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Is the quiescent centre only found in monocot roots?
I read that the quiescent centre is present between the dermatogen and calyptrogen. As calyptrogen is only present in monocot root, does that mean quiescent centre is only found in monocot roots?

I don't know the answer specifically but unlike the dicot roots the monocots donot show secondary growth in case their roots suffer injuries. So even if the quiescent centre be present in the dicots it makes more relevance in the monocots...

that's a very valid point, thanks for the answer!

Note that quiescent centers are typically defined by cell division activity not anatomical placement and are not confined to monocots.
For example, this paper discusses the quiescent center in Arabidopsis roots1.

Reference:
1: Doerner, P. (1998). Root development: quiescent center not so mute after all. Current Biology, 8(2), R42-R44.

Thanks for the article! I found it very informative.

You're very welcome!


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Identify this wild plant with brilliant scarlet red flowers
Location is Virginia, USA
They seem to last all summer

Possibly a species of Monarda?  AKA bee balm... https://www.wildflower.org/plants/result.php?id_plant=MODI

It looks like some kind of Lobelia. A close up of the flower itself would be very helpful.
I believe it is a Cardinal Flower:

This 1-6 ft. perennial has showy, red flowers in 8 in., terminal spikes. Each flower has three spreading lower petals and two upper petals, all united into a tube at the base. Erect leafy stems, often in clusters, with racemes of flowers resembling flaming red spires. The lower portion of the erect stem is lined with lance-shaped leaves.

That's it!  Thank you.

source: Stack Exchange

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

sort: votes


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Why don’t plant cells need centrioles?
I’ve just learned about cell division and I noted that plant cells don’t have centrioles but still undergo cell division. I’ve read a few documents about it and wondered why plant cells don't have centrioles.
How is it that plant cells can divide without centrioles?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done some research on your own before asking questions here — a quick search turns up this: https://biology.stackexchange.com/questions/10210/how-do-plant-cell-divide-without-centrioles ——— Please also take the time to take the tour and then the help pages starting with How to Ask questions on this site. Thanks!

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


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How much does capillary action contribute to blood flow to the human brain?
The BBC News Universal Wonders short video Why water is one of the weirdest things in the universe says after 01:50:

Water molecules can float upwards against the force of gravity. That’s because they love to stick to each other. They’re so good at it that they can actually pull each other up through tiny channels, such as the tiny blood vessels in your body. That’s how oxygen and nutrients reach the edges of your brain.
The same process, called capillary action, allows plants to move water from deep below the ground to nourish the leaves and branches that grow in the sunshine.

We learn about the importance of capillary action in water transport in plants, but I'd never heard that it was important for blood transport in Humans.
Question: How much does capillary action contribute to maintaining blood flow to the human brain? Is it a small effect compared to the difference between arterial and venous blood pressures, is it a substantial contributor?

None. I have no idea what that video is talking about.
Capillary action of water happens when you have a thin tube and water likes to stick to the "edges." Blood vessels are already full of water, there is nothing for them to capillary up against: there is already water there, so there is no surface tension (there is no surface at all). Blood flow through capillaries is caused by the heart which creates a pressure gradient between the arterial and venous circulation, in the brain and everywhere else.

Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2009. Chapter 2, Anatomy and Ultrastructure. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53086/

Capillaries are very fine vessels that exist everywhere blood is distributed to tissues including the brain, and capillary action is a physical phenomenon of fine spaces that absorb liquids allowing anti-gravity pull of water on top of trees.
Same word, but unrelated objects here. Both come from the same Latin origin meaning hair. Capillary action is not the way capillaries work (blood is pushed in because of pressure).

While "Capillary action is not the way capillaries work (blood is pushed in because of pressure)" sounds like a common-sense statement, can you actually support it somehow? Can you exclude any influence of capillary action in addition to the effect of blood pressure? Good Stack Exchange answers need good supporting links or references. Thanks!

You are welcome. Look up capillary action definition and tell me how it could possibly take place in vessels with varying diameter already filled with blood, having no equivalent of evaporation or other depressurization at the other end you find on a tree leaves besides blood lower pressure. And importantly, there is almost no attraction between the walls and blood. Unless you are talking about a non physiological situation where you dry up a piece of brain and then puts it in a water bed to get it wet, I have no idea how you can mix up those two different concepts in the first place.

It's not my place to tell you how something could possibly happen. This is Stack Exchange and an answer should try to support assertions whenever possible. Rather than tell me to look up something for you, it's more appropriate for you to find something suitable and cite it or quote from it. Concepts and phenomenon are not exclusive, two or more can apply simultaneously with different weights. Thus my question begins: "How much..." If you are certain it is zero, then you should state zero, support that, and let people vote on your assertion.


