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Compliance lung chest wall together
I do not understand compliance better why do the lung chestwall together system compliance is less than the individual compliance of lung and chest wall? shouldn’t it lie in middle? Please clear it.

Can you provide the source of this information?

Guyton and hall

The compliance can be represented by the change in cavity volume caused by the change in unit transmural pressure. It is determined by the equation "compliance = ΔV/ΔP", which ΔV refers to the change of volume and ΔP is the change of transmural pressure.
The transmural pressure mainly counteracts the effect of elastic resistance while enlarging the volume of lung/chestwall. So as we can see from the equation, compliance is inversely proportional to elastic resistance（which determines the pressure required for inhalation）.
The total elastic resistance is the sum of (also is larger than) the individual elastic resistance of lung and chest wall. So according to the equation, the total compliance is less than the individual compliance of lung and chest wall.


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Muscle contraction and closing in of z line/disc
I have studied that during a contraction of myofibril, the globular heads of myosin attach to actin filaments and pull them towards the centre of the sarcomere pulling the z line/disc as well.
What I don't understand is that the z line must also in turn be connected to another sarcomere's actin filaments and they must also be getting pulled in the opposite direction by their myosin filaments. So how does the z line move in a particular direction?

What do you mean by particular direction? Do muscles ever move in a particular direction?

What I meant was that th he sacromeres contract individually and the z lines get pulled by 2 opposite forces. Then how does the I band get shortened? Is it not by moving of the z line towards the centre ( towards A band)?

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Evolution of Anoles
For context, I am currently looking at this virtual lab of Lizard Evolution by HHMI biointeractive.
Trunk anoles from an island called Iron Cay were placed in a few experimental islands filled with small bushes and grass.Over four years, the researchers measured the length of the hindlimbs of the anoles. After four years, they found that the average hindlimb length of the anoles in the experimental islands was shorter than that of those on Iron Cay.
I was wondering if the anoles from the experimental island were brought back to Iron Cay, would the anoles still mate with each other?
Thank you!

On the face of it, this seems to be a question regarding the behaviour of artificial constructs in a computer program and not a biology one. I gather it's an educational program, but I'm not familiar how it's programmed or how it can be adjusted to behave. Perhaps you should just try it and see. If you've an actual biology question about the scenario in real life, (about speciation) then please ask it, but the question as it is now seems to me to be off-topic. Please take our [tour] and read up in the [help], noting the [ask] section.

This is also definitely a homework question... note our homework policy

I'd recommend reading up on the different mechanisms of reproductive isolation. It's possible that changes in hindlimb length or morphology could be a source of behavioral or mechanical isolation, though post-mating barriers to reproductive compatibility would be unlikely on such short timescales

to clarify the two lizard populations have only been separated for 4 years right?  There's no reason to expect too much evolution to occur in 4 years.  If the surviving lizards have longer legs then I'd argue that all that happened is just the short legged lizards died.  While that is evolution, since the lizards are the exact same individuals taken to the island 4 years earlier, there's no reason to expect they'll have changed their mate choice behavior.

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Bacteria genetic screen for mutants
Is there a simple screen for bacterial mutants with increased mutation rates? For example, detection of some loss-of-function mutation that causes increased mutation rates.
Any screen I can think of (for example, just testing on several different selective mediums) would select for bacteria with several mutations, but that does not necessarily imply an increased mutation rate.

You may give a look at the Ames test, and possibly adapt it to your needs. Basically, the test was developed to identify genotoxic substances, i.e. substances that increased mutation rates in bacteria.
The standard way is to use strains of bacteria that are classified as His-, i.e. they need an external source of Histidine to survive.
In the Ames test you prepare two cultures of such bacteria. One of them is exposed to the hypothetical mutagen, and one acts as a control. You grow both of them in plates with minimal amount of Histidine, so that all bacteria grow for a while.
When Histidine is over, only the revertant mutants will survive. If the hypothetical substance is a mutagen, you should notice that in the corresponding plate there are more revertant.
This can be easily adapted to your case if your strain are His- (or can be convinced to become His-) or have some other identifiable mutation.
So, assuming that you are happy to compare mutation rates in a series of strains that are His-, you just need to compare the growth of those strains on minimal histidine and the faster growers are likely those with the higher mutation rate, according to Ames postulate.
If your strain do not have such a property, it may be more difficult (and actually, I wouldn't know what to do, right now!)


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Identifyication of small delicate shell found on the beach
I found this item on the beach today in north west England. It’s very light weight and delicate, about 3cm long and some interesting patterns on it. Any ideas on what it is would be greatly appreciated

This is almost certainly the shell of a Sea Urchin. These are spiny echinoderms that are found almost world-wide in many different species in the littoral down to ~5000 m (16,404 feet) depth. They have five-fold symmetry, meaning the shell is divided into 5 parts that are more or less symmetrical, like a five-pointed star.
The reasons I say this is so, is that the shell (called a "test") is hollow, it is covered in small protrusions that are the remains of the spines. You can also see some of the smaller spines in the top picture at the edges of the bottom two seams in the shell, and you can see the symmetry in the top picture. You can see a sea-urchin shell with the spines removed, in a bit better state than your one, at the bottom of this page from Arizona State University

I knew it was an echinoderm, but didn't think of a sea urchin, as I've seen a bunch of different ones, but never this. Is it a heart urchin/sea potato (here and here)?  I've never seen those.

@anongoodnurse No idea on the species at all. Chances are it's one of the common ones. Having had a quick look for "heart urchin test" it could well be a heart urchin - it's definitely an asymmetric test, so something along those lines is probably right.

This is a Sea Potato (Echinocardium cordatum).

Welcome to the Biology Stack Niels. Please take a [tour] and visit the [help] for more information on how this particular Stack works. Your answer looks like a good start for an answer as we value answers that provide a bit more than the basics - reasons why you think it is E. cordatum and some references/links to back it up would help.


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Identification of an insect found near the Rhine, Germany

It was about 2-3cm long
It has two small wings and 6 legs

Is that the only photo you have? A side view would be very helpful.

possibly larval cicada, but I don't have access right now to figure out if true.

It would be helpful to know the size.

Hey thanks for the answer and yes I have more pictures just not as good quality.

Also I wrote the size under the picture it was about 2-3 cm long

That side view is very helpful, thanks.

It is the larva of a hemimetabolous insect for sure. Considering it was close to a water body I would say a nymph of some Odonata ?
The legs are a bit bulky though, I might be completely wrong.
These are not wings yet, they will be there at adult emergence.
Maybe check these out :
https://www.pentaxforums.com/gallery/photo-dragonfly-nymph-20082/
https://www.flyfishbc.com/threads/april-2011-fly-o-the-month-dragonfly-nymph-gomphus.5843/
Edit : my colleague Dirk Mikolajewski says it is a Gomphidae larvae. He will probably tell you which species soon.

Nice links! (Not a very pretty insect, though.) +1

Odonata larvae are the only insect I am scared of. I resent them a lot for eating amphibians.

I'm relieved to read that. I thought, "That thing would scare me to death!" It looks like it could take a chunk out of someone's hand, too.

Thanks everyone for the help

I also have a short video of it Walking but can't upload here I think


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Can a symptomatic, recent recipient of live attenuated dengue vaccine Qdenga transfer the virus to mosquitoes if bitten?
Can a symptomatic, recent recipient of live attenuated dengue vaccine QDENGA transfer the virus to mosquitoes if bitten?

When you say "the virus" do you mean the original Dengue virus? Or do you mean the attenuated yellow fever virus with a couple Dengue genes?

Dengvaxia is the older yellow fever-based vaccine, Qdenga is based on attenuated DENV2.

@timeskull Ah, thanks for that clarification!

The possibility of mosquitoes becoming infected with vaccine-strain DENV by taking a blood meal from a vaccinated human has been found to be low. Transmission of vaccine-strain DENV to unvaccinated people was found to be "very unlikely", but not ruled out completely.
From Limited Transmission Potential of Takeda’s Tetravalent Dengue Vaccine Candidate by Aedes albopictus:

It is critical that live-attenuated dengue vaccine viruses will not be transmitted by mosquitoes from vaccinees to the unvaccinated population, and part of the vaccine safety evaluation requires confirmation of low mosquito transmission potential.[13–18] To be transmissible by mosquitoes, the virus needs to be able to infect the mosquito midgut (infection), escape the midgut infection barrier, replicate in the salivary glands (dissemination), and be released into the mosquito saliva (transmission).[19] The TDV viruses were previously found to be inefficient at infection, dissemination, and transmission in Aedes aegypti, the primary vector of DENV.

TDV (Tetravalent Dengue Vaccine) refers to QDENGA in the above quote.
QDENGA is attenuated by serial passage through dog kidney cells, so the virus becomes better at infecting and replicating in those cells but worse in human and mosquito cells. The vaccine strains (there are 4 separate vaccine-strain viruses, one for each natural serotype of dengue) are much less effective than wild type at infecting mosquitoes, even for blood with the same concentration of virus particles. Vaccine-strain DENV on average reaches 1000x lower concentrations than wild type, these two effects are cumulative. This study couldn't measure the likelihood of transmission because 0 vaccine-treated mosquitoes (out of 186) developed measurable levels of virus in the salivary glands, which are what can transmit the virus to human hosts.

I wonder if the levels of virus in mosquitos' salivary glands are sufficient to infect dogs, now that the new strain is more infectious for dogs, and apparently they can be infected.

well, the new strain was passaged through dog cells, but that doesn't guarantee it's particularly good at infecting dogs. To give a crude analogy, if you forced humans to adapt to living in water for 6 generations, they still wouldn't be able to compete with fish.


