We are not dealing with bad traits, but different methods of dividing labour in relation to highly evolved fundamental systems of nucleic acid synthesis.


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Are there any cases where broadening the tissue tropism decreases the virulence of viruses?
Broadening the tissue tropism often increases the virulence. For example, poliovirus normally replicates in the guts and causes minor febrile illnesses. In rare cases (1%) the virus invades neurons and causes paralysis. But are there any cases that broadening the tissue tropism decreases the virulence? Imagine that we have two strains. One specifically infects the upper respiratory tract while the other specifically infects the lungs. The first strain is easily transmissible but very rarely fatal (few upper respiratory infections kill people as far as I know), while the second strain is difficult to transmit but highly lethal. Now imagine what will happen if there is another strain which can infect both the upper respiratory tract and the lungs. It’s intuitive that the new strain will combine the high transmissibility and high lethality. However, infection of the upper respiratory tract does little help to kill the patients, but can alert the immune system to neutralize the infection in the more critical part (lungs) especially if the virus invades the upper respiratory tract first. This is just my thought experiment. Are there any papers supporting this hypothesis?

This is a good question, but I would recommend changing pathogenicity in your title and text to virulence. See https://pubmed.ncbi.nlm.nih.gov/15707863/ -- "Specifically, pathogenicity is the quality or state of being pathogenic, the potential ability to produce disease, whereas virulence is the disease producing power of an organism, the degree of pathogenicity within a group or species. Pathogenicity is a qualitative term, an 'all-or-none' concept, whereas virulence is a term that quantifies pathogenicity."