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Single-cell ATAC seq arrays
As part of a data analysis project, I encountered two kinds of single-cell assays
for transposase-accessible chromatin using sequencing (single-cell ATAC seq) methods. The first uses combinatorial indexing (also called sci-ATAC seq  [link]), whereas the other counts the number of Tn5 cuts in peaks (called sc-ATAC seq  [link]). I'm not a trained cell biologist or biotechnologist so I am possibly overlooking subtle similarities between the two methods here.
To my knowledge, sci-ATAC seq generates a binarised array, whereas sc-ATAC seq generates a counts matrix. (I'm also aware that there are post-processing tricks to convert binarised arrays to other array types, eg, normalised counts arrays.)
My question is, what about combinatorial indexing results in the array being binary rather than integer-valued? I'm looking for an explanation that relates the data collection method and combinatorial indexing with the resulting array type.
Thanks in advance!


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Leaf formation on unknown tree: cocoon or something else?
A small tree in my yard has leaves which appears to double over themselves. The first two pictures show this phenomena, and the third is the same tree to maybe aid identification.

I can't absolutely guarantee when this first appeared, but I believe it was this growing season, and I know it's been there at least a month (unless it's reoccurring, I am not tracking the individual leaves).
My first thought is cocoons or some other insect behavior. Can anyone tell me what it is?
(What kind of tree it is will also be valuable, in case we can't find the answer to the leaf question here)
EDIT: Location is outside Boston, MA (USA).

Looks like a filbert (hazelnut) but I'm not certain of species...your location might help a bit and should always be included for species-identification questions. A picture of the full tree might help, too, I believe the "bushiness" of a filbert might help identification. Your "cocoons" are full of immature nuts at the moment.

@BryanKrause: Added location, outside Boston.

What a blast from the past! I used to pick wild hazelnuts when I was a child. The wild ones were covered with sharp spiny projections, but the nuts were worth it. Lucky you!

Based on the location and assuming this isn't a domesticated hazelnut there are two likely hazelnut species.  The lack of the distinctive "beak" seen on the Beaked hazelnut means this is most likely an American hazelnut (Corylus americana):

The hairs along the young branch are also consistent with this (see for example the Plant Guide from the USDA).
Note, however, there are hybrids between American and European hazelnuts so it is beyond my ability to be completely sure by visual inspection alone.


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Per Capita Population Growth Rate and Exponential Growth. Rate constants
As many of us might know, the set up of a differential equation relating instantaneous population growth with respect to time to the per capita population growth rate and current population size at an arbitrary time is as follows:
dN/dt = rN
Now, we are told that the constant, r, is the per capita population growth rate. N is the current size of the population at some time. "r" is the "organisms added per reproductive period" divided by the total population at that time. For instance, if 10 rabbits are born per month and the current population is 100 rabbits, then r = 0.1.
Let's consider a case where a population is doubling every reproductive period, modeled by 2^t. we can choose to model 2^t in base e and equivalently we have e^ln(2)t. So  2^t = e^ln(2)t = e^kt where e^kt is a general formula for exponential growth or decay. For doubling, k = ln(2).  In differential equation form we have dN/dt = kN , k = ln(2)
You can't get natural log of 2 by taking the number of organisms added to the population and dividing by the current total population. r does not equal k no matter how you set up your growth rate, but the structure of the relationship is the very same differential equation for exponential growth: dN/dt = kN, which we can integrate to a general form such as A*e^kt.  Why do we use this "r" contrivance at all? I am not sure I understand this choice. How is r different from the standard exponential growth factor k? What does it help us to understand in modeling the population growth rate?

I'm confused.  Your first two paragraphs basically make sense (except that I don't understand why you switched notation from r to k, these seem to be exactly equivalent). I don't understand your last paragraph at all; can you try to clarify?  Are you confused about the switch between discrete- and continuous-time models?

Integrating $\frac{\mathrm{d}N(t)}{\mathrm{d}t}=rN(t)$ gives you $N(t)=N(0)\exp (rt)$. Doubling would mean the ratio of the population at time $t$ to time $0$ is 2; i.e., $2 = \frac{N(t)}{N(0)} = \exp (rt)$. You can see how $r \neq \log (2)$. As pointed out by @BenBolker above, I think you may be cofounding instantaneous, continuous-time growth (differential equation) with incremental, discrete-time growth (difference equation).