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Reading list to understand the theory of mycelium based materials for beginners
I have read tons of articles and seen presentations about people making materials with mycelium. From mycelium bricks to mycelium fabrics. I want to understand the processes that allow this. That is, I want to learn the theory about how mycelium can be used to create materials and what properties those materials will have. What should I read?
I guess it should be possible to start by reading the patents I have seen, but they probably assume some knowledge. My background is mostly computational, so I have read up on systems biology, computational biology and mathematical biology. However, I don't know how much of that is relevant, so for the sake of this question, lets assume I am a complete beginner.
What is required to understand the patents in this field?

Unfortunately this question is a bit too open-ended for a Stack Exchange format. I can see tons of tutorials on how to make the mycelium products - what exactly is it that you want to know? Systems and comp bio will be more or less useless here, mathematical slightly - growth curves etc. But all that is moot because you will need to actually grow the fungus and the best way to do that is to have a go...

@bob1 I am not looking for tutorials. I am looking for theory. That is, I want to understand what is going on and how it can potentially be modelled. That is, which variables can be tweaked to change material properties.

But there's nothing in your question that indicates what you want - all you say is "From mycelium bricks to mycelium fabrics. I want to get into this." Which to me means you are interested  in making them, not the theory. If you had said "I want to understand the theory" that might make it a suitable question .

@bob1 Fair enough, I agree that it is poorly worded; I assumed that the remainder of the question would be enough to clarify what I was looking for. I'll edit it.

@Avatrin The first thing that comes to mind when it comes to “mycelium modeling” is finite element analysis. I think that you can find a lot of deeper theoretical materials there (for example): https://www.sciencedirect.com/science/article/pii/S0264127518307482

As one of the early investors in the field of mycelium based materials, I can give a brief answer.
Mycelia are the underground cellular network of some fungi and bacteria.  Under some conditions they can form dense enough networks to produce various materials.

The main effort in mycelial materials I believe is in private companies right now.  Mycelial materials are being used to make leather, packing materials, and scaffolds for plantbased meat.  New applications are coming on line regularly these days as fungi are deeply interesting, so this list should be longer.
The details on how to create these materials is rarely made public but starting by growing your own fungal mats is available and a great place to start. The founder of Mycoworks, Phil Ross is an artist who made furniture and some building material from mycelia as well. He has done workshops and kits to grow his favorite fungi, the medicinal mushroom reishi are available.
Image uploading doesn't appear to be working at this moment but if you follow the links you can see
that the texture, flexibility, hardness and toughness of mycelia represent a broad range of material properties.  It should be expected that the field will continue to broaden.
In addition to these topics, a good place to start is reading the renown mycologist Paul Stamets.  His book, "Mycelium running" talks about the uses of fungi in sustainability exhaustively, touching on this topic and quite a few others.


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If race doesn’t exits; why do humans look so different?
I was talking about a speculative new race of humans that could be created with genetic engineering and several people told me that race does not exist and is a social construct. I get what they are saying but I also read many times over the years that different groups of humans all have slight genetic differences even though we are all the same species. Racism in the world usually relies on aesthetic traits, e.g. different skin color, facial features, hair. Those things seem trivial but I would think that phenotypes would definitely be a big thing in our genomes. Therefore, why cannot race exist?
Also I am applying for jobs and they always ask for my ethnic background. The options are White/Caucasian, Black, Hispanic, Asian, Hawaiian, and Indigenous American or Alaska Native. First off, I think not separating Pacific Islanders with East Asian and South Asian is a big mistake. There is a huge difference in Asian and Indian culture and I think they should have their own box. The same goes for Middle Eastern or Arabic as I feel their culture is significantly unique as well. Lastly, isn’t Hawaiian an ethnic background and determinate by geographical location not genetics?
This post is totally open-minded and I have ZERO beliefs that any “race” is superior

This here states that there is more variation within a "race" than there are between two different races. https://scienceandsociety.duke.edu/does-race-exist/ I'm guessing what it is referring to is that what we can see is only a very small contributor to the overall genetic variation. But what is specifically referred to in the article is there is a gradual spectrum between every "race" based on geographical proximity rather than clear delineations.  Sort of like colours. We say red and green are separate colours in regular speak, but if you look they are not distinct groupings.

It's not that race cannot exist theoretically, it's that is doesn't exist empirically among the lines drawn for humans as a socially-imposed phenotypic construct. In non-human animals and plants we might refer to "subspecies" as biologically legitimate groupings.

what makes you think a unique culture would be genetic and not say a unique combination of environment and history. Also cultures are not as different as you think, agricultural cultures are very similar compared to everything out there.

I think your friends are misunderstanding social constructionism and race theory. Countries are social constructs, but that doesn't mean that Italy doesn't exist. Money is a social construct, but good luck telling your landlord that it doesn't exist. Also, most US employers follow the federal government's five categories for data on race, so the one should read "Pacific islanders or Native Hawaiian." White and Asian folks living in Hawaii mostly know not to refer to themselves as Hawaiian in any context, even if they were born there and spent their whole lives there.

Definitions of race as we normally use it varies greatly from culture to culture, ones based on actual Biology don't match our preconceived ideas.
You could break humans into races, but if you do based on any kind of biological grounds, it can't be by the superficial things we traditionally use.
The biggest problem with race is if you split humans into races, everything 'not an African native' is one race. Or hundreds of native African races before the Norse and the Mayan are not the same race.
Almost all of human genetic diversity is inside Africa and that is for a species that has very little genetic diversity. one subspecies of chimp has more genetic diversity than all of humanity. A Norwegian native and an Australian native are more similar genetically than the Berber and Bantu two different native African lineages.
Source
On top of that there is more diversity within populations than between them because of how low the genetic diversity is. Only around 6% of human genetic diversity falls along classical racial lines, meaning they are superficial differences not representative of deep relationships. Humans almost went extinct at one point, and we are all the descendants of likely less than a thousand survivors, so we are all super related. and most of our differences are small changes since that point.

Skin color is useless, since it is a superficial adaptation to latitude. Native skin color correlates really well with yearly UV levels, and the adaptation happens fairly fast. thanks to 'Cheddar Man' we know the British people of 10000 years ago had black skin.
Skin Colour:

UV levels:

John's answer is the correct one about race, and this answer makes no attempt to address the biology.
However, to address why you only get those options in you questionnaires, it is because you are apparently in, or applying for jobs in, the USA, as that is really the only country that might be interested in Alaskan Natives  and Hawaiians.
There are reasons beyond race for such questions.
These groups are the ones specifically addressed in the law that was passed by executive order on the 25th of June 2021 in the USA, and are also ones included in things like Census questionnaires. You can read the full text of the executive order here. The order is titled

Executive Order on Diversity, Equity, Inclusion, and Accessibility in the Federal Workforce

and begins:

By the authority vested in me as President by the Constitution and the laws of the United States of America, including sections 1104, 3301, and 3302 of title 5, United States Code, and in order to strengthen the Federal workforce by promoting diversity, equity, inclusion, and accessibility, it is hereby ordered as follows:

The definitions section mentions the groups (note the similarity to your list), including whole groups whom you definitely couldn't term races. You should also note the wording - it specifically does not ask about race, rather about communities (emphasis in quote is mine), so this isn't a "race" driven question you are seeing in your applications, as you noted, but perhaps not realized, when you inquired about Hawaiian in the question:

In the context of the Federal workforce, this term includes individuals who belong to communities of color, such as Black and African American, Hispanic and Latino, Native American, Alaska Native and Indigenous, Asian American, Native Hawaiian and Pacific Islander, Middle Eastern, and North African persons. It also includes individuals who belong to communities that face discrimination based on sex, sexual orientation, and gender identity (including lesbian, gay, bisexual, transgender, queer, gender non-conforming, and non-binary (LGBTQ+) persons); persons who face discrimination based on pregnancy or pregnancy-related conditions; parents; and caregivers.  It also includes individuals who belong to communities that face discrimination based on their religion or disability; first-generation professionals or first-generation college students; individuals with limited English proficiency; immigrants; individuals who belong to communities that may face employment barriers based on older age or former incarceration; persons who live in rural areas; veterans and military spouses; and persons otherwise adversely affected by persistent poverty, discrimination, or inequality. Individuals may belong to more than one underserved community and face intersecting barriers.

Now, I am aware that this is titled for the "Federal Workplace" meaning that you might think it only applies to those organizations that are federal. In fact, I believe that this would apply to any organization that has federal funding, which includes a huge range of organizations, any of whom can get federal grants - all would need to comply with this law. This includes private businesses, research organizations, hospitals, charities; in fact just about any employer you can think of.

These categories were absolutely not laid out in an executive order in 2021

@BryanKrause See the large quote in the middle and reproduced here: Black and African American, Hispanic and Latino, Native American, Alaska Native and Indigenous, Asian American, Native Hawaiian and Pacific Islander, Middle Eastern, and North African persons That's pretty similar to the list in the question. The link provided is even whitehouse.gov...

These are standard US census categories.

@BryanKrause Yes, but they wouldn't be asked about in job questionnaires if there wasn't someone looking for them and having to fill diversity measures. The point of my answer (and perhaps I should make this more clear in there) that there are reasons besides race for asking these questions.'

@BryanKrause edited. I was unable to find any other law that specifically addressed these categories; even the civil rights laws don't go into them. By fill on my previous comment, I meant fill out as in report, not to imply that diversity needed to meet a quota of some sort, as the comment could be read.

