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How are DNA virus cladograms actually calculated in practice? Is the procedure different for RNA viruses? Are these processes somewhat subjective?
The May 24, 2022 Bloomberg opinion piece Monkeypox Isn’t Looking Like a Covid-Sized Threat; It’s still early, but contact-tracing efforts and analysis of the virus’s genome offer hope that this outbreak can be contained. includes the following:

Why now, monkeypox?
Scientists are scrambling to answer this key question. Two strains, or clades, of monkeypox are known to exist, and the one currently circulating seems to be the milder West Africa one. (For more on that, see this explainer from Therese Raphael and Sam Fazeli.)

One challenge is that researchers lack a good baseline measure on the transmissibility of this clade of the virus. Over the weekend, Maimuna Majumder, a computational epidemiologist at Harvard Medical School, provided an initial analysis of the monkeypox virus’s R0 (R-naught) — the number of people expected to be infected by a single case. These findings, which have yet to be peer reviewed and are based on very limited data, suggest an R0 of 1.15 to 1.26 — low enough to imply that the virus can be kept in check by contact tracing, vaccination and isolation of infected people.

While the present chain of monkeypox transmission differs from earlier patterns, this clade of the virus is generally mild for most infected people (albeit with a long period of isolation and recovery). And, critically, vaccines and antivirals are available to address infections.

I'd never heard the term "clade" before. I've found News Medical/Life Science's (Last Updated: Jan 11, 2022) What are Viral Clades? which which introduces the concept of the cladogram and basal clade and uses the RNA virus SARS-CoV-2 as an example is somewhat helpful but it's more of an explainer than a procedure, consistent with the site's mission to be

a tight-knit community of scientific, medical, and life sciences experts that produce and share the latest information, in a readable, understandable way.

So I checked Wikipedia's Cladogram which has a general discussion but doesn't go into great detail.
So I'd like to ask:

How are DNA virus cladograms actually calculated in practice? Is the procedure different for RNA viruses? Are these processes somewhat subjective?

By "subjective" I mean do scientists producing cladograms have to make any decisions as to what genetic differences are important for the diagram, or would several groups working independently always arrive at identical diagrams from identical data sets because they apply a standardized methodology?

I understand that there are three question marks in the title and one might at first suggest this is multiple questions, but in this particular case I don't think it's better to break this up into three separate question posts because they are so closely related and answers will likely come from the same sources and require the same expertise to write and future readers will find them equally interesting. But if a potential answer author feels strongly otherwise I am certainly willing to consider a breakup.

potentially related: How can I classify the 3 clades(S, G, V) of the coronavirus that are found on GISAID? and in bioinformatics How can I classify the 3 clades(S, G, V) of the coronavirus without using protein data? As I'm not a bioinformaticist and not likely to understand answers written in bioinformatic-ese, I've chosen to post this here rather than there.

For what it's worth, clades are not something specific to viruses, but all biology. A clade is a group of organisms with a common ancestor; cladistics is the study of the ancestral relationships of organisms and classification by those relationships.

This question is slightly different than the suggested similar questions about the S,G,V clades. This question is about phylogenetic reconstruction generally, while the others were asking more how to identify an unknown sample within an existing phylogeny.

Too short for an answer, but consider that some people construct trees with BEAST2.

@Galen "...strict or relaxed molecular clock models." This is great, I'll read now, I think this will help me a lot. It seems that since there can be such flexibility in one's choice of clock models, one could argue that the answer to "Are these processes somewhat subjective?" is "Yes!"

How are DNA virus cladograms actually calculated in practice?
A cladogram, or phylogenetic tree1, is constructed by comparing similarities and differences between organisms, and placing those within an evolutionary model.2 In practice, especially for viruses and microorganisms, the analysis is performed on the organisms' nucleic acid or protein sequences.3,4 For example, a simple model might assume that all nucleic acid changes are equally likely; others might treat transitions and transversions differently; still others may have a unique substitution rate for each possibility, with the overall likelihood depending on the gene under analysis, position within the gene, frequency of each nucleotide, etc. The choice of model may be directly selected by the researcher, but is often selected from an analysis that balances model fit against over-parameterization. The researcher selects the tree that optimizes some aspect of the model, for example the likelihood that the selected tree could produce the observed data under the chosen evolutionary model.5,6
Is the procedure different for RNA viruses?
No, the procedure outlined above applies to both DNA and RNA viruses, although aspects of the model parameters may differ.
Are these processes somewhat subjective?
The same model, applied to the same data, will produce the same result (assuming a thorough tree search was performed), so that aspect is not subjective. However, model choice implies assumptions about the nature of biological evolution, and researchers may disagree on the validity of those assumptions.
That being said, the methods for analyzing viral outbreaks are very well characterized and it's unlikely two competent researchers will produce greatly conflicting trees. In reference to the monkeypox example, the two clades mentioned are strongly supported, to the point where it would be innaccurate to call them subjective.
Extra
It should be noted that for any given tree, the identification of clades is not at all subjective. Every node in a phylogeny represents an ancestor of a clade. However, researchers find some clades especially relevant to the study system, so they will call them out with a name or label. For example in monkeypox the West African/Central African clades are very relevant to most discussions.
The above generally applies to any group of organisms. Viruses and other microbes may differ in that we have access to specimens that were the actual ancestors of the current generation. For example, apart from what we learn from fossils, we can only infer the characteristics of the common ancestor of chimps and humans. However, for SARS-CoV-2 we have samples of the original isolate, even if viruses with that exact sequence are no longer present in the wild. When constructing a tree with this sample we would place that specimen at the node representing the ancestor of all current SARS-CoV-2, rather than at one of the tips of the tree.
Finally the phrase "basal clade" is nonsensical. All clades, by definition, contain an ancestor and all of its descendants. There are clades where the ancestor existed earlier in time and has more descendants than others, but then, that clade is itself just a part of a larger clade. The linked article states, "a basal clade is one closest to the root common ancestor", but of course, that ancestor had more than one successful descendant, and so both descendants are equally close to the root. The article also states, "The S clade... mutated to produce the V clade," but if the term is being used properly the V clade is a part of, and a subclade within, the S clade.7 Here is a longer discussion of why "basal" is usually an inappropriate descriptor of phylogenetic placement. (However, as mentioned above, for some microbes we do actually have samples of the ancestral strains, so "basal is a bit more meaningful there.)

1A phylogenetic tree is a broader category of analysis where the lengths of the branches in the tree have meaning. A cladogram only shows topological relationships, while a phylogenetic tree shows both topology and some magnitude of change (usually either evolutionary or temporal).
2A tree can also be produced by simple similarity clustering, which is fast, but can be positively misled compared to the true phylogeny.
3Phylogenies can also be constructed from other information, such as morphological similarities/differences, as in fossils, for example. Still, some evolutionary model is used to transform the similarity matrix into the phylogeny.
4Of course, the protein sequence can be derived from the nucleic acid sequence. Which is used usually depends on the nature of the question and the breadth of the organisms included in the analysis.
5This is the maximum likelihood method, Bayesian methods are also common.
6Selection of the optimal tree is NP-hard, and there exist many methods to tractably estimate the solution.
7SARS-CoV-2 has its clades named after specific mutations that "define" (are synapomorphies for) the clade. However, this isn't strictly informative, since there's no reason a member of that clade couldn't mutate back to the previous state, or that a member of another clade couldn't pickup an identical mutation.

This is very helpful, as are the linked papers, thanks! "...the procedure...applies to both DNA and RNA viruses, although aspects of the model parameters may differ" The nature of that difference could be the basis of a new question at some point, but I'll need to give it some careful thought.

Very nice answer.

Disclaimer: I'm not a bioinformatician, though I occasionally dabble in it, so I may well have some things incorrect. Please feel free to correct or make your own answer.
As I see it, you are asking how cladograms/dendrograms are generated for viruses.
The answer is basically that you take the genetic sequences and compare them for changes in sequence and conserved regions. The more similar the sequences are, the greater the likelihood that they are closely related and they should come out on the same branch or leaf of the tree. Conversely, the more changes in a sequence (compared to a reference) should have greater divergence and come out in a different branch of the tree.
Edited to add regarding "more similar": Similarity in sequences is based on a few parameters, but is largely based around conservation of energy. So, if you had 3 DNA sequences (AA codes underneath)
AATTCCGGG
AsnSerGly

AAATCCGGG
LysSerGly

AACTCCGGG
AsnSerGly

Compared to 1 as reference, 1 and 2 are more similar because they conserve the A/T pairing (lower energy), whereas 3 substitutes a C, which results in a C/G substitution pairing (higher energy). Of course, if you were looking at this from the possibility of translation into protein (no frame given), then 3 actually makes more sense given that it retains the coded amino-acid sequence. Substitution matrices for these sorts of things have been worked out that produce odds-ratios for a particular substitution type. The commonly used ones are PAM (Point Accepted Mutation) and BLOSUM (BLOcks SUbstitution Matrix).
The procedure to generate a cladogram is essentially the same for any organism that you care to analyze and follows these basic steps:

Sequence
Assembly
Alignment
Tree building

Now, while this all sounds good and easy, it really really isn't. The first two of those steps are more or less unambiguous, though with the advent of single-molecule sequencing these have changed a bit too in the past 10ish years. The latter two are dependent on exactly which alignment algorithm you use. There are quite a few different alignment algorithms out there, many of which are now considered out-dated or have been superseded by a newer one.
If you want to have a go at some basic alignment and tree-building, I recommend using Clustal Omega, which is a web-server where you can put your sequences (in DNA, RNA or protein) in FASTA format, and hit the button. Grab a few sequences for the mRNA/CDS (because this cuts out the introns) for a gene from different species from GenBank and have a go. It should have an alignment output and a tab on the output with a cladogram.
It also depends on exactly what sequence and what form you use for analysis. For instance, to take a recent example - The trees and all of the variant names you see for SARS-CoV-2 (e.g. these ones at nextstrain.org) are based off the genomic sequences for the spike protein only. If you used the sequence for the RNA dependent RNA polymerase (RdRp) you would get a different picture (almost no divergence because these are highly conserved, so highly you can use these to find novel viruses that infect all clades of life), and these trees would also be different to those generated if you used the whole genome. In addition, you can convert the genomic sequences into protein, and you might well get a more conservative tree out - because of the redundancy in the codons for each amino-acid.
As with much in biology it also has to do with exactly what you use as reference sequence(s) and how divergent those are from your target. For instance if you were to attempt to build a tree of all Humans (Homo sp.), you might use Chimpanzee (Pan troglodytes) as an out-group (reference), but you could also use Orangutan (Pongo pygmaeus) or Gorilla (Gorilla gorilla), or a combination of these, and you likely would get slightly different results each time. Appropriate choice of out-group is one of the hard questions in this sort of analysis.