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What are the various parts of an ant hill
How can I identify the parts of an ant hill structure from a casting?  Specifically, if there is no real commonality between species, I would like to identify the various parts of a fire ant mound in Florida


text:
Can you predict what the metabolites of pipradrol would be? Are they similar to those of methylphenidate?
As these drugs are structurally very similar, I am curious about how the body would handle them. Ritalinic acid is a major metabolite of methylphenidate, but that's about all I know.
Thanks

Methylphenidate:
https://en.wikipedia.org/wiki/Methylphenidate#/media/File:Methylphenidate-2D-skeletal.svg
Pipradrol:
https://en.wikipedia.org/wiki/Pipradrol#/media/File:Pipradrol.svg
Ritalinic acid:
https://en.wikipedia.org/wiki/Ritalinic_acid#/media/File:Ritalinic_acid-2D-skeletal.svg


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Preserved flowers in epoxy resin
I want to cast flowers in resin. The problem is that everyone is casting dried flowers in order to prevent the moisture from fresh flowers evaporating while the resin is curing and I need to cast fresh flower. I tought of freeze dried flowers but could not find any company that could do it in my country nor online shop where to buy in europe. I am thinking of castin stabilized roses which are dehydrated first and the soaked with glycerin, propyl glycol and som dyes for colors. I wonder  if the glycerin with propyl glycol will evaporate with the higher temperature during the resin curing process.


text:
What is the probability of an offspring sharing identical HLA typing as one of their parents?
DISCLAIMER: I have yet to thoroughly study HLA 100% to the bone, and hence I won't know everything about it at the back of the hand.
Recently I came across this information on a San Francisco hospital website claiming the chance of a full HLA match between 2 randomly selected people is 1/1,000,000 and the chance of a full HLA match between a child and one of their parents is 1/200.$^{[1]}$
What struck me as odd is the 1/200 chance of a parent matching their offspring's HLA, which seemed too high of an estimate. The immediate intuition is for a child to have identical HLA typing as one of their parents, their parents need to share some HLA haplotypes, which on its own should be a rare occurrence. Hence I decided to attempt verification of this number to confirm if it was within the realm of possibility
According to Stanford$^{[2]}$, the HLA cell surface receptors that mix during inheritance are HLA-A, HLA-B in MHC I, and HLA-DR in MHC II. A set of these 3 forms a haplotype. [HLA-C and HLA-DQ are probably involved too, but we'll omit them for simplicity's sake.]
For our estimation, we use data from the same Stanford source$^{[2]}$ and find there are 59 HLA-A serotypes, 118 HLA-B serotypes, and 124 HLA-DR serotypes. This gives us $59\times118\times124=863288$ different possible haplotypes.
To get the probability of 2 parents sharing at least 1 common haplotype, we do some math: $\frac{1}{863288} \times \frac{863287}{863288} + \frac{1}{863288} \times \frac{863287}{863288} + 2 \times \frac{1}{863288} \times \frac{1}{863288} = 1/431644$
The above is assuming the parents have met randomly in the world and no inbreeding has taken place. Inbreeding will pretty much ensure 2 parents share common HLA haplotypes.
This means the chance of an offspring to even possibly have the same HLA typing as one of their parents is 1 in 431,644, which is already way lower than the 1 in 200 chance stated on the hospital's website.
Just for calculation sake, the precise chance of an offspring sharing the same HLA typing with either one of their parents after accounting for different possible haplotype combinations produced by the parents would be: $100\% \times \frac{1}{863288}^2 \times 2 + 25\% \times \frac{1}{863288} \times \frac{863286}{863288} \times 2 + 50\% \times 2 \times \frac{1}{863288}^2 = 5.792 \times 10^{-7}$
An exceedingly small chance.
Issues with my estimation:
There were 2 assumptions made during this estimatey computation. I didn't take into account the weighted and uneven distribution of the haplotypes, and just assumed they are all statistically evenly distributed. Some haplotypes are more common than others, and this factor was not considered during the estimation. If existing data on haplotype occurrence is used, it will likely affect the estimation quite a bit, however, this is highly difficult as the data varies by region and ancestry.
I also did not take Genetic matchmaking into account, which is a factor that will lower the chance of 2 parents sharing common HLA haplotypes.
If exact computation for the probability proves to be difficult, what would be a reasonable estimation on the order of magnitude of said probability? Is 1/200 within the realm of possibility once you take into account the uneven distribution of haplotypes caused by certain more common ones?
Sources:
$^{[1]}$https://www.ucsfbenioffchildrens.org/education/types_of_bmt_donors/#2
$^{[2]}$http://web.stanford.edu/dept/HPST/transplant/html/hla.html