Laws are rarely written that way. One law says you can't discriminate based on race; somewhere in administrative code they categorize race for some other purpose; someone collects information based on that definition to show they're in compliance with the law because they know it's something they can defend in court by pointing to the government document.

Also, Federal employees are only US Federal Government employees. Contractors aren't federal employees; my salary is paid by a federal grant but I'm a state employee in the state that my university is in, etc. This is all quite off-topic for Biology and perhaps belongs in Politics.

Let us continue this discussion in chat.


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Examples of Differential equations in Biology
I am a mathematician currently teaching some math classes at a university. Next semester, I'll have bachelor's degree biochemistry students. I want to know where certain math tools might be needed in such a field.
Where do differential equations arise naturally in professional Biology? Maybe from some data analysis of a complex phenomenon? What scenario?
I was thinking of a scenario where, for a complex set of variables, you would take one of them, say $x$ and plot $\frac{\Delta x}{\Delta t}$ vs $x$ and find that the relationship was e.g. polynomial ($\frac{\Delta x}{\Delta t} \propto x^{3}$).

Unless you’re teaching in Harvard or MIT, the most you can expect from biochemistry students is simple algebra. That doesn’t help you, but “Blessed are they that expect nothing…”.

@David I was interested in numerically approximating systems of differential equations to model metabolic pathways when I was an undergrad. I was not allowed to pursue this. Not because it was explicitly disallowed, but rather because I was kept too busy memorizing multisyllabic terms (a little bit of physics and graph theory would have been better IMO) that I promptly would forget after finals.

@Galen: Did those multisyllabic terms include "multisyllabic"? =P

@user21820 Who knows! I forgot!

I'll just say I don't miss reciting "Phosphoribosylformimino-5-aminoimidazole carboxamide ribonucleotide isomerase".

All the posts are very helpful! Thank you to everyone!
I am quite familiar with the use of Differential equations in population biology, but I sensed that wouldn’t be that satisfying to biochemists. You provided me with a lot of useful references :)

The only time I ever used my Ti-89 calculator to do anything of use was calculating sedimentation of proteins in an ultracentrifuge.  It totally worked though.

For biochemistry students the obvious link to differential equations is the Michaelis–Menten equation which is a simple model of the kinetics of reactions involving enzymes. Your students will be hearing a lot about Michaelis–Menten in their biochemistry classes if they haven't already. It's also very accessible to students having their first exposure to differential equations.
Considering the wider field of biology there are several major topics that revolve around differential equations. Population Biology and the related field of Population Genetics are heavily mathematical with lots of differential equations involved.
Expanding beyond ordinary differential equations there is Alan Turing's Theory of Morphogenesis which tried to explain striping and spotting in animal hides using a system of coupled partial differential equations to model reaction rates and diffusion.

Michaelis-Menten is super obvious, can't believe I didn't think of it.

Update
please follow Charles E. Grant's advice and do Michaelis-Menten!
Hodgkin-Huxley as suggested by commenter ctwardy is a great idea too.
Original answer
I would strongly recommend the book mathematical ideas in biology by J Maynard Smith.
A couple of examples that spring immediately to mind with relevance to biochemistry might be:

gene expression
structure of the coiled-coil protein fold (see e.g. equation 4 in Quine's book)

Less biochemical but still very fun is Lotka-Volterra modeling of predator-prey interactions.
Another book that seems to directly address your question is this one.

Also neurophysiology! The Hodgkin-Huxley equation won a Nobel prize.

Are Twelve ODEs for mitochondrial membrane potential (ΔΨm), and matrix concentrations of Ca2+, NADH, ADP, and TCA cycle intermediates, used to model the response of mitochondria to changes in substrate delivery, metabolic inhibition, the rate of adenine nucleotide exchange, and Ca2+ good enough for you?
Generally speaking, many biochemical process would often be modelled on the macro-molecular scale by differential equations. These include rate equations for the chemical processes, as well as diffusion kinetics within the cytoplasm or across membranes.
On the larger scale of organs and entire systems, we also have alveolar gas exchange, digestion and absorption processes, renal filtration, homeostasis, and of course many others.

Logistic differential equations in modeling population dynamics is the first to come to mind.
Populations grow under the constraints of limited resources, capturing the transition from initial exponential growth to a plateau as the carrying capacity of the environment is approached.
For a detailed exploration of logistic differential equations you can refer to this comprehensive guide on Brilliant.org.

The other answers offer many examples of differential equations for initial-value problems where you solve an (most often here) an ODE or a PDE. There are also boundary-value problems in biology, for example when modelling the strengths and elasticity of various structures supporting a plant (e.g. https://doi.org/10.34133/ehs.0007) or of animal bones (e.g. https://doi.org/10.1007/s12018-015-9201-1 for human medicine, but the principle is the same for other living and fossil vertebrates) or modelling the elasticity of plant leaves based on the plant's turgor (https://doi.org/10.1111/tpj.12042). Similar simulations had also been done for individual cells. In these cases the PDEs are elliptic and are most often solved by the finite element method or similar methods.


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Extremophile hunting and identifying unknown microbes
I'm going extremophile hunting! We're doing a trek by boat between some islands with semi-active volcanic terrain to try to document some interesting species, and running into a problem I've never tackled before.
Usually I'd send samples into a lab for genetic analysis, and then go from there, but in this case we won't be able to get samples to and from the lab until the end of the trip. At that point we won't be able to go back and follow the most interesting organisms without a second trip.
The temptation is to bring along whatever equipment we need for our mobile lab and do the genetic analysis on-site. Space and budget are at a bit of a premium, so I thought I'd ask the community if anyone has any good ideas for microbe identification on the go. We'll have power and refrigeration and even a small amount of freezer space, though no -80C freezer. We're most interested in extremophilic fungi, though I'm sure we'll find other interesting things along the way.

If you have some money: portable -80. Approx $8K. I've heard good things, but never used one. We'd need a bit more info - just trying to ID (sequence?)? Want to culture?

If "identification" is your goal, I would suggest a MinION sequencer and associated equipment for library preparation. These are capable of generating large informative reads for e.g. metagenomics/isolate sequencing and are extremely portable. They have field sequencing kits, and there have been papers evaluating use in the field (see also here).
If your goal is "bring them back", then bob1's comment about a portable -80º is probably the more pertinent piece of equipment.


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How did the Zinder-Lederberg experiment on Transduction work?
In the paper that introduced TRANSDUCTION (J Bacteriol. 1952 Nov;64(5):679-699), Lederberg and his student Zinder reported that S. typhimurium

"LT-22 is lysogenic for a virus active on LT-2. This virus is capable
of inducing lysogeny in LT-2."

I read this line as: LT-22 carries a prophage that, upon induction, can infect LT-2.
They then used subsets of these strains: LA-2 (also known as SW-414), which required methionine and histidine; and LA-22, a collection of strains with different metabolic requirements.
Zinder and Lederberg commented that

Prototrophs appeared in the platings of LA-22 but not of LA-2. Sterile
filtrates of LA-2 broth cultures did not elicit prototrophs from
LA-22.
However, filtrates from mixed cultures of LA-2 and LA-22 elicited about one prototroph per million LA-22 cells.
Thus LA-2 produced a filtrable agent (FA), under stimulation from LA-22, that could elicit prototrophs from LA-22.
Filtrates of LA-22 cultures, containing substantial amounts of phage (PLT-22) active on LA-2, also stimulated FA production from
LA-2.

Thus, LA-2 produced a phage that infected LA-22 to produce a prototroph.
But if the phage was present in LA-22 (derived from LT-22), how could it infect LA-2 (derived from LT-2)?
Is there a detailed explanation of this experiment?
Thank you

Regarding the bolded sentence, it's not surprising that a prophage from one strain of salmonella would infect another salmonella strain. What part of the process needs explanation?

The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it)

There certainly are detailed explanations of the experiments. For this answer I'm using a 2016 retrospective in J. Bacteriology, the same journal that published the original paper. However those descriptions will tend to gloss over the points that concern you as described in your comment:

The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it)

Remember, these experiments took place in a very early time for biochemistry. The Hershey-Chase paper that established nucleic acid, not protein, as the carrier of genes was also published in 1952! The "how" of transduction wasn't worked out until later.
The Filterable Agent responsible for transduction between LT-2 and LT-22 is now known as phage P22. Its prophage tends to be integrated into the host genome. When it switches from lysogenic to lytic phase, it replicates its genome while still integrated into the host.

The headful mechanism fills the first capsid with part of the prophage genome and continues through the adjacent bacterial chromosome for up to seven or more successive capsid headfuls.

So, a significant fraction (about 2%) of the virus particles produced by lytic P22 contain host bacterial DNA and little to no phage DNA.
Why superinfection exclusion (SIE) fails in the LT-22 is an interesting question, but it turns out to not be surprising. P22 has four separate SIE systems, and one, sieA works by binding to and blocking the exit of P22's "ejection proteins", so it can stop transduction by preventing entry of any kind of DNA. However, it looks like this system doesn't perfectly prevent DNA injection. From a 1971 paper on P22 SIE:

The frequency of transduction of wild-type lysogens is reduced by a factor of 250, indicating that transducing particles are excluded by P22 prophage

So, if the concentration of P22 particles with bacterial DNA is high enough, a few will get through.
Incidentally, I found that LT-2 was first isolated in Sweden, and LT-22 in Chile, both in the 1940s.

Thank you, I also read that paper. Your answer gives a better understanding of the issue. Tx

I hav found more info in two more papers. In Microbiol Rev 1978;42:385 it is said: "P22 ... generalized transducing particles consist primarily of host DNA... the transductant carries the transducing material as long as the prophage is present". Thus, lysogeny is actually needed for transduction to occur.