Accidentally posted before finished...

@uhoh If you have three sequences 1: AATTCCGG 2: AAATCCGG and 3: AACTCCGG then 1 and 2 are more similar (conserved base pairing) than 1 and 3 or 2 and 3, though this might not hold-up if you went to the protein sequence because of the codon redundancy... Just one of the problems...

yep, in addition to substitutions there are also additions and deletions of single base pairs and complete codons, and those can happen in areas that vary in the amount of impact on expression rate and on the nature and activity of the resulting protein (if that's what the stretch is doing). It still seems quite hard to unambiguously define or decide what "more similar" means with all this going on, which is why I ask about the subjectivity.

The similarities have been worked out over time and basically it uses an odds-ratio for the positional changes. Substitution matrices are available. The common ones are PAM and BLOSUM

thanks for the edit!


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In traditional plant cloning, why do we require two different vectors (plasmids)?
So I was recently taught cloning in plants and I came to wonder what is the need to first put the gene of interest in the entry vector plasmid and then the final vector plasmid before finally transforming agrobacterium? Can someone make it make sense to me?

Welcome to the site. Please visit the [help] and take a [tour]. If you could explain (edit into your question) which cloning procedure you are using in detail it would help us to know exactly which methodology you are using. In addition, this site has a requirement of evidence that you have had a go at answering this question for yourself, otherwise it will be closed as homework.

There are a lot of different vector systems and some have 2 components, so including the details for your vectors would help. As bob1 notes, reading the material for that system might allow you to answer the question yourself.

If you mean the binary system using the Ti plasmid:
The main issue is that on the massive Ti plasmid there is a difficulty locating unique restriction sites (see section "Introduction of Genes into Plants by Using Agrobacterium"):

However, Ti plasmids are very large and T-DNA regions do not generally contain unique restriction endonuclease sites not found elsewhere on the Ti plasmid. Therefore, one cannot simply clone a gene of interest into the T-region. Scientists therefore developed a number of strategies to introduce foreign genes into the T-DNA. These strategies involved two different approaches: cloning the gene, by indirect means, into the Ti plasmid such that the new gene was in cis with the virulence genes on the same plasmid, or cloning the gene into a T-region that was on a separate replicon from the vir genes (T-DNA binary vectors).

Both of these approaches mentioned involve a two-step cloning procedure for using the entry vector to add the payload to the Ti plasmid.

Edited to link ref and add quote.

source: Stack Exchange

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Is there "limbic mimicry" in real life to distract animals? (like it was portrayed in "Fantastic Beasts: The Secrets of Dumbledore")
In the movie "Fantastic Beasts: The Secrets of Dumbledore", one of the characters comes up with the idea of "limbic mimicry" to distract dangerous animals from violent behavior. Please see the details below to have a better idea (in a spoiler tag because it contains spoilers from the movie):

  While freeing his brother Theseus Scamander from Erkstag prison used by the German Ministry of Magic, Newt outmaneuvers an army of baby Manticores (scorpion-like creatures) using "limbic mimicry" to distract them from violent behavior, forcing them to copy his dance-like movements that mimic the appearance of the creatures. Theseus begins to copy Newt's movements as well when they were escaping.

Is there an example of this from real life?  Of course, in the movie, it is a bit exaggerated for cinematic effect and they are fantastic animals.
However, I wonder if certain movements can distract animals from violent confrontations and is there a term for this in biology? (it can be animal vs animal also)
I know there is mimicry in biology which is an evolved resemblance between an organism and another object or another species as an anti-predator adaptation. However, it is about appearance. I couldn't find examples related to movements.

There's lots of different behaviours to avoid angering animals and to avoid attack. There are various technical terms for those things, but they aren't a formal field of study as far as I know.
Here is an example of someone with experience interacting with lions. https://www.youtube.com/watch?v=tC7DuEEk-zY I'd say the main reason why the lion stays calm is that the human stays very calm and portrays a sense of absolute certainty in his movements.
Someone in Botswana walked up to a female lion who was keeping some babies, and she looked very angry... So he walked backwards very slowly, maintaining eye contact, trying to appear tall. and everything was fine. If he'd turned his back and run that's is a behaviour that would have provoked an attack. Most carnivores are triggered to attack by flight or fear.
I was confronted with 50 angry bulls in a field once, and having lived near cattle for many years, I could see that they were particularly menacing and angry. I mimicked a different gait than I would normally have to look like a non-menacing animal, and their behaviour changed and the looked at me confused rather than angry, while i walked past them, I noticed the difference because at first they charged towards me, and then they didn't take a single step when I changed my behaviour to look like a weak old human.
Angry predators are particularly difficult to dissuade, i.e. dogs.
As far as scorpions go, they attack pretty much anything that has the right size and movement to represent a prey, i.e. generally a lot smaller than them.

I knew some erudite geek(s) would downvote this so i kindof wrote it for that purpose :)/

+1 I upvoted. Some people don't appreciate interesting/challenging questions (unless it includes some bloated babble perhaps). This is not an easily answerable question as it is in the field of ethology, and possibly a less studied category of mimicry and you tried your best to answer with observational experiences.

Thank you for the lion vs. man video also. It is very much related. I can't believe he did something like this for the sake of science :)

Locomotor mimicry is what I've found while searching and it is very related.

Locomotor mimicry is a subtype of Batesian mimicry in which animals avoid predation by mimicking the movements of another species phylogenetically separated. This can be in the form of mimicking a less desirable species or by mimicking the predator itself. Animals can show similarity in swimming, walking, or flying of their model animals.
https://en.wikipedia.org/wiki/Locomotor_mimicry

There are three types mentioned: Terrestrial, Aerial, Inanimate object. However, the examples include small animals like spiders and insects like butterflies, moths, drone flies.

The most common form of locomotor terrestrial mimicry is found in ant-mimicking spiders. These mimics are capable of antennal illusions and similar gait patterns as an ant, which is shown in the jumping spider family (Araneae, Salticidae).
https://en.wikipedia.org/wiki/Locomotor_mimicry

The ghost pipefish is the only bigger animal mentioned as an example of inanimate object locomotor mimicry and they resemble sea vegetation and also sway in water like them.

Good call, was about to add locomotor mimicry and you noted it first. Most weird locomotion dissuasion i've seen this year is a stack of 50 processionary caterpillars in the grass, all twitching together in sychronous waves 1-2 times per second. Looked very extraterrestrial. Same as this with 50 of them https://youtu.be/mzhGebtRmgI

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Identification: tall conifer with tamarisk-like leaves
I am looking to identify a conifer that I found in a public park. Please see below for pictures of the leaves, bark and habit (click for full-size view).
I normally use Pl@ntNet for identification, but in this case it fails: it would only suggest French tamarisk or other tamarisks based on the leaves. But those are more like shrubs, while this was a tall tree, very comparable in shape and size to the bald cypress (?) standing a few meters from it. The upward-curving leaves shown in the picture may not be entirely typical, but this small lone branch was the only one I could reach to take a photo.
Additional information:

Location: Dresden, Germany.
Google street view link, it's the one on the right.
Leaf size: about finger length.

@theforestecologist Updated as best as I could. I really can't put a number on the height, but it's a "tall tree", as you can see on the Google street view link I just added.

This looks like pond cypress, Taxodium ascendens, (sometimes considered a variety of bald cypress: T. distichum var. imbricatum).

 Source: Wikipedia ; Credit: NOAA (2005)
The specific epithet, ascendens, comes from the fact that the plant's awl-like (sumbulate) leaves (3-10mm long) tend to grow along erect ("ascending") green stems ; whereas bald cypress (T. distichum) tends to have leaves that grow in a more distichous growth pattern.
The bark also tends to be greyer than bald cypress, but retains fibrous/shreddy bark that can become furrowed with age:

 Source: Ebben Nurseries
You can see multiple high-quality photos on Will cook's Carolina Nature site.

For example, this image showing the peely and furrowed bark.

Although native to the SE US, I found numerous records of this tree being planted in Germany (e.g., inaturalist). The Dresden Garden also mentions housing Taxodium trees here.


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Position of vascular bundles in angiosperm leaves
In both isobilateral and dorsiventral types of leaf, xylem is present near the upper (adaxial) epidermis and phloem towards the lower (abaxial) epidermis.
Why is this so?