If you follow your math, you will definitely not find a 1/1,000,000 chance of two random people being an HLA match, so it seems clear that the independence and equal weighting of types is not a great assumption.
We can make a different set of back-of-envelope assumptions, and just say that the 1/1000000 number comes from having 6 combined matches. In that case, you would interpret 1/1000000 as due to 6 independent matchings of probability 1/10. In that case, with a parent you only have to randomly match the other three. 1/10^3 = 1/1000, much closer to the 1/200. Further non-independence, unequal frequencies, and homozygosity makes 1/200 seem reasonable in a whole population (though individuals with more rare HLA would be less likely to match a parent or a random individual), and I presume the 1/200 number comes from actual observed frequencies rather than theoretical calculations.
Perhaps someone with more HLA expertise (I have basically none) will provide a better answer based on more specifics, but I just meant this as a quick napkin calculation for whether the numbers given are plausible, and I think that they are.

After googling around, I'm not too sure about the accuracy of the 1/1,000,000 chance claim of HLA matching between random individuals either, as there are rarely any sources making direct claims of the estimation chance.


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Water sample preservation
I am taking my students to collect water samples from different bodies of water. These bodies of water include the local river, a park pond, and water accumulation from recent rain. Once we gather the samples students will be analyzing the samples under standard light microscopes. I was wondering what is the best way to preserve any life that may be found in the samples in case there is no immediate opportunity to analyze the samples under the microscopes? Is there a specific time frame to analyze the samples before they have to be replaced? Also if they are kept in a bottle/jar does the container have to be unsealed or with perforations to allow air flow? Thank you.

What sort of timeframe? Collect in the morning & analyze in the afternoon would be good. Next day? Next week? Next month?

The samples will be analyzed within a week. Collection will take place Monday and the analysis of samples no later than the Friday of the same week they were collected.

Things start changing in minutes in sea water: I picked this up from some book on salt water aquariums when I had them.. I can tell you delicate inverts start dying in one day when power failure shuts down the circulation pumps although battery powered air pumps are running.  The main reason I gave up on salt after about 15 years.

Depending on what you are trying to look at, for zooplankton you can take water samples and filter them through a 100-200um mesh and store them in glass or plastic bottles. For my research we used mason jars that were cleaned thoroughly. After filtering just submerge the biomass in 70-90% ethanol and they can be stored in a fridge for quite some time.
If you want to look at phytoplankton, you can look into using Lugols Solution for preserving your samples. The nice thing about using lugols is that it will stain the phytoplankton as well. Your best bet for these is to store in amber bottles and keep in cool dark place. Here is a decent guide on how to collect the samples and prep the solution.


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Did the first cell self-replicate or was it multiple first cells?
We're almost sure by now that the first cell was born in a some kind of underwater vents environment which harvested all the necessary conditions for it to exist.
However, did the first cell self-replicate to have other cells or did the same process lead to the birth of others as well? If the latter is true, doesn't this make the evolution of cells more common once the primitive conditions exist?

Your question implies that the first life form (however you want to define that) had a cellular shape, but this is not necessarily the case: you can have i.e. self-replicating RNAs that don't need any form of 'cell' and could represent some sort of precursor stadium to cellular lifeforms in general

Welcome to Biology.SE! This is an interesting area to speculate about, but due to the paucity of evidence there is no consensus about the origins of life. As a result your question is probably beyond the scope of this site. ——— To learn more you may wish to check out the help pages starting with [Ask] questions effectively on this site. Thanks!

Good question. Simple answer here: we have absolutely no idea.
I would hazard a guess to say that the first proto-cell probably did not have the ability to replicate, so there must have been many proto-cells prior to the occurrence of the first true cell with the property to replicate itself with some degree of fidelity. Whether or not at some point cells existed that could be traced to two or more independent abiotic generations, that is unknown. The likelihood of this event is all we can talk about. I defer to biochemists working on this (still very open) problem, but I think it is honest to mention that they too have no idea, really. This is because, as we can surely appreciate, likelihood and outcome are two entirely different things. And unlikely events happen all the time. Each life form and individual is astonishingly unlikely, but historical contingency so happens to have brought us all here despite the odds.

"The likelihood of life occurring by chance is fantastically improbable". Everything indicates that life shouldn't exist and yet here we are. Plus, everything is connected too; if a single link was missing, we wouldn't be here. It will always blow my mind. I'll give time for other answers to be fair. Thank you!!