In the same paper, P22 superinfection exclusion is described as follows. There are 3 mechanisms (1) "chemical modification of the cell surface component (the 0 antigen)" but " P22 lysogens still adsorb P22 virions, but less efficiently"; (2) "preventing entry of the DNA of superinfecting phages into the cell" but " The sieA exclusion system can be saturated by high multiplicities of infection"; (3) "sieB" which " does not act on wild-type P22". Thus, one can assume either that there were many viruses that saturated sieA or that Zinder used sieA mutants...

In both cases, the model is more complicated than that delineated by Zinder himself.

The second paper (doi: 10.1128/mbio.02169-23) indicates 4 mechanisms of P22 superinfection exclusion; which Zinder had to bypass to obtain transduction. The additional one is the C2 repressor, which assures the non-expression of lytic genes (but does not exclude the insertion of new prophages).


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Why electrical synapses are more common in invertebrates?
I suppose it's because they live in an environment where there's a constant vulnerability to predators and they need to respond quickly. But it's not really the case for many invertebrates and besides many vertebrates too live in such environment.

I think this falls under this Q&A: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont There's not really going to be an answer besides "that's how they evolved".


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How is opsin of rhodopsin is different from that of iodopsin?
Rhodopsin contain retinal, an aldehyde of vitamin A and opsin protein and iodopsin also contains retinal along three different types of opsins namely erythropsin, chloropsin and cyanopsin. But kind of opsin does rhodopsin has ?

You'll need to clarify what you mean to ask.

What I want to ask is, like in iodopsin, there are three different types of opsin protein erythropsin, chloropsin and cyanopsin. But in rhodopsin we have retinal and opsin but how is this opsin different from the opsins of iodopsin ?

Different how? What sort of differences are you looking for?

See, rhodopsin consists of retinal and opsin which on separation of which we are able to perceive light. Now in case of iodopsin which is found is cones also contains retinal and three different kinds of opsins namely chloropsin, erythropsin and cyanopsin. Now the opsin that we find in rhodopsin, how is it different from these chloropsin, erythropsin and cyanopsin that are found in iodopsin ?

How is it different how? Imagine you have cats and dogs and you want to know how they are different. The list would be endless: you could talk about how they make different sounds, have different diets, their color, the texture of their fur, their history of domestication, etc. Which characteristic of these opsins are you asking for a comparison of?

I'm asking how they're chemically different ?

They're different proteins; they have different amino acids. Is that what you want to know?

Yes, what kind of groups they have in their structure ?

What do you mean by "groups"? What are you trying to learn or do?

I'm talking about functional groups such -CHO, -OH, -CO- etc that we usually find in organic compounds.

There are a few hundred amino acids in an opsin protein; each are going to have one or more of those functional groups in addition to the amino backbone.


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What are the chances that two children of the same couple will have the same genes without being identical twins?
If I randomly select half the chromosomes of the male and female eventually I will select the same exact half for both a second time. How often does this occur? Is this considered a twin if it is born at a different time as in years apart?

Just because the poster might not have an intuition for why this is obviously very low doesn't make this a bad question. In fact, this is interesting.

The chances are effectively zero.
Even in the absence of recombination, this calculation involves choosing the correct member of a pair from each of the 23 chromosomes, from both the father and the mother.
223 × 223 = 246 = 70,368,744,177,664
So, less than a 1 in 70-trillion chance. For some context, only about 117 billion humans have ever been born in history.

A more accurate calculation would include recombination, which occurs on all chromosomes (except the XY in males). Incorporating this would require knowledge of the recombination profile and number of genes for each chromosome. It would make the above probability many, many orders of magnitude less likely. (Like, it's very possible there are more potential combinations of two parents' chromosomes than there are atoms in the universe.)

If this were to occur, I personally wouldn't call them twins. That term is consistently used to reference a single pregnancy, regardless of whether the children are genetically identical.

There is a one in 1/(0.5)^46 = 70 trillion chance of this happening in theory without accounting for recombination. However, there is a 6% chance of this happening when there are 4 chromosomes, which is applicable to real plant and animal species! With real human data, which takes into account recombination, hotspots, etc., there is a one in 4.771 * 10^39 chance of this happening. This is one in a 5 thousand billion billion billion billion chance, and only 100 billion humans have ever lived.
Extra information:
Theoretically, there is a one in 17.59 trillion chance of independent assortment happening so that the exact autosome combination is the same (0.5^44).
There are chromosomes A and B. Uppercase: from mom. Lowercase: from dad
Mother: A1 A2 B1 B2
Father: a1 a2 b1 b2
1st step: assort chromosome A. 4 options. (A1 a1, A2 a1, A1 a2, A2 a2)
2nd step: assort chromosome B. 4 options. (B1 b1, B2 b1, B1 b2, B2 b2)
Now, there are 16 options for the child for 2 chromosomes.
Imagine a pairwise matrix of these options; the top left to bottom right diagonal represents the pairs in which two children have the same chromosome combination. This is 16 children out of a total 16*16, or 0.0625 = ~6% chance of happening. This means this must happen regularly for some animal species! https://en.wikipedia.org/wiki/List_of_organisms_by_chromosome_count
If we increase the chromosome count to 22, there are 4 options for each chromosome, so there is a one in 1/(0.25)^22 or 1/(0.5)^44 or one in 17.59 trillion chance.
Different-sex siblings can never be 100% genetically identical.
For men, the Y-chromosome will always be the same and brothers will have a 1/2 chance of having the same X chromosome. For women, the X chromosome from the father will always be the same and there is a 1/2 chance of getting the same X chromosome from the mother. Since they have to be both the same sex (50% chance) and get the same X chromosome, this increases the odds by 4 to (1/(0.5)^44)*4 = 70 trillion. This is why the sex chromosome acts like an autosome.
For full siblings, there is an observed mean of 0.50146 relatedness with an SD of 0.03761 (from the supplementary table). To get this halfway to twins, we would need 0.25/0.03761 = 6.6471683063 SDs above the mean. This occurs, on average, once in (1 / (1 - norm.cdf(6.6471683063))) = 66,937,665,852 events. To go the rest of the way to full twins, we will need to be (1-0.50146)/0.03761 = 13.2555171497 SDs above the mean, which is one in 4.771 * 10^39 events!
Since about 100 billion humans have ever lived, and a “chance” half-twin half-sibling occurs once every 67 billion humans, this has probably happened before. Interestingly, this 75% genetically related sibling pair, derived from empirical data, has about the same probability of about 75% of the chromosomes happening to assort the same way.
More extra information:
Darlingtonia's answer is good. However, there is recombination, which makes it extremely more unlikely than it already is. The existence of inbreeding helps with this a bit, as sequences might be exactly the same between mother and father already.
Let's look at some data.
This paper used real allele frequencies to generate a relatedness distribution for full siblings.
https://academic.oup.com/beheco/article/20/2/410/219031
Another paper looked at relatedness of full siblings had has standard errors available.
https://academic.oup.com/beheco/article/29/2/468/4819097
But this isn't fine grained enough. Let's make a simulation. Also, let's assume the siblings will both be women or both be men. Since this only happens half the time, the real odds are halved. We will also ignore recombination hotspots, discussed here: http://adamauton.com/adam_auton_thesis.pdf
23*2 chromosomes. 1.6 recombinations per chromosome (we are ignoring variation between different chromosomes): https://book.bionumbers.org/what-is-the-rate-of-recombination/.
Length of the average chromosome: 6.3 Giga-base-pairs divided by 46 = 136,956,522. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391780/
136,956,522 base pairs make up each of the 46 chromosomes. Recombination happens 1.6 times on each chromosome.
137 base pairs make up each of the 46 chromosomes. Recombination happens 1.6 times on each chromosome. Allow two parents to produce 10 offspring in this way. Then, calculate the average relatedness coefficient between the children.
We could use the infinite allele model but adjusted for the baseline relatedness we’d expect due to chance, which, for four alleles, is 0.25. However, this would incorrectly classify genetic twins as only 75% related.
Therefore, we could use chunks. The length of shared chunks can be used to estimate genetic relatedness. We would also need to use SNPs, not total base pairs, as most base pairs will be the same for all mammals.
At this point, we are making way too many assumptions for this simulation estimate to be realistic.
Instead, let’s look at real data:
“IBD sharing between pairs of full siblings in the SAMAFS and Hemani20k data, which have mean IBD proportions of 0.501 and 0.502”
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007979
We want both homologous chromosomes in one individual to be identical by descent to make “twins.”
For full siblings, there is an observed mean of 0.50146 relatedness with an SD of 0.03761 (from the supplementary table). To get this halfway to twins, we would need 0.25/0.03761 = 6.6471683063 SDs above the mean. This occurs, on average, once in (1 / (1 - norm.cdf(6.6471683063))) = 66,937,665,852 events. To go the rest of the way to full twins, we will need to be (1-0.50146)/0.03761 = 13.2555171497 SDs above the mean, which is one in 4.771 * 10^39 events!
Since about 100 billion humans have ever lived, and a “chance” half-twin half-sibling occurs once every 67 billion humans, this has probably happened before.


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Human Eye Diagram: question about some dimensions
Does anyone know any of the answers to these questions about this human eye diagram:

What points should be the center of the circle for the radius numbers (Rn) in the following diagram?
The difference between the two values R1 and R2?