Establishment of the dorsoventral polarity of the leaf is under the control of a large array of regulators, including, but not limited to proteins pertaining to various transcription factor classes.
To summarize (read more here):

One aspect of leaf development that is of particular interest
is the establishment of dorsoventral polarity: the distinct
adaxial (upper) and abaxial (lower) sides of the leaf. Studies over the past decade have defined genetic details of this model, and uncovered diverse mechanisms of gene regulation that facilitate development of leaf dorsoventral polarity, including transcriptional regulation, chromatin modification, DNA modification, regulation by short RNAs
and translational and post-translational regulation.

REV/PHB/PHV transcriptional factors promote adaxial fate, while the identity of cells in the abaxial domain depends on the expression of KANADI transcription factor (source).
Vascular development in turn, regulated:

Central regulators for vascular development involves the REV/PHB/PHV/CAN/ATHB8 genes which are members of HD-ZIP III family and KAN (KANADI). These regulators act antagonistically to maintain xylem and phloem, respectively.

Also, notably:

Auxin plays an essential role in regulating vascular formation through PIN1 transporter by early markers like ATHB8.

PIN1 mediates auxin transport and manifests polarized localization on cellular membranes, while:

Phloem differentiation is induced by low-grade auxin stimulation, whereas xylem differentiation requires higher-auxin levels.

Thus, the mechanisms of leaf vascularization are highly complex (I merely touched them) and require a high understanding of Biology (as do the provided sources).


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Why is a genome of an organism only given in the 5' -> 3' direction?
If u look up a genome of a certain organism or virus, it's always given in the 5' to 3' direction. I understand that one can derive the other direction very easily by just constructing the complementary strand.
Since genes can lie on both strands, why is only one strand given?

Think a little about how complementary strands bind to each-other with respect to 5' and 3' ends....

Welcome to SE Biology. We use standard English here, rather than text abbreviations so please edit your question, replacing "u" by "you". This may seem pedantic, but it is all part and parcel of our aim to provide good clear questions that will attract answers of lasting use. All nucleic acid sequences are written in the 5' to 3' direction, to indicate the asymmetry of the phosphodiester bond, so are you asking for both strands to be presented, or the reverse complement of the genome sequence? And in what context? Cite a Genbank page and explain to us how you would like it different.


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Biological reason for "deadlift face"?
Always when I deadlift at the maximum load, my face looks more or less like this:

or this:

The same applies for when I do other heavy-weight exercises.
But what biological mechanism causes that? Face muscles, to the best of my knowledge don't participate in the mechanical system that contributes to the lift. Also lifting doesn't cause any uncontrollable emotions, that would cause my face to go >:( Furthermore, I don't see any biological gain my organism gets from a "deadlift face". It doesn't increase oxygen intake or improve cooling.
So why do I uncontrollably flex my face? I suppose it is something about my nervous system going into overdrive, but I have no idea what's the actual mechanism.
I did some research, but google only directs me to dubious "fitness lifestyle blogs", and I have no idea how to word my question in a way that would make sense on google scholar.

On this site, you need to show evidence of your efforts to solve the question. Google ugly gym face or something similar, and if you still have any questions, edit your post to show the specific problem you have.   Many people take offense when informed that they need to show their attempt to answer this question first. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many. Every site has a culture. This is ours. Thanks.

@anongoodnurse ah sorry. I tried some research, but google just returns some "fittness lifestyle" dubious blogs. And I don't know how to express it in scientific wording to do google scholar search.

Did you actually try ugly gym face? Because that search was spot on for me. It’s so strange that almost everyone who’s asked to google something can’t find what I find easily. It’s a real mystery to me. Anyway, if you don’t show your research, you won’t get an answer. Sorry.

I don't make that face when I do my one rep max so it's not biologically necessary. I don't see it as any different from someone who tenses up when doing something where tensing up is of no benefit, like playing a musical instrument. The only difference is in this case is that it doesn't hurt either way so no one tells them to learn not to do it. Not all things you automatically do have benefit.


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Targeted gene sequencing and specialist analysis compared to WGS and DYI searches
There seem to be a lot of "genetic consulting" services that focus on things like cancer, with a modus operandi of:

Do targeted gene sequencing (usually on a few tumor suppressor genes related to cancer the customer is at-risk of)
Analyse the respective data and compile a genetic report outlining risks

The few analyses that I've seen around WGS compared to targeted sequencing claim fairly high accuracy of WGS, including on tumor suppressor genes, sufficient that I wouldn't worry about it, given that TGS will also have some degree of error. So it seems to me like there's little point in using a targeted approach compared to WGS nowadays, given that I can buy a 100x WGS for 1k and some of the targeted tests cost upwards of that.
The other question would be whether the clinics have any "specific" data. I doubt this? I've not heard of a lot of closed-source genetic data, besides maybe that of pharma research companies on a few niche topics. So it seems like a Promethease report could match whatever a specialist would be doing here... or even just searching the variants of concern on clinvar.
Is there any reasons I'm missing why these services still exist? Is it just consumers being misinformed? Or am I glancing over some big problems or benefits?

I guess this might be a bit of a silly question, but hopefully the answers to this will help me elucidate some underlying questions about applied genetics.

Leading question that may help you self-answer: you mention the depth of WGS, but what depth does targeted sequencing (such as these genetic counseling services provide) usually have? With what frequency would you expect to see mutations implicated in cancer risk?

The frequency itself depends since we're not talking single base mutations, the depth for most targeted sequencing offers I could find is unspecified.

First of all: one thing is the cost for research, one is the cost for diagnostic.
Diagnostic tests undergo a series of validation procedures (of which I am not expert) that inevitably lead to an increase in price.
So, the cost of a research WGS can be as low as 1K; the cost of a WGS test validated by FDA would be much higher.
The same is true for targeted. You can sequence an amplicon for 4$. But if you want to use a test that is approved by FDA the price would probably increase.
Also, interpreting variants you get from WGS is not an easy task. There may be false positives, false negatives, difficult situations. It's not that you can do it yourself, unless you are REALLY an expert.
In addition, targeted test are designed to screen for genes responsible of the majority of cases, so in a large majority of cases you would spend more money and still get the same result you would get with amplicon sequencing.
This said, I am sure that the direction we will see in the near future (if personalized medicine stops being a buzzword and starts being reality) is a shift towards more comprehensive screenings such as WGS.


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How sensitive are "cheap" genetic sequencers these days?
It is in the news that tomatoes with a Sl7-DR2 knockout are being trialed in England, with a view to being commercially grown and available to consumers.  While this would be legal in England, it would be illegal in Wales and Scotland, and there are concerns that the food industry may not effectively distinguish between them such that they enter the food chain in these countries.
If one was concerned about that, as I understand it, one could use the sequence given in the paper as a guide sequence (TGTTTCACTGGGCTGGTTTAGC) to detect the presence of a small amount of GM tomato in a pooled product, say tinned tomato's.  If one used a conventional next generation sequencing machine costing 6 figures of dollars this would be incredibly sensitive, such that any amount of contamination is likely to be detected (I think).  There are a number of different technologies that allow for much cheaper sequencing machines, for example the Oxford Nanopore MinION costing about $1000.
How sensitive are these cheaper sequencing machines, in relation to detecting the presence of a specific allele within a mixed population with many copies of the alternative allele?

I would hope that a similar law would be passed in Scotland, although it is interesting politically as the SNP is in hock to the Greens.

Surely you would just use PCR, not sequence the whole genome.

@PolypipeWrangler's point is correct. To answer the question not asked (What's the cheapest way to detect this sequence?), some kind of direct PCR solution would probably be the answer. You could just do vanilla PCR and run the product on a gel if you had good size standards, you could use a qPCR solution, or you could maybe test it in the field with an isothermal PCR solution.

Note: user @Polypipe Wrangler's comment about using PCR for this application is very pertinent. My answer is mostly about distinctions in sequencing technology.
Cost
An important distinction is between cheaper machines and cheaper sequencing.
You can buy time/services on instruments owned by service providers, and in that comparison Illumina remains a cheaper option (MinION is actually one of the more expensive options per sequencing run).
The upfront cost of the instrument, while relevant, is ultimately not the practical point of comparison between these different methods.
Sensitivity
Either instrument is roughly comparable at this point for finding a given sequence per sequenced base. Illumina is still more accurate, but with bioinformatic advances you can overcome that limitation pretty easily.
The advantage of Illumina comes in that it provides many more sequenced bases- that is where your sensitivity comes from. You will have to run a lot of MinION flow cells to get comparable numbers of reliable bases compared to Illumina.
For specific information about estimating limits of detection for high-throughput sequencing, see here. The short version is that detection of a given chromosomally integrated sequence in a sequencing run should be excellent, assuming that the sequence's copy number is comparable to chromosomal copy number.

I would start by pointing out that PCR-based detection methods are generally found to be more sensitive and specific than sequencing for applications like this one. (see reference). While qPCR methods are still considered the gold-standard for genetic detection, digital PCR (dPCR) has several advantages and can often achieve greater sensitivity and specificity.
Ultimately, the sensitivity depends on the sequencing depth and assay design. Speaking from experience in methods development and validation for pathogen detection in complex biological specimens, even massively high-throughput next-gen sequencing systems like Illumina MiSeq or HiSeq platforms don't really match the sensitivity of PCR-based detection method unless you implement them with some form of target enrichment, like hybrid-capture probes.
And in terms of cost, a standard endpoint PCR or qPCR will probably win out each time, if you're only interested in the one target. Especially if you factor in the target enrichment, which usually involves some kind of amplification using a thermocycler like the ones you use for the PCR detection anyway. The one area where a targeted sequencing approach might make sense is if you were screening for large panel of different targets in each sample, which doesn't seem to be the case here.