@Odin You are mistaken by saying "Everything indicates that life shouldn't exist and yet here we are." . The probability of life forming is unfathomably low but the sample space is unfathomably large. With sufficient time and sufficient chemical reactions, it becomes a statistical inevitability for a molecule like RNA to form. The period of almost a billion years between the formation of the earth (4.5 Ga) and the emergence of life (ca. 3.7 Ga), along with the inordinate number of molecules in the primordial soup outweighed the miniscule probability of life emerging


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Estimate for number of genes changed in speciation between a megafauna parent and child species
At least in terms of a back-of-the-envelope calculation, what is a believable range for the number of gene changes between parent and child species to represent speciation between species of megafauna?

Why duplicate this : https://biology.stackexchange.com/q/86139/38451

To paraphrase an old saying, gene changes should be weighed not counted. There are a plethora of types of gene changes, and they vary by orders of magnitude in their impact. In particular, which genes are affected has a huge impact. Some point mutations (change in a single or a few nucleotides) can be lethal. On the other hand there are trisomies where an entire chromosome is duplicated. These may cause severe health problems but don't result in a different species.
As is discussed in many other questions on this site, the definition of a species is fuzzy and context specific.

What you say is all very well but it does not seem to be an answer to this question. The poster's question may be unclear and naive, but he seems to be interested in the rate at which new genes appear as species diverge to something different. The fact that the definition of species is fuzzy is irrelevant. The sort of answer that would be useful (but which I am not able to provide) is an estimate of the number of different gene between two species with a common answer (mouse and rat?) and the evolutionary distance between them. This would give some sort of approximate rate.


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Probability for a megafauna specimen to exhibit a gene not present in either parent
What is the rough probability for a megafauna specimen to exhibit a gene not present in either parent?
I'm looking, ideally, at the chance for one specific individual to be the first in a breeding population to have a given gene.

So similar : https://biology.stackexchange.com/q/86138/38451

Not similar at all.

@Christos Similar to what iayork's answer has expressed, when do you think a mutation results in a new gene? If you had a protein with one function (e.g. kinase activity) that gradually evolved another function (e.g. trafficking), where is the cutoff between them? Which is the kinase gene and which is the trafficking gene? For this reason, your question is incomplete and cannot have a definite answer.

well for scale every single human carries around ~100 mutation in is sequence. but this is going to depend a lot on the size of the genome.

@Jam See my comment on iayork's answer. If you think about it, a gene duplication occurs, if the gene is functional that event produces an extra copy. If at some stage a mutation occurs or mutations accumulate to give the gene a new function (including a dormant mutation gene acquiring a promoter) a new gene has arisen. It has to happen during evolution at some stage, so it is reasonable to wonder about rates and probabilities, although unreasonable to expect anyone here to be able to answer.

@David I completely agree that when the question is expressed in terms of rates, it is answerable but in terms of instantaneously switching from one gene to another, it is incomplete.

The rate of evolution (as a result of germline mutagenesis) depends on many environmental factors. Scally (2016) suggests that germline mutation rate is approximately $0.5 \times 10^{-9} \text{bp}^{−1} \text{year}^{−1}$ in humans. You may be able to calculate the probability from here. It may be different for other organisms. Moreover, evolution can also happen because of gene duplication (as David said) and horizontal gene transfer, transposition etc. So you may narrow your question down a bit.

You need to define “gene” for your question to make sense. In humans, each individual has roughly 100 novel mutations (that neither parent had) (Human mutation rate revealed). However, those are not necessarily “new genes”, since many occur in non-functional DNA, even those that occur in functional regions may not alter any function, and even those that alter function may not be part of a gene, depending on your personal definition.

I wouldn't think the poster needs to define gene. It's evident that he's talking about new genes, not mutations that change existing ones. Most new genes appear to arise by duplication, and it's possible to compare species and identify differences e.g. in gene families like globins or blood group antigens. If someone has some figures for differences between rodents or primates and estimates of time of evolutionary divergence this would give a rate. To calculate a probability you would probably have to estimate the number of generations and the population of each. So this is not an answer.


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Can you help me identifying this spider?

I took this picture in Ohrid, Macedonia, it is the first time I see this kind of spider here.
This spider was 2-3 cm long and was outside in urban building.

It's probably an Araneus, but I'm not sure about the species.

Welcome to Biology.SE! Thank you for including location information, but please edit your post to add an estimate of the size of the spider and the environment you found it in. —— The size and environment can be essential clues for identification. Thanks!

It was 2-3 cm long and it was outside in urban building. Thank you too

@CveteRisteska Better edit your question and insert the size and location information in the original post. Information in comments might get lost or people won't read them.

I tried to identify it by your photo via Seek app and the result is "cross orbweaver / Araneus diadematus
The result seems true when it's compared to description in this site
For comparision see this image:

You're welcome. I strongly recommend this app for that kind of situations.