My suspicions: From what I can tell, Cornea R1 refers to the left side (front) of the Cornea measured from the right side (rear) of the Lens at its apex.  I'm not sure why R1 differs from R2.  Lens R1 values represent the lens between its changing diameter when it focuses (due to muscles) and is measured from the center of the largest circle of the eye in this picture.  Again, not sure how R1 differs from R1.  Retina is measured from the center of the largest circle of the eye in this picture.

ref: reference


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Can instincts disappear after a long period of non-usefulness?
I recently dived into the topic of instincts and now I have a question, where I haven't found anything about.
There's this thesis (I think mentioned here amongst others) that, through epigenetics, learned instincts can be passed along in genes and can over time be permanently integrated into the genome.
But...
Why is there no mentioning about how instincts can disappear over time, if they're simply not useful anymore? Or is it just not possible?

If its like any other genetic trait, there needs to be selective pressure for it to be counter-productive to be weeded out. Merely not being useful is not necessarily sufficient. though I suppose over extremely long periods of time it may get diluted out by mutation if it presents no beneficial or ill consequences.

@DKNguyen - That would make a good answer.

OP: The Russian fox farm experiment would give you a lot of information on the loss of instinctive behavior through selective pressure.

@anongoodnurse That's super interesting. I had no idea there was an experiment being run like that and with such definitive results showing themselves so quickly.

@DKNguyen - A solid example of your very on-point  answer. The back story of the experiment is also very interesting. :)

so basically how does the evolution of behavior work. simple question do you know  how tissues or organs are lost in evolution

@John what does that have to do with behavior?

Because behaviors are lost in the same way, it can take a long time to lose a an organ or tissue if it has no direct detriment. it is lost through drift.

oh, thanks. very interesting. I guess, I'll read into that somewhere soon

If it is like any other genetic trait, it will only be weeded out if there exists selective pressure that makes it counter-productive. Merely not being useful is not necessarily sufficient. Though I suppose over extremely long periods of time, it may get diluted out by mutation and propagation of those mutations if it persists in having no beneficial or detrimental effects.


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Why don't all cells have active telomerase?
If telomere degeneration plays a role in aging, and extending them is biologically possible with telomerase, why isn't it active in all cells? Humans use it in their germ cells, so why not all somatic cells too?

We don't want all body cells dividing indefinitely. When that happens we call it "cancer".
Telomeres are one of many ways to regulate cell division and prevent runaway growth in a last-ditch manner where a cell becomes non-viable after dividing too many times without telomeres. From Wikipedia:

With telomerase activation some types of cells and their offspring become immortal (bypass the Hayflick limit), thus avoiding cell death as long as the conditions for their duplication are met. Many cancer cells are considered 'immortal' because telomerase activity allows them to live much longer than any other somatic cell, which, combined with uncontrollable cell proliferation[46] is why they can form tumors. A good example of immortal cancer cells is HeLa cells, which have been used in laboratories as a model cell line since 1951.

and:

Telomerase activation has been observed in ~90% of all human tumors,[48] suggesting that the immortality conferred by telomerase plays a key role in cancer development. Of the tumors without TERT activation,[49] most employ a separate pathway to maintain telomere length termed Alternative Lengthening of Telomeres (ALT).[50] The exact mechanism behind telomere maintenance in the ALT pathway is unclear, but likely involves multiple recombination events at the telomere.


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What indoor plants or groups of plants are significant consumers of CO2?
I am experimenting with the goal to reduce CO2 ppm in a 4200 sqr ft (12 rooms) dwelling by either distributing more plants through the space, or using a hydroponic garden's air as a source in the dwelling for a CO2 filtering system.
Using plants that are high consumers of CO2 will provide ppm data measurements to influence which solution I take.
What plants or groups of plants should I consider?
Thank You!
Greg Messer

the type of plant might be less important than the growing conditions.

I would imagine there are other criteria that are equally as important as just CO2 consumption such how easy they are to grow and maintain and how much space they take up. And cost. I just used snake plants. Humans have pretty exhaustively gone through the list of what plants are suitable as houseplants.

What type of ventilation system is used in this dwelling? Is the CO2 mostly coming from the occupants, or are there combustion sources too?

Possibly one of the extremely fast growing aquatic plants such as Azolla might be an option. Plants in this genus are sometimes mentioned as carbon dioxide remediation mechanisms due to their extremely fast doubling times.
Anything else that shows high productivity (rate of carbon fixation/photosynthesis) might be an option. You would obviously need to tailor the environment to suit that high growth rate, as suggested by commenters.
I was surprised to read just now that plants apparently are (can be!) actually effective at indoor CO2 remediation. I had not thought that they were terribly effective. Though some of this is due to other associated organisms e.g. bacteria in potting soil.


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Current Fern Taxonomy
In our school, the manual exhibits an outdated taxonomy as expressed by my teacher. We're following the Kingdom Plantae, Division Pterophyta, then divided into three Orders:

Order Filicales
Order Ophogossum
Order Marattiales

However, I tried to look up what is the currently accepted taxonomy for ferns. What phylum is it under? Are its children taxa changed drastically? Does it still have a taxon dedicated to ferns only? What are also the morphological differences eyed in classifying these plants? These are some of the confusions I have. Thank you for answering :)


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Can genetic recombination occur between DNA viruses?
Single stranded RNA viruses like coronaviruses can recombine with each other. During the viral RNA replication, the viral polymerase can jump onto another template strand and result in a chimeric genomic RNA.

However, trying to extrapolate this model to DNA viruses will encounter a big problem. Most DNA viruses have double stranded genomes. The replication of dsDNA is semiconservative, which means the template (parent DNA) is also a part of the daughter DNA. Even if the DNA polymerase jumps in the halfway, the template DNA won’t move with it. Does that mean DNA viruses don’t recombine, or recombine in different ways?

Summary
Certainly DNA viruses do recombine — some of them encode proteins specifically for this purpose. And this is unsurprising if one reflects on the fact that recombination is a fundamental characteristic of double-stranded genomic DNA in prokaryotes and eukaryotes. What is surprising is that recombination occurs in RNA viruses — the starting point for the question. However the mechanism by which this can occur — apparently in a random manner — is completely different from the long established way in which double-stranded DNA genomes recombine.
Apologia
The literature on recombination is vast. For the purposes of an answer to this rather naive question, I think it sufficient to refer the reader to a Wikipedia article on recombination in general, and draw on a single review of recombination in DNA viruses.
Answer
Quoting from the aforementioned review by Weller and Sawitzke in Ann. Rev. Microbiology (2014) 68, pp 237–258:

“Homologous recombination plays many important roles in the biology of all living organisms including DNA replication and repair of DNA damage. Recombination is essential for genetic diversification required to enable organisms to adapt and evolve.“

The Wikipedia article deals first with ‘standard’ recombination in DNA genomes, which, although not identical in all situations, generally involves a double-strand break, pairing to a homologous region on another chromosome, and often ‘crossing-over” of the strands between the two chromosomes:

This is illustrated in more detail in the article, but one should emphasize that crossing-over involves an intermediate Holliday junction of four strands of DNA, as shown below for PDB file 1M6G.

The idea that single-stranded nucleic acid is a requirement for the process (as assumed by the poster) is false.
Recombination is catalysed/promoted  by specific proteins — recombinases — the most well-known being perhaps RecA in Escherichia coli and Rad5 in eukaryotes. Specific nucleases are also involved in making the strand breaks. What the review by Weller and Sawitzke focuses on is the evidence for similar recombination and recombinases (and nucleases) in DNA viruses as diverse as bacteriophage lambda and herpes simplex virus type 1. They examine the mechanism and identify the viral and host proteins involved and conclude that:

“Both bacteriophage λ and herpes simplex virus display high rates of recombination, both utilizing their own proteins and commandeering cellular proteins to promote recombination reactions.”


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Why using Fokl as an enzyme in the zinc finger nuclease method?
I started reading about CRISPR, and then about older methods of gene editing. I recently learnt about zinc finger nucleases, where Fokl (a restriction enzyme without specificity) gets specificity, thanks to the zinc finger domains, and can do one stranded breaks. So my question is, why do we need an enzyme which only cuts on one side of the DNA? Is there no other restriction enzyme which has no specificity and can cut on both sides of the DNA? I tried to research on my own, for example in papers, where the zinc finger nucleases method is described like in “Genome Engineering With Zinc-Finger Nucleases”, but I didn’t find the answer to this question.

In short, yes, there are restriction enzymes that induce double stranded breaks. In fact, unmodified FokI is a  restriction endonuclease (indicating it creates double-stranded breaks) ¹. Modified domains of FokI can turn it into a nickase (single-stranded breaks) ².
The reason these nicks are desired is because the repair of single-stranded breaks (SSBs) promotes different DNA repair pathways, I quote ²:

"Here, we demonstrate that site-specific DNA-nicking enzymes (nickases)—constructed by engineering the FokI nuclease domain of ZFNs—can induce SSBs in the genome, whose repair via highly accurate HR gives rise to targeted genome modifications. Importantly, SSBs are not repaired by error-prone NHEJ, and, therefore, do not give rise to indels at both on-target and off-target sites. Thus, SSB-inducing zinc finger (ZF) nickases could serve as highly specific mutagens with no or little off-target effects."

Nicks can be repaired via the less error-prone Homology Directed Repair (HDR) pathway. It is important to note that (in humans) the HDR pathway may be different between double- and single-stranded breaks ³.

https://www.neb.com/en-gb/products/r0109-foki#Product%20Information | 2024/02/12
Kim, Eunji, et al. "Precision genome engineering with programmable DNA-nicking enzymes." Genome research 22.7 (2012): 1327-1333.
Davis, Luther, and Nancy Maizels. "Homology-directed repair of DNA nicks via pathways distinct from canonical double-strand break repair." Proceedings of the National Academy of Sciences 111.10 (2014): E924-E932.