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What mammalian species has the greatest relative variance in adult size?
The smallest adult chihuahuas weigh about 2 kg, and the largest adult English Mastiffs are around 104 kg, making them 52 times larger by weight.
Of course, this enormous variance is the result of selective breeding (i.e., artificial selection). What's the greatest variance, in relative terms, that has been observed in the naturally selected adults of a given mammalian species?  For example, are there any mammalian species for which it is possible to observe (in the wild) individual adults that differ in size (be it weight, height, length, or some other measure) by a factor of 50, or even 20 or 10?  Are there any environmental factors that might encourage such a large size variance within a species?

Is the difference between male and female individuals something you are interested in?  This is the biggest difference I am aware of, with elephant seal males being up to 10 times the size of females (from wikipedia, females 400 to 900 kg males 2,200 to 4,000 kg)

If the greatest variance is from sexual dimorphism, then sure, that certainly counts. But in that case it would also be nice to know the greatest variance that doesn't involve sexual dimorphism.

I bet you would like this paper, about how much variation there is and why.  I do not think it answers your question exactly though.  This paper is about sexual dimorphism in pinnipeds like elephant seal.

Finding the most variable wild mammal in size is difficult because it is not usual (except the artificially selected breeds like dogs, horses, pigeons etc.). It is probably a small animal like a rodent species. I've found "variegated squirrel" as a promising candidate but the variation mostly comes in color, although this paper talks about some morphological variety also. I've found the fish "arctic charr" as the most variable vertebrate (within most categories: size, phenotype, range, ecology etc.)

I tend to find trivia-style questions to be not particularly useful contributions to this site, unless you can express some biologically interesting question to address with that trivia answer. The help asks that you should only ask practical, answerable questions based on actual problems that you face - what's the actual problem to solve here?

If you're after trivia, the Guinness World of Records is great for individual specimens. Jon Brower Minnoch comes in at around 300 times heavier than Lucia Xarate in humans, for example.

Generally no - because you are essentially limited to clinal species (e.g. ring species) and the lack of ability to interbreed kind of limits the species definition. The only way a Chihuahua can breed with a Great Dane is artificially.... but I'll leave it to a better ecologist to answer.


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Why is protein turnover necessary or important for cells to function?
Cells constantly create new proteins in order to maintain their normal function, this is called protein turnover.
Why is that? Do the old molecules wear out as time passes, so that they need a replacement?

Clarification: creating new proteins is only part of protein turnover.  A more accurate succinct description would be that protein turnover is the replacement of old proteins with new ones.  The original, unedited version of the question (which focused specifically on new protein creation) makes more sense than the current version.  Turnover is part of the answer to that question.

Biology is an intricate orchestration of chemical reactions and their products. Generally, this fete is accomplished by enzymatic facilitation of certain reactions that would otherwise occur too slowly.
However, "unwanted" reactions occur spontaneously all the time, too. One important mechanism for these reactions is the presence of free radicals causing oxidative stress: reactive molecules are present in cells as a consequence of the energy necessary for metabolism, and these can react with proteins and other cellular components and change their structure. Modified proteins may fold incorrectly and lose their function (or gain harmful function). There is very little that can be done to prevent these reactions from occurring except to clean up afterwards.
Half-lives vary by protein, but for most proteins are measured in the scale of hours (Chen et al, 2016) to a couple days (Boisvert et al, 2012). By constantly degrading and replacing proteins, cells ensure that their proteins are functional and fresh. You might consider this as analogous to performing regular maintenance on a machine like an automobile, using replacement parts as the originals become worn.
Both protein degradation (e.g., via the ubiquitin-proteasome system) and synthesis are highly regulated.

Boisvert, F. M., Ahmad, Y., Gierliński, M., Charrière, F., Lamont, D., Scott, M., ... & Lamond, A. I. (2012). A quantitative spatial proteomics analysis of proteome turnover in human cells. Molecular & Cellular Proteomics, 11(3).
Chen, W., Smeekens, J. M., & Wu, R. (2016). Systematic study of the dynamics and half-lives of newly synthesized proteins in human cells. Chemical science, 7(2), 1393-1400.

"Half-lives vary by protein, but for most proteins are measured in the scale of hours"Wow that's wild

@AzorAhai-him- Indeed it is, though I want to be careful that I'm not exaggerating things too much. I've added a second reference with a different range of estimates; still hours, but possibly more in the range of tens of hours. Some can be much longer, though; this Biology.SE answer: https://biology.stackexchange.com/a/67698/27148 refers to a couple of those.

Good answer. tl;dr Proteins turn over because they're consumed, modified, or escape homeostasis and require regulation or degradation. Semi-unrelated note, as a tangential rant, how does nobody think to provide keratin/spider silk as an example of a long-lived protein? Keratin (main structural protein composing hair, wool, feathers, nails, horns...) in its native environment can easily and routinely last (tens/hundreds of) thousands of years. If it's a dry place, you'll find it, especially since it's built in bulk. Hooves. Spider silk. Claws. Feathers. Keratin strong.

Still, my haven't-taken-bio-since-HS self would have been off by an order of magnitude

Many aspects of cellular function are related to feedbacks and cycles wherein proteins need to fluctuate in abundance to maintain cellular function.
One example of protein cycling would be cell cycle dynamics. Another would be circadian protein cycling.


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Why did the requirement for coronary circulation arise?
Why the heart does not absorb the blood directly(for it's oxygen requirement) rather than taking it through coronary circulation?
Is it related to the permeability of myocardium?
Having such a circulation system can help in avoiding diseases which arise due to issues in coronary circulation.

Oxygen and nutrients diffuse out of capillaries into surrounding tissue.
If you don't have sufficient density of capillaries, diffusion distances are too long, and tissue becomes anoxic and dead. See for example:
Henquell, L., Odoroff, C. L., & Honig, C. R. (1977). Intercapillary distance and capillary reserve in hypertrophied rat hearts beating in situ. Circulation Research, 41(3), 400-408.
In other words, the heart muscle is far, far too thick, even in a rodent, for enough oxygen to be delivered without vascularization of the myocardium.


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Plasmid Design and Integration events [Single vs Double cross over]
When linearising a vector by restriction digest within the middle of a homologous region can a single cross over integration event only occur if the plasmid is re-ligated within the cell after transformation? If so, why do some organisms require transformation of a linearised vector rather than plasmid DNA?
An example:
You amplify and clone GeneA into a vector containing an expression cassette. Before transformation, you digest this vector with a restriction enzyme at a site within GeneA to form a linear DNA fragment such as: GeneAStop_ExpressionCassette_StartGeneA.
My understanding is a double cross over event would occur in StartGeneA_ExpressionCassette_GeneAStop and the expression cassette would integrate between the two parts of the gene in the genome.
However, as the gene is cloned directly into the plasmid as one part and then digested to form a linear fragment, the expression_cassette is not in the region between two homologous fragments.
Does this mean a double cross over event cannot occur and a single cross over event would have to occur for the transformed DNA to integrate?
Can this single cross over event happen without relegation of the digested plasmid into circular DNA?
What would happen if you amplified by PCR rather than digested, as it would not be able to religate?

Your post contains many different questions, so I responded to what I considered being the central question. If you were looking for a different answer, please focus your post such that the main question becomes clearer.

Single crossover is not the result of religation in the cell. The double-stranded break (DSB) in the plasmid instead stimulates a homologous recombination event, causing the entire plasmid to integrate into the homologous region in the chromosome. The result is two tandem copies of the homologous region, interspaced by the rest of the plasmid.
The figure below shows (1) a plasmid carrying a wild-type copy of the gene YFG1 (purple) and some selection marker AUXA (blue); and (2) a genome region with the gene yfg1 (pink) that is homologous to YFG1, but carries a mutation (black star). Arrows are shown for orientation.
After introducing a DSB in YFG1, this region will line up with homologous yfg1 region in the genome and integrate as shown. Note how the two tandem copies of YFG1/yfg1 resulting from the integration will both be "chimeras"; i.e., one part originates from the plasmid and the other from the chromosome. Also note how in this specific example, the mutation ends up in the second copy, since the DSB was introduced "upstream" of the mutation.

Figure adapted from (1).
References and further reading

Guthrie & Fink (1991): Guide to Yeast Genetics and Molecular Biology, Part A. pp 285-287. ISBN: 978-0-12-182095-4
Orr-Weaver et al. (1981): Yeast transformation: A model system for the
study of recombination. PMC349037


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Is this an instar of the red fire bug?
While inspecting some yarrow that seemed to be having problems, I found a few of these bugs. I think they may be an instar of red firebug, but the photos of the nymphs that I found had only one row of black dots (e.g. here along the back) whereas these have two, maybe more. (US, midatalntic, tiny!!! Maybe 1.5 mm?)
Are these firebugs or something else? (Sorry for the poor quality photo.)


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Can the Monkeypox virus be spread by mosquitoes?
I am wondering if the Monkeypox virus could be spread by mosquitoes since it is part of the Smallpox family.
While doing some online research on this possibility, I came across this abstract taken from an article titled 'Role of Mosquitoes in the Spread of Smallpox' in The Journal of Infectious Diseases, Volume 128, Issue 6, December 1973, Pages 781–783:

Smallpox is endemic in Calcutta, where Culex pipiens fatigans and Aedes aegypti abound. In a study of the role of these two species of mosquito in the spread of smallpox, laboratory-bred mosquitoes were allowed to feed on variola-infected, viremic infant mice. The engorged mosquitoes were tested daily for 15 days for viable variola virus. Virus could be recovered from C. pipiens fatigans for 72 hr and from A. aegypti for 96 hr. The separated proboscises of the latter mosquitoes were tested and were found to contain virus for the entire 96-hr period. It appears, therefore, that mechanical transmission of smallpox by these mosquitoes, especially A. aegypti, is possible.