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How fast do hummingbirds fly?
Hhhmz! A hummingbirds flew past me while I was in the garden and yet, it still managed to halt perfectly in front of a blooming flower nearest to me. Just as soon I began to wonder, how fast do hummingbirds fly and in which way do they achieve their flight in addition to their distinctive hum.

"distinctive humming sound"??  Are you sure you are talking about mockingbirds?

Thanks mgkrebbs, I meant to write hummingbird although I wrote mockingbird.

Have youo tried to google your question? Are you talking of the flapping frequency or the distance they can travel per unit of time?

You also need to differentiate between the speed they can achieve for a short distance, and their average speed in migrations.  Answers are easily found with a search engine: about 30 mph in level flight, up to 60 mph in dives, and the rufous hummingbird can migrate between southern Mexico to Canada & Alaska in a couple of months.

Hummingbirds can give the impression by their small body size that they are very fast and of course they are. The Anna-Hummingbird, about ten centimeters in size, reach speeds of 385 body lengths per second (27. 3 m/s or 98 km/h).
So they can get acceleration values of about ten times the acceleration due to gravity.
To the comparison: Peregrine falcons come on speeds of up to 200 body lengths per second in the nosedive and fighter jets, like e. g. the MiG-25 (a Mach 3 fast interceptor), reach only the approximately by 40 times of its total length by one second.
They got this enormous achievement mostly by their biological construction.
For example: the heart of the hummingbird is very large in relation to the body and beats 400 to 500 times per minute, its respiratory rate is up to 250 strokes per minute, so  lots of oxygen gets into their wings and they can perform so strong. During sleep, many hummingbirds reduce their heart rate to save energy.

Thanks for answering Mr. Amstrand, are you able to expand on hummingbird's biological construction?


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How are single cells sorted in an scRNA-Seq protocol by FACS?
I am computational guy trying to understand how FACS sorting works in an scRNA-Seq protocol. About sorting single cells in each well of a 384-well plate, I have a question that would be grateful if you could answer it.
The protocol reads that cells are sorted in the wells based on their marker levels. For example it says:

NK single cells were collected from the CD19-/TCR-β- events by gating
  for NK-1.1+ events in NK-1.1 vs. Gr1.

The part that I don't understand is that how it is possible to know positive/negative events or even to gate on events beforehand? I know that FACS first examines markers and then sorts them into positive, negative or waste collections. Here is my question:

But how do we know what an expression level is acceptable for calling
  a cell positive, and also in more complicated case, how do we to gate
  on a subpopulation of cells (like top right quadrant) when no events
  have yet crossed the laser beam because we don't know the baseline of
  CD markers' expression levels yet?

For instance, It could be possible that in my panel setup a CD marker can never reach a value more than X, but in your setup it can never reach a value more than X/2.
N.B. As protocol says, subsampling of the main sample for FACS is not possible to infer these values beforehand because it is very likely that the populations of different cell types is not conserved in the subsample.

I will append the previous sentence in your protocol, and put what might help you in bold:

To  obtain  B  cells,  NK  cells  and  monocytes,  a  splenocyte  suspension  was  stained  with PE-Cy7-conjugated  CD19,  eFluor  450-conjugated  NK-1.1,  PerCP  Cy5.5  Gr1,  FITC TCR-β,  APC  CD11b  and  PE  B220  (CD45R).  B220+ and  B220neg (germinal  center)  B cells  were  collected  by  gating  for  CD19+(TCR-βneg)  cells  and  then  by  B220  against  theCD19  marker.  NK  single  cells  were  collected  from  the  CD19neg/TCR-βneg events  by gating  for  NK-1.1  positive  events  in  NK-1.1  vs.  Gr1.

The cell types in question have unique properties that can be stained for using (immuno)histochemistry, i.e. chemicals and/or antibodies. The antibodies themselves tend to be conjugated, i.e. they are covalently bound to fluorophores typically which are fluorescent. That means a cell type can be labeled by fluorescence, and the FACS machine can sort fluorescent cells from non-fluorescent cells.
They stained the different cell types with different markers. The markers are sufficiently different from each other to be able to use them together in some cases. For instance, whatever FITC is could be used simultaneously with PE-Cy7-conjugated antibody.

First, they collect two subsets of B cells (the B220 positive and negative cells) by using the CD19 marker (PE-Cy7-conjugated antibody that binds CD19).
Then, from one of the subsets, the B220 positive one, they sort another subset which is positive for eFluor 450 (which is conjugated with an NK-1.1 antibody). This collected subset fulfills their criteria for being NK cells.
This subset is used for single cell capture on a plate (e.g. for SMART-seq2) or using microfluidics (e.g. for 10X Chromium).