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Will “ground hornets” come back to the same place after winter?
We recently moved into a new house and when we mowed the yard we were being stung by these huge hornets. We couldn’t find anyone to remove them and I am terrified they are going to come back this year. They are in the ground and are about 1-2 inches long and chunky. They also come out at night when we are trying to sit on the patio. I need some advice. If they will be there this year, what can I do to rid of them.

Welcome to the Biology Stack Exchange. Please take a [tour] and visit the [help] page for more information on this site and how it works. There are quite a few different wasp/hornet species world-wide and this question will probably need an ID to be able to answer properly. If you can, can you please edit in a picture of the insects in question and a location in the world - something like your nearest major city and/or state and country usually works well.

Yes, they are likely to return to the same zone and garden if it is a good habitat for them.
Knowledge of them will protect you, and give you confidence that you can reclaim your garden.
1/ research dissuasion of ground hornets.
2/ put together some protective clothing, in case you have to spray a biocontrol agent or another deterrent. I don't know what your budget is, but you could get by with a hat protected by netting, from some instructions online, and some gloves, they won't swarm you in great hives.
3/ Invest in a lot of diligent research, to know what month they start burrowing, what day temperature they prefer to wake up to, how to protect yourself physically if you have to approach an active nesting hornet, if it's ok to keep a good long-handle net near the porch and intercept them when they venture too close in the evening. Read stories of others who have had the same adventure.
I am an experienced zoologist I have been stung by wasps many times, and fortunately not a hornet.
I climbed a tree with 20 in nest just above me and climbed down again, and many other encounters.
The biggest danger is that a wasp or bee falls in a cola when someone is briefly distracted.
Folk should know to be conscious of not mouth-breathing when running near them, and what to do if your friend is stung inside the throat on a hike far from help and breathing becomes difficult.
With this knowledge, I am became confident to let wasps and bees forage and walk on my hands and face which can be annoying after a minute or if they insist on foraging over an eyelid or a nostril, however it is better than startling them, I know how to tell the difference between more and less aggressive lookalikes based on their flying patterns, leg length in flight and other markers, It's a good thing to teach children. I became confident to stay very calm near a hornet nest and try to avoid it, to immediately suck a wasp sting and very fast put cola, or vinegar is better, on a sting, to greatly diminish its effect, and run fast if a nest is disturbed so they go into an aggressive mode.
Good luck.


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How do organs grow to the exact shape and size?
We all know that organs begin to grow in a foetus around three weeks after fertilization. But how does the body know exactly which shape and size the various organs need to grow to?

I think this is too broad; you're talking about a whole field of biology ("development") that would be taught across multiple university courses, and the answer won't be quite the same for each organ and can be answered at multiple levels of analysis (e.g., at a systems/overview level, down to individual regulatory genes and products).

"Organogenesis" might help you in your research. It appears "signalling" is key, but not the only factor.

other search terms that may help are "developmental biology" Hox genes" "intrinsic regulatory mechanism" and "feedback mechanism" here is an article to start with. https://www.frontiersin.org/articles/10.3389/fcell.2021.820391/full

The other answers are good. The other part of this answer is that we don't exactly know how it happens in all cases, but we have a lot of knowledge of what influences it.

Thank you @BigMistake!

Thank you @BryanKrause!

Thank you @DKNguyen!

Thank you @John!


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Help identifying this fossil
Found near alexandria mn

enter image description here

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Pictures of the ends and sides would be helpful. Standard practice for photos like this would be to take them with the tape measure off to one side so that you don't obscure relevant details. Beside MN (Monaco? Mongolia? Myanmar? Montana?), what sort of rock did you find it in? Are you sure it is a fossil and not a random concretion?

It was in a bunch of random rock and black dirt and minnesota i will get more pictures it is def not concrete though

Ah - concretion is a type of rock caused by minerals joining particles of sand etc together. They can form some pretty odd shapes.


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Use of ADP hydrolysis for driving energy-requiring processes?
The free energy of the hydrolysis of the β-γ phosphoanhydride bond of ATP is used to drive energy-requiring biological process such as chemical synthesis, movement, ion transport and production of light.
However the chemical structure of the α-β phosphoanhydride bond of ADP appears very similar, but I am unaware of instances where its free energy of hydrolysis is used in a similar way. Is this theoretically possible, and are there any actual examples?

I have edited your question as the term "potential energy" is not generally used in relation to biochemical reactions, the expression "used for energy" is imprecise, and the title poses as different question to the body of your question.: ADP can be used for other purposes (as a regulatory molecule, for example) besides driving energy-requiring reaction, but it appears that it is the latter that you are asking about.

It is theoretically possible

The structures of ATP and ADP are shown above, with the phosphate groups designated α, β and γ. The value of the Gibbs standard free energy of hydrolysis of the α–β phosphoanhydride bond of ADP is similar to that of the β–γ phosphoanhydride bond of ATP at approx. 30 kJ per mol. Hence it is theoretically possible to couple the hydrolysis of the α–β phosphoanhydride bond of ADP to an energy-requiring process and produce an overall negative ΔG.(The reader may wish to consult an external source — e.g. this previous SE Biology answer — if unfamiliar with a chemical account of the popular but imprecise idea of ATP as a “source of energy”.)
The hydrolysis of the analogous bond of ATP is so used
Most reactions and processes for which ATP provides the driving free energy change involve the hydrolysis of the β–γ phosphoanhydride bond in the reaction:
ATP → ADP + Pi
However in several synthetic processes the energy is provided from the hydrolysis of the α–β phosphoanhydride bond in the reaction:
ATP → AMP + PPi
These include RNA synthesis (to form a phosphodiester bond) and amino-acyl tRNA synthesis (to form the aminoacyl bond, which itself provides the energy to drive peptide bond formation).
Examples of ADP hydrolysis driving energy-requiring reactions?
Although this may merely reflect my ignorance, I know of no reactions of the sort:
ADP → AMP + Pi
where the energy of hydrolysis is used to form a chemical bond etc.
So, although I may be proved wrong, my answer is NO. But…
…a possible exception — not producing inorganic phosphate — is the adenylate kinase reaction, for which the overall standard free energy change is near zero:
2 ADP ⇔ ATP + AMP
This could be considered as using the energy of hydrolysis of the α–β phosphoanhydride of one of the molecules of ADP to form the β–γ phosphoanhydride bond of ATP. This is thought to be important in the regulation of glycolysis, the AMP produced serving as a signal for the requirement of energy and acting as an activator of the enzyme phosphofructokinase.
Why — or why not?
“Why” questions are dangerous in biology, as there is a tendency to argue that the way things are are the way they must be; and there are generally no tests of hypotheses in support of such a view. Nor did the original poster ask why. But with the strict understanding that what follows is just speculation, I offer these thoughts in support of my generally negative answer:

I have argued previously that an NTP (ATP — perhaps by chance)
developed as the “universal energy currency” because it was already
involved in RNA synthesis in the hypothetical RNA world. Clearly this
requires hydrolysis of the α–β phosphoanhydride bond of a nucleoside
phosphate molecule. The argument for ATP over ADP would be that the
pyrophosphate produced in the former process is further hydrolysed to
inorganic phosphate by pyrophosphates, and the irreversibility of the
reaction (heat is produced) is important to prevent RNA synthesis
reversing. As NTPs had to be synthesized anyway, they could also be
used for other purposes, but it was energetically more efficient to
hydrolyse the β–γ phosphoanhydride bond if irreversibility was not
crucial (e.g. the product removed).
Once ATP became fixed as the energy currency, metabolism was tuned
for its production and, later regulation. Thus the development of
systems for anaerobic and aerobic synthesis of ADP would not have
conferred any advantage on an organism. When regulatory systems
developed in involving the relative concentrations of ATP, ADP and
AMP (as mentioned above), using ADP to drive reactions would have
been disruptive.


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What is the unit for the vertical axis in multicomponent plot of qPCR

This is a typical multicomponent plot for a multiplex qPCR. Does anybody know the unit for the vertical axis representing the fluorescence?


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Could multiplexed CRISPR disable the mitotic and meiotic genes of cancerous cells?
Although I believe there is a good reason -- or reasons -- why this theory, that CRISPR could disable the genes for division in cancerous cells, is incorrect, I haven't been able to find them.
In short, the theory is that multiplexed CRISPR could knock out the genes responsible for cellular division (mitotic and meiotic genes) and thereby prevent the uncontrolled division of the cancer cells.
I understand that off-site edits, multiple mitotic and meiotic pathways, and the resiliency of cancer are difficulties, but in theory the idea makes sense.
Obviously, if the theory would work, probably someone would have done it already, so there must be a good reason why this won't work. Please could someone explain it to me? Please let me express my gratitude for your consideration in advance!

As with all cancer therapeutics one of the biggest problems is how you get the therapeutic to kill cancer cells without also killing so many healthy cells that the therapy kills the patient.
For CRISPR to work you have to get the CRISPR components into the target cells. Right now this is done using relatively harmless viruses like adenoviruses. The viruses "smuggle" the CRISPR components into the cells as they infect them. Nanoparticle containers are being researched as an alternative to viruses. The problem with your proposed therapy is that there is no way to target the viruses only at the cancer cells. You'd end up shutting down the cell division genes in healthy tissues too. Turning off cell division of a bunch of your healthy tissues is likely to kill you. There is also no way to ensure that all of the cancer cells would pick up the CRISPR components. You leave a few cells behind and the cancer quickly comes back.
Currently the most promising CRISPR cancer therapies are aimed at enhancing immune therapies. You take blood/bone marrow from the patient, sort out the immune T-cells, edit their genome using CRISPR to enhance their ability to identify and kill cancer cells, then inject them back into the patient. The result is hopefully a robust, ongoing immune attack on the cancer cells.