Can the Monkeypox virus be spread by mosquitoes?

“Is possible”. But unlikely because smallpox has been eradicated whereas malaria hasn’t. At the start of the covid pandemic we had a question whether it could be spread by the plagues of locusts prevalent at the time. And some people worry about catching AIDS from public lavatory seats.

As yet there are unlikely to have been any studies looking at this particular scenario with Monkeypox virus, as it hasn't been widely studied.
However, the poxviridae are all similar in that they are large, robust virions with the capability to persist in the environment for some time (for some species up to 6 mo in winter outside), meaning that they can survive conditions that would be unusual for many other viruses. So, it is likely that if smallpox was capable of being transmitted by mosquitoes, then the same is possible for monkeypox and potentially other pox viruses too.
Having said that, the places where smallpox was last found during the global eradication program, were largely places where mosquitoes and mosquito borne diseases are common (India, Somalia, Bangladesh). Despite this, the eradication was successful using contact-tracing and ring-vaccination. If the virus was actually transmitted by mosquitoes, then these strategies would have been unsuccessful because the mosquitoes could have carried the virus to people who were not direct contacts. As this was not seen, I doubt that mosquitoes were a common vector for transmission of smallpox, if they were at all, and hence it is unlikely that mosquitoes will be a vector for transmission of monkeypox.


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How does the total number of genes increase throughout the course of evolution?
Campbell Biology says:

A typical prokaryotic cell has  about 3,000 genes in its DNA, while a
human cell has about  21,300 genes.

If evolution depends on random mutations occurring in the genome, this means that only certain genes are altered, but not add up to the total number. Supposing that we and the bacteria come from a common ancestor, then what is responsible for the tremendous amount of genes that has been added throughout the evolution?

"If evolution depends on the random mutations occurring in the genome, this means that we only alter certain genes, but not add up to the total number" - Why? Are you thinking only of point mutations? Also note that bacteria and humans have been evolving for the same length of time, and bacteria have had far, far more generations to evolve than humans have.

"Are you thinking only of point mutations?" - This is the case, mutations are the only thing I can think of right now. Can you point out other factors?

I didn't say "mutation", I said "point mutation". You may even only be thinking of specifically substitution mutations. You could start with https://en.wikipedia.org/wiki/Mutation to learn about others.

Look up gene duplications, copy number variations and transposons. That may give you a clue.

For a less mechanistic and more theoretical view, I would suggest looking into the evolution of complexity (that's just one ref it's a large literature). Obviously expanding to a view of mutation beyond substitutions is essential, as suggested by other commenters.

It's possible that interspecies hybridization resulting in temporary allopolyploids is a driver in this. There's some interesting material on carp, I'd recommend reading.


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Abnormally fast nerve conduction
Is there any neurological condition or disease where nerve conduction becomes abnormally fast?
We know that myelinated neurons conduct impulses much more rapidly than non-myelinated ones as the myelin ensures that the ions carrying the signals don't leak while flowing through the axons, acting as an insulating material. In demyelinating diseases, the myelin sheath gets lost, affecting the conduction velocity leading to abnormal nerve conduction, which can be rescued by certain therapies such as introducing NPCs that differentiate into oligodendrocytes promoting remyelination.
So I was wondering whether there is any form of disease or at least some theoretical possibility where the nodes of Ranvier are at abnormally long distances from each other leading to conduction velocities much greater than normal.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Action potential amplitude decays between nodes of Ranvier, which is why they exist and are spaced the way they are: to boost the signal at appropriate intervals.
Demyelinating disorders reduce the distance at which the propagated signal can extend without being 'boosted' at a node of Ranvier, leading to conduction failures. See another Q&A here:
Why does damage to myelin sheath in multiple sclerosis lead to a decrease in information reaching the brain from sensory receptors?
If you separated nodes of Ranvier too far apart, the same thing would happen: you might increase conduction velocity a bit, but you'd also cause propagation failures.
It's not really possible to prove a negative, so while it would be possible to provide a reference if there was a "neurological condition or disease where nerve conduction becomes abnormally fast?", it's not really possible to give a reference if the answer is "no", but at least it would not work the way you propose.
You might describe some forms of epilepsy as involving "too much neural activity" (as a simplification), but not "abnormally fast".
Speed of transmission is a function of the diameter of nerve fibers, so obtaining faster conduction would be at the expense of reducing space for the number of fibers in the PNS, or additionally the number of neurons in the CNS.


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Do the cells of any multicellular lifeforms discard their genetic material after differentiating?
There are many types of cells which will never again divide. Some of them may not need DNA to perform their function. Are there any cases where the DNA is discarded after a final differentiation?

I recommend looking into terminal differentiation.
As one extreme example of terminal differentiation, xylem cells that form plant vascular tissues are simply dead. This is a case where not only the genome but also physiologic activity in these cells is irrelevant to their function.
A more famous case is red blood cell enucleation, wherein the genome of mature cells is lost in cell division.
In other words, yes, this happens.

But how does this answer the question? The instance  you explain is for cells that just die — not an example of what the poster is asking about, and we have no idea from your answer what is in the review you link to. Please either explain in your answer or restrict yourself to commenting.

Your answer didn't answer the question I meant to ask, but it did answer the question I wrote in the title. Rather than say your interesting reply was unfit, I have decided to change my question to match it. I'll ask a new question about what I really meant later. :-)


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Are there any species whose cells do not copy the DNA that has been inactivated during cell differentiation?
According to this paper, the ATP cost of a having (not counting transcribing) a gene in a diploid eukaryote is about $5\times 10^3$ ATP per base pair, while the lifetime ATP usage of a mono-cellular eukaryote might be around $10^{9+3}=10^{12}$ ATP. The human genome contains about $3\times 10^9$ base pairs, and all taken together this implies that the cost to the cell in a multicellular organism of copying its genome may be a respectable fraction of its total lifetime energy costs. (I am not willing to say anything more specific than that, because these are ballpark numbers and vary widely from organism or organism and even cell to cell.)
The process of cell differentiation inactivates large blocks of genes. This paper suggests that only ~6% of mammalian genes are ubiquitously expressed, while each tissue tends to express only 30-40% of the whole genome it carries.
Taken together, these two facts imply that an organism whose cells did not copy permanently inactivated genes could save as much as half the energy it would have to spend otherwise on genetic replication, which in the first paragraph I argued was not insignificant. Nonetheless, all of the organisms I can think of put full copies of their entire genomes in every cell that will ever need to multiply (mature red blood cells do not contain copies of the full genome, but that is only because they do not have a nucleus). Are there any species that exhibit this parsimony?
I recognize that a mechanism for doing this would be nontrivial, because some genes are inactive during differentiation but must be present to become active later, but life, uhh, finds a way.

To put these numbers in context, the human body has a daily ATP budget on the order of 100 moles. Translating that to numbers of ATP molecules ($\approx10^{26}$), the quantities you cite are minuscule. Looking at figure 3 of the paper you link, those estimates are more burdensome (accounting for the whole genome) but are still tiny as a fraction of the energy budget (bottom axis).

Also: you might be interested in the ciliate micronucleus/macronucleus organization as a related strategy.

@MaximilianPress The ATP budget of the whole body is not a good number to compare the costs of a single cell with. There is a lot of ATP available every day, but there are also a lot of cell divisions.

Fair enough, to me it was not clear which those numbers referred to, though going back and rereading I see it now. Also, only just noticed: you write $10^{9+3} = 10^{11}$ where I'm pretty sure it should be $10^{12}$. I still think that Figure 3 pretty much has the answer, which is the same: this is not a very large cost for selection except at astronomical population sizes (bacteria), which have quite compact genomes already (possibly related).


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Is the formula of cyclic adenosine monophosphate (cAMP) $\ce{C_{10}H_{11}N_{5}O_{6}P}$ or $\ce{C_{10}H_{12}N_{5}O_{6}P}$? Does it matter?
For some reason, half the sites on the internet say that there are 12 hydrogen atoms in one molecule of cAMP, and the other half claim 11.
Who is correct?  Does a single, free, unbounded and unresolved cAMP molecule in isolation possess 12 hydrogens, and in all other cases have 11? I am confused.

OK. Despite my reservations I have provided an answer as there was some interest in the question. As you are more active on physics and chemistry SE sites I'm a little surprised that you didn't see the answer yourself.

Without links to, or presentation of, examples of the two formulae it is not possible to be sure that the following explains the particular experience of the poster, but nevertheless I provide it as there has been some interest in the question
The chemical formula depends on the actual molecular structure
This statement may seem obvious, but certain molecules can exist in different states — in biochemistry acids and bases especially can be ionized or not.
If one consults the catalogue of a chemical company, one finds the following diagram of one type of cAMP that they sell in powdered form, in which the phosphate group is shown protonated:

The chemical formulae is given with 12 hydrogens, to reflect this: C10H12N5O6P.
If one consults the Wikipedia entry for cAMP, one is provided with chemical information in the standard form used in Wikipedia, with the phosphate group shown ionized in the diagram of the molecule:

The chemical formulae is given with 11 hydrogens, to reflect this: C10H11N5O6P.
Does it matter?
It matters if you are in the laboratory and preparing a solution of cAMP at a particular concentration. In this case the error would only be about 0.3%, but if it were a salt of an acid, that would have a greater effect. Use the MW written on the label of the bottle.
It matters if you are doing metabolomics and identifying species by their molecular mass, but the species present will depend on how the experiment is done, and one is unlikely to be dealing with this oneself — your software will identify the species for you.
So, in practice, not very much. But in general it matters a lot that one thinks about the ionization state of molecules in solution in biochemistry, and understands how this will vary with the pH.