For a FACS machine, you can select the threshold level of e.g. florescence that will be used as a cutoff between positive and negative events (cells). This is arbitrary and is usually subject to trials.

Thanks for your answer, but someone told me they do index sorting today for scRNA-se but I don't understand it wither! :-)

I think index sorting is when you sort the cells into individual wells, and each well or cell is assigned its fluorescence value (each well is indexed). Then using this data in retrospect, you can choose which cells/wells you want to combine or eliminate. I'm not entirely sure but I think that's the gist of it.

we don't know the baseline of CD markers' expression levels yet?

There are standard settings that can be used between runs that will give consistent results from one sample to the next. There are also controls (fluorescent beads) that can be run beforehand to set the machine to ensure that those standard settings will work, and that allow you to make the relatively minor adjustments to bring them into a consistent range.
But you also have another misapprehension:

subsampling of the main sample for FACS is not possible to infer these values beforehand because it is very likely that the populations of different cell types is not conserved in the subsample.

Just because the positive cells are not in the subsample doesn't mean you can't set normal values.
The key is that a positive cell isn't a subtle thing. In a typical flow cytometry stain, your positively stained cells will be much brighter than your negatives; at worst tens of times, often thousands of times brighter. Setting a gate fairly close to the upper end of your negatives (in your subsample) will in practical terms guarantee that your positives will be outside the gate.
I grabbed a random example from a Google search; this is a pretty typical looking gating:

Notice that in each gate, the positive population is (eyeballing) a thousand times, to several thousand times, brighter than the negative (the X axis is a log scale). When you have that much room to work with, delicate subtle effects in baselines settings can be safely ignored.

Thanks for your answer, but someone told me they do index sorting today for scRNA-se but I don't understand it wither! :-)

Index sorting, very simplistically, is just a retrospective analysis of the cells that are sorted. You collect single cells without a specific sort (or more typically, after they are sorted for many but not all parameters); you perform some other kind of analysis on the cells (like sequencing); and then you go back and link the full analysis of the cell, to the further data you collected. It means you can assess parameters that you didn't explicitly sort for.


text:
About the definition of ketogenic amino acid
I am studying biochemistry and have been looking at metabolic network diagrams showing the different intermediates of glycolysis and the citric acid cycle that amino acids can be converted to.
I have gone over a list of which amino acids are considered ketogenic and which are considered glucogenic. I was surprised that Serine, Glycine, Cysteine, and Alanine are not considered ketogenic as they can be converted to pyruvate and pyruvate can be turned to acetyl-CoA, so that these 4 amino acids seem like they can then be used for ketogenesis.
I then looked at the definition of ketogenic amino acids on Wikipedia and it says "A ketogenic amino acid is an amino acid that can be degraded directly into acetyl-CoA".
The question is if there's some reason this is the definition of ketogenic amino acids; it seems to make more sense to me to classify Serine, Glycine, Cysteine, and Alanine as ketogenic due to what I said.
Thank you.

The fundamental 'problem' with acetyl-CoA is that it cannot be converted to glucose via the tricarboxylic acid (TCA) cycle: a two-carbon compound (acetyl-CoA) enters the TCA cycle, but two carbons are lost as CO$_2$ during each round of the cycle (in the two decarboxylation steps, ie in the reactions catalyzed by isocitrate dehydrogenase and by the alpha-ketoglutarate dehydrogenase complex).
There is no 'net gain' of carbon when acetyl-CoA is 'burned' in the TCA cycle.
This is why animals cannot convert even-number fatty acids (even-chain fatty acids) to glucose, and a basic principle of animal nutrition is that triglycerides, with the exception of the glycerol backbone, cannot be converted to glucose.
This, is seems to me, is also the key to understanding the difference between 'ketogenic' and 'glucogenic' amino acids.
Amino acids that directly give rise to acetyl-CoA (or acetoacetyl-CoA) cannot be converted to glucose but that can be converted to ketone bodies (such as D-3-hydroxybutyrate)  are referred to as ketogenic amino acids.
Pyruvate can be converted to glucose (via glucneogenesis), and amino acids that may be converted to pyruvate are considered glucogenic. A very good example is alanine which may be converted to pyruvate simply by transamination (alanine aminotransferase).
Alanine is a key protein-derived glucose precursor, especially in times of starvation (Felig, 1975). A commentary on the discovery of this key finding is given in this citation classic
In addition, amino acids that may be converted to TCA intermediates that in turn may be converted to phosphoenolpyruvate (and are thus precursors of glucose) are considered glucogenic (Lehninger, Biochemistry, 2nd Ed, 1975, p629).
We need to be aware that propionate (a three-carbon compound) is glucogenic (and this is particularly important in ruminants): it is even-chain fatty acids (and their CoA derivatives) that are non-glucogenic.
Furthermore, an amino acid may be both ketogenic and glucogenic.