Thanks for the clear and detailed answer, Charles!

@ColinPace do not forget to upvote answer and accept it - if you like it.

@AlexanderChervov thank you for the note about etiquette. I believe I have already accepted the answer (clicking the green check mark), and I tried to upvote the answer, but I do not yet have enough experience points.

Bezeljak (2022) discusses recent advances in targeting cancerous cells with viral vectors: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884858/


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Why do wasps have "wasp waists"? What's been optimized?
I photographed these (unidentified) wasps on a sunny but cool winter day in northern Taiwan because they were conspicuously hanging out on a hand railing and had much lighter coloring than I'd ever seen before.
But after I took the time to look at a close-up I realized "Wow, they really have long, very thin waists!" Mechanically, it looks like they are two large masses connected by a very long thin beam, which must have quite a tiny canal in the center to let all the "juices" flow through.
While other insects and spiders may have segments separated by a tiny connection, this one is both small in diameter and quite long.
Why? Does this specific configuration provide some benefits to them?

 click for full size

companion question: What are the three dots (eyes?) on the top of this wasp's head? What species might it be?

Note that mechanically, the required slenderness ratio of a self-supporting beam is inversely proportional to scale. So this feature is much less costly for insects than it seems to be from macro photos.

@Therac agreed for sure - but... why? The reason I mentioned that it looks like two masses connected by a beam (and with wings attached to one of them) is that I wondered if this configuration has some mechanical advantage - perhaps during flight. As you suggest, it can be small in diameter and still plenty strong for the job, but I also wonder why it's so... long.

Why do humans have such a flexible shoulder?  Our ancestors relied on throwing things so the ones who could throw things better did better.  What is the wasp's equivalent weapon?  The stinger.  Wasps have such thin "waists" to facilitate maneuverability of the stinger.  This is especially important in wasps because for many, and for the ancestors who first evolved this feature, a flexible thorax with an ovipositor capable of depositing eggs into grubs and caterpillars was fundamental to their reproduction.  The path to their current form seems to have been as follows:  1) early stingless wasps develop an ovipositor and begin implanting their eggs into other insects, 2) the thorax evolves to be thin and flexible to facilitate this method of reproduction, 3) the ovipositor modifies into a stinger and, combined with that flexible thorax, the wasp becomes the Zorro of the skies.
See New Scientist's 20 November 2019 Hourglass figure: Why do wasps have such narrow waists?

I had also thought about that, but for the specific types I wonder whether it could also have aerodynamic reasons (in terms of efficiency and balance).

The ovipositor argument sounds (to me) like special pleading.  While the wasp-waist may make ovipositoring somewhat more efficient it seems unlikely that this is of such major selection advantage to drive such a change in so many wasp variants. || Stinging flexibility as suggested by one respondent in your link sounds more likely. But even that seems an unlikely selection driver.

@RussellMcMahon hmm... we have to remember that the stinger is a modified ovipositor, so only females can sting or "oviposit". In Sexing a Black & Yellow Mud Dauber Wasp "abdomen (A) to petiole (B) length ratio (A/B) - (male = 0.6 to 1.3, female = 1.5 to 1.9)" the abdomen is significantly longer for females. That's one species only, and I don't know if males have different aerodynamic requirements...


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What are the three dots (eyes?) on the top of this wasp's head? What species might it be?
I photographed these (unidentified) wasps on a sunny but cool winter day in northern Taiwan because they were conspicuously hanging out on a hand railing and had much lighter coloring than I'd ever seen before.
But after I took the time to look at a close-up I realized "Wow, this wasp has three dots on the top of it's head!"
If it was a spider I'd assume they were eyes, but like many insects these wasps already have to large wrap-around eyes that extend towards the top of the head already?
Question: What are the three dots (eyes?) on the top of this wasp's head?

 click for full size

companion question: Why do wasps have "wasp waists"? What's been optimized?

This is like the mud dauber wasp

I don't know what species this is but a lot of bees and wasps have those three dots on their head.  They are sort of eyes, but they can't actually make out images.  They basically just detect light above the wasp's head.  By having three there in a triangular configuration, the wasp can determine the direction of any shadow that appears overhead, like a bird swooping down for a snack.

University of Houston - What Bees See
Wikipedia: Simple eye in invertebrates; Dorsal ocelli

Neat. We often forget as mammals with a paltry two eyes that in other creatures, different eyes may have different purposes and be more highly specialized.

If I recall, these might be horizon sensors or sky polarization compasses.


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Bruhathkayosaurus matleyi current status and size estimates
https://www.youtube.com/watch?v=BqVqW9A-6eo
I watched this YouTube video about Bruhathkayosaurus matleyi and he basically makes three interesting assertions:

The illium used to define Bruhathkayosaurus matleyi was not of a sauropod but of a 9 meters abeliosaurid.
The huge femur (incorrectly) assigned to Bruhathkayosaurus matleyi is indeed a huge sauropod but needs to be defined as a new genus (the author suggests "Fangorn").
The size estimations coming from the huge femur now lost are valid and suggest a 110-170 metric tonnes animal of length 38-48 meters.

The video is based on a 2023 paper by Gregory S. Paul, a free-lance paleontologist and paleoartist whose hypotheses are often disputed (especially in taxonomy) and are not mainstream.
I ask if these three assertions are accepted by the scientific community? what is the status of the giant sauropod formerly referred to Bruhathkayosaurus matleyi and whether is it a valid species? And I ask if the size estimates are widely accepted, making it the largest dinosaur?


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species that alerts predators in order to mate
I read once about a species of animal that engages in, and please forgive me for the terminology but I cannot for the life of me think of any other way to describe it, mutually-assured destructive sexual blackmail.
If a male attempts to mate with a female, and the female shows signs that she is going to reject the male's advance, the male will start making a loud call that will attract this species' common predator.
Essentially, the male is threatening the female that they will both get eaten if she doesn't accept his advance.
I can't remember what the name of this species was and I really do not like what it's doing to my search history.
What species, if any, engage in this type of behavior?
What terminology should one use to describe this behavior?
I tried asking ChatGPT first (less judgmental) but came up empty.
There's a species of orb-weaving spider that will mimic the web vibrations of prey struggling to get free when a female seems likely to reject his advance, in the hopes that the female will accept the male's advances in order to avoid being mistakenly identified as prey.
There's the vampire jumping spider, which risks predation during courtship displays.
Neither of those quite fits the pattern I'm thinking of, where the male exposes both himself and his potential mate to predation.
If you downvote this question, I... completely understand.

A similar phenomenon occurs in begging nestling birds: https://www.nature.com/articles/nature.2013.12774

I finally found an answer, probably after getting put on some kind of watch list:
water striders.
If the female looks like she's going to reject the male, the male will tap on the water surface to attract fish.
The female, being closer to the water, is more likely to be eaten.

Excellent answer, what a memorable phenomenon. Not sure, but for the term for this you might try [english.se], with the tag [single-word-requests].


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Spider ID: What is this?
This crawled on my husband. It didn’t bite him, he was able to swat it away so that’s why it looks a little messed up. I honestly just want to know if this is poisonous. We live in AZ, Goodyear area and there’s usually only regular house spiders running around. There were no marking on the abdomen or thorax, the legs seem 2 toned but I couldn’t get a good look. It wasn’t more than an inch big but it has a thicker build.
enter image description here

This looks to me like a female of the common and harmless Southern House Spider, Kukulcania hibernalis (see below).
https://bugguide.net/node/view/508965

Yes, nice match.


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What is the mechanism by which an animal has behavioral instincts?
I understand (at a layman's level) how evolution and natural selection work in regards to anatomy.  The offspring has a slight mutation that makes it a better survivor in some way -- faster, stronger, more agile, better camouflage, more efficient respiration, whatever.
But I have no idea how instinctual behavior is developed and/or transferred.
Observing my house cats, I can see that they have all kids of instincts for hunting, fighting, playing, grooming, etc etc.
Where did these instincts come from?  Animals (including humans) are born already knowing a lot of things, right?  That's what "instinct" means.
How does that work?  Do we even know?

Instincts are formed the same way anatomical attributes do: genetically. The nervous system has developed instincts (or reflexes, if it helps you to understand them better) through millions of years of selection; those individuals with beneficial instincts had a better chance of survival to reproductive age.

@anongoodnurse So instincts are also anatomical differences, localized in the nervous system?  And organisms with "bad instincts" died out?

I believe so, yes. Instincts can mean different things to different people, so there's room for debate. They can be said to be genetically coded for neurologically, though they can also be altered by the environment. A neuroscientist might argue that there is no one satisfactory explanation for instincts, but that we are born with many of them is irrefutable. Dogs bred over time to hunt and kill small animals (e.g. vermin) will have a very high prey drive whereas those bred solely for companionship may have a very low prey drive.

This site has a policy of the OP showing evidence of research (e.g. links to an article and a quote) in an attempt to answer the question; if you [edit] your post to include some, you may get a much better answer than mine. I think it's a very interesting question.