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Are these little white fuzzy insects "scale"? What species and what is their lifecycle like?

These appeared on three small, similar houseplants I bought about a month earlier at a nursery. There were dozens. I physically removed a few and just pruned stems that had many, and put the clippings in a plastic container with some water to keep an eye on them.
I noticed that they moved around each day and saw one moving in real time. Included are some top-side closeups and some from below through the wall of the plastic container.
Location is northern Taiwan in April, but since the source is a nursery they could be from elsewhere perhaps.
They're about 3 to 4 mm long, and all white. They are white, fuzzy and "pill-shaped" with little fuzzy extensions around their edges. From below they have six (short?) brown legs that are hidden when looking from above.
Question(s):

Are these little white fuzzy insects "scale"?
If so, what species and what is their lifecycle like? (should I be looking in the soil for the next generation?)

They look very much to be cochineals, small insects closely related to aphids.

@JakobTougaard Wow I think you've nailed it! :-) https://www.alamy.com/close-up-view-of-female-cochineals-dactylopius-coccus-scale-insects-in-the-suborder-sternorrhyncha-image356065881.html

@JakobTougaard just asked Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?

@JakobTougaard I have a lot better photos, some through a microscope, I'll upload a some in a few hours.

Mealybugs. They're small, sap sucking insects related to aphids, cicadas, stink bugs and assassin bugs. The name come from the coating of distasteful, powdery white wax they secrete as an antipredator defence. Squash them, as they reproduce and their feeding weakens the plant and can introduce plant viruses. These things are particularly damaging to fleshy, slow-growing plants like cacti and succulent euphorbias. Since your plant appears to be a poinsettia(Euphorbia pulcherrima), I'm not surprised.

This is great, thank you! Yes mealybugs seems to be the right call. I have some additional photos I need to upload that I took through a microscope but I'm sure it won't change the answer though it may make it easier to address "...and what is their life cycle like?" Generally Stack Exchange answers should include links to at least one or two supporting sources. Thanks!

Glad I could be of some help. Their lifecycle is similar to most other true bugs, being egg>nymph>adult


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What unmanned monitoring techniques are available to measure coral reef health?
Most biological data for coral reef monitoring are collected by human observers. This could be resource-intensive for long-term studies and thus hard to maintain consistency on large spatial scale. While remote sensing can be applied on a macro scale, are there any automated observational platforms that are available to look at events on a smaller scale such as behavior of fish colonies around reefs?

There are several researchers I know, including myself and others in my former grad school lab that are collecting acoustic data, or video data, for monitoring coral reefs using deployed underwater microphones and/or cameras that run for days to months at a time.
There are some papers exploring how reef sounds can be measured to monitor health, e.g., some have found healthier reefs to be 'louder' and have more fish calls, and sometimes these correlate positively with metrics usually obtained from visual surveys, such as coral cover and fish abundance.
For some examples of different sensing platforms, I recommend looking at the following papers and others by these authors. Some are in habitats other than coral reefs, but utilize methods that could be applied to coral reefs:
Mooney et al. (2020) Listening forward: approaching marine biodiversity assessments using acoustic methods (a review of this topic)
Kaplan et al. (2015) Coral reef species assemblages are associated with ambient soundscapes. Marine Ecology Progress Series
Pagniello et al. (2021) An Optical Imaging System for Capturing Images in Low-Light Aquatic Habitats Using Only Ambient Light
Archer et al. (2018) First description of a glass sponge reef soundscape
reveals fish calls and elevated sound pressure levels
Some camera or acoustic systems were custom built for these studies. Others, like SoundTraps, are commercially available.


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Disease-causing allele frequency and modern medicine
I was thinking about what the impact modern medicine might have on human evolution based on a couple assumptions.
If we assume that:

modern medicine has massively cushioned the selection pressure against people with inborn errors of metabolism, weak immune systems, disabilities, and genetic defects more broadly.
that these people, due to modern medicine, are able to live past reproductive age.
and that these people (broadly speaking) go on to produce offspring at the same or marginally lower rate as those without these defects.

could we expect to see these defect-causing alleles increasing in frequency in the now and more so in the future? or maybe at some point, given the constant improvements in modern medicine, these alleles essentially become fixed in subpopulations or maybe even the global population?

Can you please provide a reliable source for the massive cushioning modern medicine has provided these individuals? Thanks.

I can't find any study, but surely its reasonable to assume it. And I don't think there will even be studies in this topic for the near future anyways, given that there is no benefit from researching this. But that doesn't mean its perfectly resonable. for instance,  as a higher percentage of people who would've died from infection are kept alive at least up until reproductive age.

Your three down votes and close votes would argue against your certainty. This site requires you show your attempts to answer your own questions. If you hover over the DVD’s button, one reason is “shows no effort”.

It's worth considering that other factors such as sanitation and a plentiful and reliable food supply play by far the most major part in decreased mortality, then other confounding factors such as pollution and increasingly sedentary lifestyles make it even more tricky to identify what effect medicine has.

@anongoodnurse https://biology.stackexchange.com/questions/64424/where-do-birds-and-squirrels-go-to-die and https://biology.stackexchange.com/questions/89886/do-air-purifiers-work-against-bacteria-and-viruses both did not cite anything. and maybe because it was phrased in anecdotal way. But my question is abstracted from anecdote, I HAVE a genetic defect and without modern medicine I'd die before reproductive age, no doubt about it. Besides, I never claimed that my assumptions were true, what I said was IF these assumptions WERE true, could we expect to see such alleles increasing in frequency

@JiminyCricket surely, in some contexts we can, take the sickle cell hypothesis, if my hypothesis is true, then we'd expect to see that west african populations with good access to antimalarial drugs, vaccines, and bed nets have gradually lower frequencies of sickle cell carriage or disease. Also, food supply generally doesn't affect the relative frequency of alleles, it increases population count but doesn't make those with genetic defects more likely to propogate (unless the defect impacts diet, e.g. the ability to fast)

@anongoodnurse I can't cite any direct evidence, but I will list you diseases that without modern medicine and scientific knowledge would've cut short peoples lifespan to before reproductive age or affected their reproducetive abilty. Phenylketonuria, Cystinuria, Glycogen storage diseases, Lysosomal storage disease, Leukemias, Type 1 diabetes, Asthma, neurofibromatosis, Fibrodysplasia ossificans progressiva, porphyrias, hemophilia, IgG deficiency, Haemochromatosis, and so on.  and this exludes infections, so my point stands. It's reasonable.

This question is strongly associated with the pseudoscience of eugenics, and specifically the idea of "dysgenics", supposing that modern interventions "weaken" the gene pool. I don't suggest this is your intention, I merely point out the connection. For more information I'd google "medicine dysgenics", which brings up scholarship such as this. Trivially... sure, there is probably some effect. Substantially, it's not clear that this has much effect at all.

I believe @MaximilianPress has put it best. I also think you do not give credit to those with inborn errors of metabolism; most would not likely choose to procreate knowing that they are passing a fatal gene to their offspring. Anyone can claim anything on the internet. Did you know that I can fly? It’s an autosomal dominant mutation, obviously, because all of my children are good flyers as well. And the sun has no effect on our wings.

Finally, speaking as a physician, of the more than 1000 IEMs, only a metaphorical handful (not a massive cushion) can be treated with the individual reaching adulthood able to reproduce (for a variety of reasons). Some IEMs aren’t diagnosed until mid to late adulthood, so are probably common enough. Frame of reference is everything. Someone with a treatable IEM might win a Nobel prize someday for something that changes the world for the better. You never know.

@MaximilianPress I understand that that was always a possiblity because how easy it is to misinterpret what I'm trying to ask. But thank you, anyways for at least providing a use term, and an attempted answer, albeit without a source.

@anongoodnurse you bring up a good point, that people who are daignosed with genetic defects, IEM's, and disabilities might not choose to procreate. So the selection pressure is definitely not mitigated for alleles that cause those conditions. But I think there's definitely a grey area where negative selection is mitigated for those with alleles that cause mild to moderate disease that doesn't warrant genetic tests, which would also apply to polygenic traits like weaker immune systems, and certain mental disorders, for instance, but probably not to flying, though, sorry.

I’m so confused about what exactly it is that you’re asking… However, if you believe with any degree of certainty that medicine has massively cushioned the death rate from IEMs, why do you have difficulty believing that my offspring and I can fly? They’re about equally true…

@anongoodnurse I think you have missed my point. first of all, I'm not referring to IEM's across the board, nor am I referring to IEM's alone, I am saying modern medicine has massively cushioned negative selection pressure for CERTAIN ALLELES causing CERTAIN DISEASES. and therefore, WITH THE ASSUMPTIONS i have made, we should expect an increase in the frequency of such alleles. This is basic population genetics; removing or mitigating a selection pressure will cause alleles selected against to increase in frequency.

@anongoodnurse and who said I have difficulty believing you can fly, the traits practically fixed where I'm from ;) ,but you seem to have difficulty merely entertaining my position, perhaps its your ideology. Here's an example I'll try to explain, where I'm from Williams syndrome is underdiagnosed, and so what happens is only the resulting complication (usually cardiovascular) of Williams syndrome is treated, without the diagnosis of Williams syndrome being given. These treatments will prolong the life of the patient to at least reproductive age and so the alleles should increase in frequency.