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How to calculate df in the chi-square test of Hardy-Weinberg equilibrium?
We often use df=1 in Hardy-Weinberg equilibrium when there are only two alleles. Some people say that it's because we've used the frequency of two alleles when calculating the expectated values, while others may give different explanations.
The website for the second explanation:https://www.mun.ca/biology/scarr/4250_Chi-Square_HWP.html
The principle is that, if you know you looked at n experimental results that could have fallen into any of three categories a b c, the value of the first category a can be anything (up to n), and the value of the second category b can be anything up to (n-a). Having determined a and b, the third value is now pre-determined: c = (n - a - b). So, only two of the three values are free to vary. For diploid genotypic data with two alleles A & G and three genotypes AA, AG, & GG, this would suggest df = 2 in the observed data. However, given f(A), the expected frequencies for all three genotypes are automatically determined, thus there is only one degree of freedom.
This affects how to calculate df when there are more than 2 alleles. The first answer is df=3, which is from the Hartl's textbook, but unfortunately it's in the afterclass questions, and it doesn't have an answer, so I don't know why. The second one gives df=2. I found another article (in a chinese website) which says that df=m*(m-1)/2 (m is the number of alleles). Which one is right, or which one is commonly used?
Now I believe that my question is solved, so I won't open this question.

It would be helpful to have links to the sources that you have found so far, particularly so for the long quote.

You'll need to at least explain what the first method is and how it results in df=3.

After the latest edits I'm still not clear what the first explanation leading to df=3 is. If the explanation is that for 2 alleles there is 1 "free" parameter to vary because if you know p or q you can derive the other as 1-p or 1-q, therefore 1 DF, then for 3 alleles you would still get 2 DF: if p+q+m = 1, you have 2 DF because you only need two of the three to calculate the third. That's the same as the second explanation, and really it's the same explanation, too. Where did you get 3 DF from for 3 alleles? You must explain this even if the original is in Chinese.

(closing for now, because even as a good question, without this piece of clarity it would be inappropriate for someone to answer your question)

@BryanKrause I agree with you on df=2. 3 DF is from the afterclass question in Hartl's textbook. It just asks "In the situation with 3 alleles, the df should be 3. Explain why." And it's with an odd number, while the textbook only gives answers for questions with even number, so I really don't know the reason. Maybe it's just wrong.

@Planarian Ah, now I understand. Yeah, if there is no explanation and just a textbook question I'd just as soon assume a typo. You could see if your library has an instructors edition that includes odd solutions.

Better yet, what does the textbook actually say about degrees of freedom for this test? It's unusual for a textbook to come with a question on material that isn't covered...


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Number of regulators required for specify the total state of genes
My course notes make the following claim:
If the regulation of each gene could include all transcription regulators
available, then in principle the total state of all genes could be specified with only $log_2(N)$ regulators.
It then gives this explanation:
To see this, imagine that one had 10 regulators that can be on or off. Then one can, in principle, specify $2^{10}$
different states, and thus specify all possible states for up to N = $2^{10}$ genes.
I don't understand the explanation given. For n genes, each of which can be turned on or off, there should be $2^{n}$ states. This would then mean N regulators would be required to regulate N genes.
Could anyone explain why this is incorrect?

Not sure what this means. what does "total state of all genes could be specified" mean? "Specified" like once we observe log2(N) regulators as on/off we can make a good guess about the state of any given gene, or we can make a statement about some overall state of the network, or something? Or like if we were god we could completely control the network by turning on/off only log2(N) regulators? What is "total state"?

@MaximilianPress I think it means that all the possible states for N genes could be specified using log2(N) regulators.

Have you asked your course instructor?

@jore1 I'm still not sure what a state is, or what it means for regulators to specify states for genes. In what context? why? I suspect that this is a description of a mathematical/graphical model of gene regulation, but the terms and structure of the model are not specified in your question, so it's hard for me to evaluate standalone statements about the behavior of the model.


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Pupae in sheoak tree
Can you identify this pupa? We found it when trimming our sheoak. It had bored into the wood. We are at Cape Jervis in South Australia.


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Are all animals “information seeking”?
I read on Britannica that all animals down to microorganisms are "information seeking", but there was no source to back up the claim.

One way to begin exploring curiosity is to understand ‘information seeking’. This behavior is observable across the entire animal kingdom – from apes and dolphins all the way down to crabs and tiny nematode worms. ‘Information seeking’ means that every animal seeks information about their environment. This is so they know how to navigate it. In fact, it’s why sensory organs exist – to supply the brain with information that helps you understand your environment and make better choices.

Are there any sources or facts to support these claims?

What are you doing right now? (Information seeking.) All animals, even the smallest "micro"organisms, at a minimum seek conditions conducive to life. That requires information seeking.

This might be a better question for the Philosophy stack.

The answer is going to entirely depend on how you define "information seeking". How do you choose to define it?

@BryanKrause. Britannica says “every animal seeks information about their environment”

@anongoodnurse Where is your evidence?

Try slime-molds - an article regarding how they sense their environment and respond to it. It's a general assumption of any organism that moves or can act in any way, it's been observed and studied at all levels of size and complexity. In a world where it's eat or be eaten, it's more likely to lead to a successful life passing on genes to offspring if you can tell your food from a predator.

As @BryanKrause stated, how you define "information seeking" matters. If you define it as intellectual curiosity, the claim is preposterous. If you define it as movement towards conditions necessary for life, then the claim is true. The burden of proof is not mine in a comment. Have you done any searches in an attempt to answer the question? Please show us, as it's strongly recommended on this site (see the [tour]). And define your terms. Thanks.

@Aruralreader - I doubt the the OP is asking about knowledge, truth, ethics, or the meaning of life. I might be entirely wrong, though.

@anongoodnurse I updated the post with edits someone recommended, and the original source and definition are there. Also, how would say a jellyfish be information seeking?

For jellyfish, see rhopalium. But you really should try to look these things up for yourself before asking, it's a requirement here to show your research when posting, and comments aren't for the purpose of answering supplementary questions or starting discussions, just for offering guidance to new users  as to how to use the site and suggesting improvements to the original post.

The answer is going to entirely depend on how you define "information seeking". How do you choose to define it? If Britannica does not define what they mean by "information seeking" then that statement is not useful by itself. It's common to encounter these sorts of statements in writing targeted to a non-specialist audience. They are not meant to be taken quite so literally, they're designed to get your mind working and exploring to help you interpret the next things they're going to say. So, let's look at what else they say:

This is so they know how to navigate it.

Not all animals even move, so for this to make sense for "all animals" it must be a pretty broad meaning of "navigate" to be true.

In fact, it’s why sensory organs exist – to supply the brain with information that helps you understand your environment and make better choices.

Every animal has some ability to sense the outside world; I'd argue that even every plant and single-celled organism does as well, this is an absolute requirement for life.

to supply the brain with information

Well, we're back to more specific then, many animal species do not have brains. Sponges, for one; cnidarians also, though they do have a nervous system they're not typically thought of as having a brain.
So, it seems that all Britannica means by "information seeking" is "somehow collect information from the outside world". That's not a very strong statement since "collecting information" can mean almost anything. But, it's also not the sort of thing anyone can prove: there could always be some hypothetical life out there that doesn't collect information but it's not anything we've found.

I thought that mobility at some life stage was one of the primary characteristics of the animal kingdom, and that they must be eukaryotes. Many bacteria are non-motile, and they are prokaryotes. However, bacteria do reproduce under the right conditions, but does this involve "information"? Is it possible to react without "information"? Yeast doesn't move towards sugars. It does metabolize (react) sugar, though.

@anongoodnurse Only as juveniles/gametes. The source quote specified animals but bacteria certainly process information about the outside world, even as simple as regulating enzymatic pathways in response to different food sources. My point is really that one can bicker indefinitely about what "counts" or not but it doesn't really provide any additional knowledge or understanding to do so.

The world “seek” is the problem in my book. For me it implies conscious volition, which would differentiate it from merely *receiving” signals from the environment. The poster could do worse than investigate the history of the usage of the word, perhaps by inflicting himself on SE English Language and Usage.

@David Yes, though a closer read of the original source does not make it seem that "conscious volition" is part of the claim being made; I'd consider the use of the word "seek" to be anthropomorphizing that is not really necessary.

@anongoodnurse Part of the problem is that "animals" is a pretty vague definition to begin with. In any case, I agree with this answer in that "information seeking" is a useless classification even if exists, especially in light of the fact seeing as how many other things also "take in, information".

@David - The entry does discuss curiosity, but the quote the OP refers to is sensory info: "‘Information seeking’ means that every animal seeks information about their environment. This is so they know how to navigate it. In fact, it’s why sensory organs exist – to supply the brain with information that helps you understand your environment and make better choices." Although then "choices" becomes a problem...

@DKNguyen - It's not that vague. Nine reasonably reliable sites out of 10 will define it exactly the same way.

@anongoodnurse I've never heard of motility as a requirement, and it seems a rather arbitrary one at that when some things border so close to being immobile.

@DKNguyen - I haven't read one yet that didn't mention motility, even so far as making the case for corals (stationary) as animals. Sponges, though, have been described as "sluggish". Heh. But they do have a motile larval form.

@BryanKrause so all animals have the ability to sense the outside world and respond according to their biological composition is a certain fact

@HasanZaeem To the extent that I can't comprehend any possible counterexample, yes, but what is it that you can do with that information? It doesn't seem very useful to me. Better to understand how organisms function specifically rather than aiming for such generalities. Biology isn't physics.

@anongoodnurse — Yes, the question is very much one of semantics, which  is why I don't think the question admits a biological answer. However in a philosophical answer I would say that if one classes a simple bacterial response to environment as "seeking information" then the same is true for the response of a plant to light or gravity. Would one really be prepared to say that plants seek information?