Yes, in principle, but it could take a very long time. Consider phenylketonuria, which is a severe genetic disease that is completely preventable by excluding phenylalanine from one's diet. Suppose that PKU is now completely neutral due to our ability to screen for PKU alleles and counsel carriers appropriately (not to avoid reproducing, which would induce selection against PKU, but to make sure that their children are tested and put on an appropriate diet).
How long will it take PKU to fix due to genetic drift?
From here, the time to fixation
$$
E(T) = -4N_e [p \ln p + (1-p) \ln (1-p)] \textrm{ generations}
$$
where $N_e$ is the effective population size and $p$ is the starting frequency (this counts fixation at either 0% or 100% but should be a lower bound for fixation at 100%).
The highest frequency of PKU in any population in the world is around 70% (Gundarova et al. 2018); starting from here, the fixation time would be $0.63 N_e$ generations. Even in a very small population (e.g. $N_e = 200$), this will take hundreds of generations/thousands of years ...
The time scale might be much shorter if there were positive selection, i.e. some selective advantage to carrying the allele that also/formerly caused disease. This is known, or speculated, to be the case for many deleterious recessive alleles (sickle-cell, thalassemia, cystic fibrosis ...). However, in many of these cases the selective advantage is against infectious diseases such as malaria whose effects have also been mitigated by modern medicine ...

Gundorova, Polina, Rena A. Zinchenko, Irina A. Kuznetsova, Elena A. Bliznetz, Anna A. Stepanova, and Aleksander V. Polyakov. “Molecular-Genetic Causes for the High Frequency of Phenylketonuria in the Population from the North Caucasus.” PLoS ONE 13, no. 8 (August 1, 2018): e0201489. https://doi.org/10.1371/journal.pone.0201489.


text:
What is meant by 'identical alleles'?
I read in my book that "two alleles are considered to be homozygous if they are identical". But at the same time I read the definition of allele to be:

genes which code for a pair of contrasting traits are called alleles

My doubt is that how can they be both contrasting (different) and identical (same) at the same time
What I think is that if homozygous is somehow a part of specific conditions in alleles then how can it be different from alleles itself.

These are just issues with singular and plural and whether you refer to individual copies or categories/types.
Two of the same allele copies are the same allele (category/type). Two different alleles (copies) can also be different (categories/types).
In the context of a diploid individual, they have two instances of each gene so therefore two alleles; these alleles can be the same or different.
So you can say you have two "red flower" alleles, meaning two copies of the red flower allele. Or you can have a population that has two alleles for flower color: red flower alleles or white flower alleles.
The same is used in English for other things. You might say a farm grows two fruits, peaches and plums, and also that I have two fruits in my hand, both peaches. You need to use surrounding context to recognize whether copy or type is meant.


text:
What colors I am looking for in the TSA stain in this paper?
I'm just having a little bit of trouble and want to make sure that I am seeing the same things that the original researchers were seeing. This is the name of the paper Hair Cycle Control by Estrogens: Catagen Induction via Estrogen Receptor (ER)-α Is Checked by ERβ Signaling. Specifically, I am looking at Figure 2 with the tyramine signal amplification (TSA) images and am wondering what colors are supposed to indicate the presence of estrogen receptor (ER)? Take the statement:

ERα IR had its peak in telogen follicles and was intensely visible in
the dermal papilla and cells of the sebaceous gland.

When I look at Figure 2, T, I don't seem to be seeing any blue in the sebaceous gland?

Is it the case that the area I circled in red is the sebaceous gland with the smaller circles around the blue indicating the presence of ER-α, as opposed to the arrow the authors had placed?


text:
Biology (DNA electrophoresis with agarose)X
I'm researching a polymorphism using restriction fragment length polymorphism (RFLP) and gel electrophoresis.
After RFLP, I should see fragments at 141bp and 111bp, but I can not see in 2% agarose, what is your suggestion, dear friends?
Here is my gel recipe:

TBE: 0.5% 75ml
agarose: 1.5gr
Voltage: 65
Time: 1 hour

Unfortunately, I do not have the ability to change the methods.

Why can't you change the conditions? Anyways, fragments of 141 and 111 bp should separate in 1,5% agarose. Can you show an image of your gel?`

How are you visualizing the bands? Ethidium bromide or SYBR green or something? What does "1hr" mean, did you run it for 1 hour? Did you load a ladder to confirm that the band didn't run off.

When you say you "can not see" the bands, do you mean they are totally absent? Or is only one band seen?


text:
How can a viral infection (like shingles) recur in a healthy individual?
I don't quite understand how a viral infection, like chicken pox (Herpes Zoster), can recur in a healthy individual. If the body has created an immune response, how can the virus just spontaneously reactivate in a healthy adult? Or is this just an unknown mystery?
I understand that in an older person, perhaps the immune system weakens, so there is a recurrence, but shingles does recur in ordinary adults. For example, apparently Justin Bieber has had shingles and he is 28 years old.

What have you learned from reading about shingles?

I once saw a 6 year old immunocompetent child with shingles. Herpesviruses are very interesting viruses. The herpesvirus responsible for infectious mononucleosis reactivates often and asymptomaticly. It makes for some interesting reading.

When I got shingles for the second time at the age of 28, a colleague who studies such things laid out a hypothesis that shingles (zoster) has gotten more among common younger adults, in part, because of more widespread use of the chickenpox vaccine. In a nutshell, the body's adaptive immune responses wane over time. Occasional re-exposure to similar antigens can help boost that response and help maintain it for longer. Now that most kids are vaccinated and never get chickenpox, there's a lot less natural re-exposure happening for those of us who were taken to chickenpox parties as kids.


text:
How many ancestors' DNA do we have per generation?
DNA can be recombined and it's pretty random which ancestor will donate how much DNA other than your parents which is an almost perfect 50/50 split. For example, my family have had DNA tests done and I have significantly more DNA in common with my maternal grandfather than my maternal grandmother (something like a 60/40 split). When you go back a certain number of generations you will find that some ancestors no longer donate any DNA to you. For instance I have ancestors from Cornwall but no detectable Cornish DNA. I imagine that this number will asymptote to a particular value. Each generation going back will double the potential number of remaining donors, but probably half of them will be eliminated from consideration.
So, potentially, if you go back 10 generations you will have 1024 ancestors but maybe only have DNA from 100 of them. Maybe 11 generations gives 110 ancestors, 12 gives 113, etc. and 125 is the limit (on average).
Is there a calculation or some research for the number of ancestors per generation you have identifiable DNA in common with?

Out of curiosity, since DNA is such a young science - what proportion of the Cornish were tested to give a baseline of what constitutes Cornishness? How far back in time/generations? We'd also need to qualify what the percentages mean in terms of base-pairs, or is it some sort of selective sample of key sequences that was being tested for rather than the whole genome being sequenced?

@JiminyCricket not many are really needed. It's possible to identify Cornwall and Devon specific clusters using ~70 samples from each as long as their grandparents are local source.

@CJ this should at least give you a clue about the answer https://gcbias.org/2017/12/19/1628/

https://en.wikipedia.org/wiki/Coalescent_theory


text:
To what extent are microtubule-filaments present in astrocyte leaflets?
I have been trying to find information about whether microtubule filaments are present in the leaflets of astrocytes. A astrocyte can have quite varied morphology but many at least, have a star-like shape, with multiple branches, that become progressively branched into thinner processes. I found a suggested terminology for the progressively thinner branches here: Diversity of astrocyte functions and phenotypes in neural circuits
Soma --> Branches --> Branchlets --> Leaflets
The leaflets are really thin, maybe around 200 nm in width, and contact synapses at the "tripartite synapse".
What I'm curious about is whether there are microtubule filaments extended into these thinner leaflets. I know they are present in the branches and branchlets. But since MT filaments are around 25 nm in width I was thinking they were maybe too thin. I also read in a A closer look at astrocyte morphology: Development, heterogeneity, and plasticity at astrocyte leaflets saying that "The peripheral, leaflet-like processes which comprise much of the astrocyte volume exclude these large filaments and instead rely on actin dynamics for their structure, much like neuronal spines" But when I read the referenced article I couldn't find the authors making any similar conclusion...so I don't know, I'm really curious about this, if anyone has any idea, intuition, or facts (though I'll welcome any hunch) that would be greatly appreciated!


text:
Where to archive web citations for molecular biology article?
In 2013 I wrote a scientific paper in the field molecular biology. I needed to quote some webpages which I feared might disappear, e.g. amazon sales offers (it was a food related topic). So I archived them at Webcite (wecbitation.org), because it was recommended to me as an appropriate place for biosciences.
However, they stopped accepting new submissions. Where should I archive now ?

You can use the Internet Archive's Wayback Machine to get "permanent" links (as permanent as anything is on the internet) to just about any webpage, and I believe you can request indexing for pages that aren't already in the archive. Wikipedia uses this functionality for permalinks, for example.


text:
How is the Staverman's reflection coefficient in the Stirling equation determined?
The Stirling equation is expressed as follows
$J = Kf ([Pc-Pi] - σ [πc - πi])$
Here, capillary hydrostatic pressure (Pc) and Bowman's space oncotic pressure (πi) favor filtration into the tubule, and Bowman's space hydrostatic pressure (Pi) and capillary-oncotic pressure (πc) .
My questions:

What does σ, or Staverman's reflection coefficient, in this equation mean?
And by what logic or method is it determined?

References:

https://www.ncbi.nlm.nih.gov/books/NBK500032/
https://pcwww.liv.ac.uk/~petesmif/petesmif/why%20do%20we%20need%20kidneys/bowmans%20capsule.htm


text:
How is a haploblock defined with only one SNP location?
I am reading Impact of estrogen receptor gene polymorphisms and mRNA levels on obesity and lipolysis – a cohort study and am looking at Figure 1. I understand that haplotypes are associated with higher levels of linkage disequilibrium and that the intensity of the red indicates a high level of linkage disequilibrium. How then is a haploblock determined for Block 2 where only one SNP location is given? I am thinking linkage disequilibrium is a measure between at least two SNP locations.

In Figure 2 how are haploblocks determined when all SNP locations compared are displaying high linkage disequilibrium? Also, why are locations 5 and 6 excluded?

Reading the methods
In the methods, it is stated that haplotype blocks were inferred with the software Haploview:

Genotype information for ESR1 and ESR2 and regions
approximately 10 000 base pairs up- and downstream of
these genes were downloaded from HAPMAP in May
2005 [33]. Genotype data for the population of individuals of European ancestry were visualized using Haploview
[34]. We initially selected tag-SNPs defining all haplotypes with frequency > 5% from the block-by-block tags
displayed in the HAPLOVIEW "Haplotypes" window.
However, sometimes these tag-SNPs were exchanged to
other SNPs on the same haplotype due to difficulties in
designing genotyping assays. In addition, in regions not
covered by common haplotypes we aimed to select one
common SNP (allele frequency > 5%) every 5 000 base
pair. No non-synonymous SNPs full-filling these criteria
were detected in the ESR genes.

Haploview documentation writes:

Blocks
Haploview generates blocks whenever a file is opened, but these blocks can be edited and redefined in a number of ways. In the Analysis menu, you can clear all the blocks in order to start over, define blocks based on one of several automated methods or customize the parameters of those algorithms. Additionally, the blocks can be edited by hand.
Confidence Intervals [DEFAULT]
The default algorithm is taken from Gabriel et al, Science, 2002. 95% confidence bounds on D prime are generated and each comparison is called "strong LD", "inconclusive" or "strong recombination". A block is created if 95% of informative (i.e. non-inconclusive) comparisons are "strong LD". This method by default ignores markers with MAF < 0.05. The MAF cutoff and the confidence bound cutoffs can be edited by choosing "Customize Block Definitions" (Analysis menu). This definition allows for many overlapping blocks to be valid. The default behavior is to sort the list of all possible blocks and start with the largest and keep adding blocks as long as they don't overlap with an already declared block.

So, assuming that they used default parameters, you can reconstruct their methodology from the default method documentation and their description:

Take that default haplotype block output.
Where that default output didn't describe a block, select a common SNP every ~5Kbp in the unblocked region.

Answering your questions
In figure 1, the SNPs displayed are all tag SNPs. They are not the only SNPs in the block, but rather the tag SNPs used to represent the block. I am not clear on why multiple SNPs are used in some cases and single SNPs in others, unless they just try to have 1 SNP every ~5Kbp in general. I don't think that's what they did, judging from the figures.
In Figure 2, presumably the blocks are the output of the Gabriel et al. 2002 algorithm using D'.
The single SNPs that are not part of any block are presumably derived from the "every 5Kbp" procedure for regions not labeled with haplotype blocks.

Thank you, Maximilian Press, for your very helpful response! I am very excited to finish reading this paper.


text:
Are the muscles of all animals mechanically similar?
For instance, is the skeletal muscle of an elephant made of the same balance of fibers and cells as the skeletal muscle of a hippopotamus?
I recognize that slow- and fast-twitch muscles are a thing, and that which animals have which vary. I also recognize that different animals might have different numbers of mitochondria per muscle cell, and that there's a difference between skeletal, smooth, and cardiac muscle, but am still conflicted on one thing would it be accurate to claim that the mechanical properties, density, and the like of all types of animal skeletal muscle are the same?
If you happen to have a source for your answer, please supply one - it'll be useful for something I'm trying to write.

I recall Comparative Biomechanics by Vogel stating the power density is roughly similar. Similar enough to group together and make comparisons with groups of man made actuators.

@DKNguyen Thanks.

This doesn't appear to be answerable by anything other than opinion — can you please specify your criteria for "similar".

@tyersome Having similar physical densities, compressive and tensile strengths, Young's moduli, extensibilities, and so on and so forth - essentially, properties of the muscle in regards to materials science.


text:
Why don’t all HPV strains cause cancers?
There are roughly a dozen high risk HPV strains responsible for cervical cancer. These strains promote hyperplasia of infected cells by encoding E6 and E7, which potently antagonize tumor suppressor genes RB1 and TP53. Overtime the episomal viral DNA gets incorporated into the host chromosomes by the cellular DNA repair mechanism, which enables stable propagation of viral oncoproteins to daughter cells (according to this paper, about 80% of cervical cancer cases harbor at least one copy of HPV DNA in the chromosomes).
However, there are many more strains causing hyperplasia of infected skins, such as the strains causing common warts, flat warts, and genital warts, but none of them have been found to be associated with cancer. Is it because these viruses encode milder oncoproteins that don’t potently antagonize RB1 or TP53; because these viruses infect wrong types of cells which are refractory to transformation by E6 and E7 compared to cervical epithelium (oncogenes are context dependent. For example, EWS-FLI1 potently transforms mesenchymal stem cells into Ewing sarcoma, but causes senescence and apoptosis in more differentiated cells); or because the viral DNA do not incorporate into the host chromosomes (which sounds unlikely because incorporation of foreign DNA by DNA repair mechanisms is inevitable after prolonged exposure)?


text:
Why does oogenesis have to begin in foetal stage itself?
In males, spermatogenesis begins after puberty and they retain this ability throughout their life time. However, in females, oogenesis begins and ends in the foetal stage itself and the female is unable to generate any more oocytes in her lifetime. Is there any reason for this assymetry in nature?

For ref: This and this.

Welcome Muralidhar. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask.


text:
Refuge impact on growth rate
I have a question related to the refuge effect in ecological models. The assumption is that the population of hosts/prey is divided into two groups. One group consists of individuals that are safe from parasitoids/predators and another group consists of individuals that are exposed to parasitoids/predators and can get parasitized. Does it affect the growth rate in the sense that hosts that are in refuge have a bigger growth rate than those that are not in refuge? Are there some known experimental results, some papers or books that deal with this topic?

The answer to this depends a lot on what kind of question you're asking. Adding more context/clarifying your question might help you get more useful answers.
If you run a short-term experiment starting with the same population sizes in each region, and little mixing between populations, the protected population must grow faster (given that the protected region is the same in every way as the exposed region except for being protected from natural enemies).
Of course, if you don't have enough statistical power (there isn't very much predation even in the exposed region, or your population counts are not very accurate, or there is lots of other random variation in the growth rate) then you might not be able to detect this difference.
There are lots of potential confounding effects:

how smart are the prey? Do they preferentially move into the refuge (in which case the protective effect of the refuge might be overestimated)?
... or do they prefer places with lower conspecific densities (in which case they might preferentially move out of the refuge as predators remove conspecifics in the exposed region; you might underestimate the protective effect of the refuge)
or do conspecific densities affect survival or fecundity in other ways? (If the protected individuals die less from predation, this might be compensated by other effects of crowding.)
how do the natural-enemy (predator/parasite/parasitoid) densities respond to changes in host density?
are the refuge and the protected area really identical in all other ways? If this is an observational study, maybe the prey species is already making a tradeoff between areas on the basis of predation risk balanced with some other benefit (such as greater resource availability)

There is a lot of research about all of these complexities (you might start by doing a literature search on "ideal free distribution" and "predator", or "landscape of fear"; however, most of this research is about short-term redistribution rather than long-term growth rates)
If none of these complications is occurring (in particular, no other environmental differences and no differences due to host densities in each area) then we could also say that the fitness (i.e., expected number of lifetime offspring) of hosts in the protected area would also be expected to be higher than that of hosts in the exposed area (this might be what you mean by "growth rate").
You might want to dig into the literature on marine protected areas, where researchers consider how population dynamics work inside and outside spatial regions where fishing is excluded (which is similar to protection from predators or parasites).
From a very narrow mathematical biology perspective, if the two populations are coupled (i.e. individuals can move back and forth between refuge and non-refuge areas), then there aren't separate growth rates for the two subpopulations — in the long run, both will grow at the same (exponential) rate as the whole population (discounting density-dependent effects). Consider the simplest possible model:
$$
\begin{split}
N_e' & = (r-p-m)N_e + m N_p \\
N_p' & = (r-m) N_p + m N_e,
\end{split}
$$
where $N_e$ and $N_p$ are the "exposed" and "protected" population sizes (and $N_e'$, $N_p'$ are their derivatives/instantaneous growth rates); $r$ is the intrinsic growth rate (in the absence of predators); $p$ is the per capita predation rate; and $m$ is the migration rate, the per capita rate at which individuals move back and forth between protected and exposed areas. (This model is horribly unrealistic because it assumes that all of the per capita rates are constant — neither the intrinsic growth rate of the prey, nor the attack rate of the predators, nor the behaviour of the prey, can change as the population densities in both regions change.)
We can do the typical mathematical analysis of this system:

find the Jacobian of the system

$$
J = \left(
\begin{array}{cc}
r-p-m & m \\
m     & r-m
\end{array}
\right)
$$

calculate its eigenvalues, $r-m - \frac{p}{2} \pm \frac{\sqrt{4 m^2 + p^2}}{2}$
conclude that the overall population size (and both components) grow, asymptotically, at an exponential rate given by the largest eigenvalue (the positive root above), unless $m=0$ (in which case the protected population grows at rate $r$ and the exposed population grows at rate $r-p$).
if you want to know the relative contribution of the two subpopulation densities to the whole population (attained asymptotically), calculate the eigenvector associated with the dominant eigenvalue and scale its magnitude to 1.0.

Great explanation, thanks a lot!