Only leucine and lysine (LK) are exclusively ketogenic
Tryptophan, Isoleucine, Phenylalanine, and Tyrosine (WIFY) are both glucogenic and ketogenic
The other 14 'protein' amino acids are glucogenic

See  D'Mello (2003) for a great ref (it must be good, he's from Scotland).
The catabolism of the branched-chain amino acids (Ile, Leu, Val) provide an example of each type (Harper et al., 1984):

The catabolism of isoleucine gives rise propionyl-CoA and acetyl-CoA and is both glucogenic and ketogenic.
Leucine catabolism yields acetoacetate and acetyl-CoA (ketogenic)
Valine catabolism yields succinyl-CoA (glucogenic)

A quote from Metzler (2001) may help to clarify the origin of the terms.

According to a long-used classification amino acids are ketogenic if (like leucine) they are converted to acetyl-CoA (or acetyl-CoA and acetoacetate).
When fed to a starved animal, ketogenic amino acids cause an increased concentration of acetoacetate and other ketone bodies in the blood and urine.
On the other hand, glucogenic amino acids such as valine, when fed to a starved animal, promote the synthesis of glycogen
... isoleucine is both ketogenic and glucogenic, a fact that was known long before the pathway of metabolism was worked out.

Thus, in feeding experiments, a glucogenic amino acid gives rise
to the synthesis of glycogen, whereas a ketogenic amino acid does not
(but does give rise to an increase in the concentration of ketone bodies)`

We may note that plants can circumvent 'the acetyl-CoA problem' as they have the enzymes of the glyoxylate cycle, where the two decarboxylation steps of the TCA cycle are 'bypassed' (the key enzymes are malate synthase and isocitrate lyase) [and plants can convert acetyl-CoA to glucose].
It is also of interest, maybe, that both arginine and taurine (not one of the 20, of course) are essential in cats (see D'Mello, 2003). Arginine is required because of an inability to synthesis ornithine and a single Arg-free meal may cause a cat to become comatose due to the build-up of NH$_3$ (see D'Mello, 2003; Bequette, 2003) , and taurine is required to prevent retinal degeneration (see D'Mello, 2003; Bequette,2003). In addition, cats need high levels of Phe/Tyr for melanin biosynthesis, otherwise hair color may change from black to red-brown (see Bequette, 2003)
Reference
Some key references given above are from the following book:
Amino Acids in Animal Nutrition (2003) Edited by J.P.F. Mello, CABI Publishing, 2nd Edition

D'Mello, J.P.F (2003) Amino Acids as Multifunctional Molecules by J.P.F. D'Mello (Chapter 1)
List Bequette, B.J. (2003) Amino Acid Metabolism in Animals:an Overview (Chapter 4)

In Addition (Taurine in Cats)

Carnivores Herbivores and Omnivores in Blondes in Venetian Paintings, the Nine-Banded Armadillo, and Other Essays in Biochemistry by Konrad Bloch

“The question is if there’s some reason this is the definition of ketogenic amino acids”

The answer from @user1136 covers the biochemistry of the degradation of ketogenic and glucogenic amino acids. However it doesn’t answer this part of the question directly, which is what I shall use my answer to add. Just as we may classify amino acids as hydrophobic or hydrophilic if we are interested in their function in proteins, this classification as related to a particular context. At least in part, this is:

The provision of glucose, especially for the brain, during starvation
and pathological states such as diabetes

Whether or not so-called glucogenic amino acids could in principle be converted to acetyl CoA, the regulatory mechanisms controlling the pathways ensure that it will be converted to glucose via gluconeogenesis — which is the raison d’être for the breakdown of amino acids during starvation.
Although certain tissues can use other fuels instead of glucose, the brain and the erythrocytes have an absolute requirement for glucose. In the case of the erythrocyte the product of glucose oxidation, lactic acid, can be recycled via the liver. However this is not the case for nervous tissue. So an alternative classification might be glucogenic or non-glucogenic. However the fact that the ketone bodies produced by non-glucogenic amino acids have important positive and negative functions themselves (alternative fuel, but can cause acidosis) presumably led to the use of the term, ketogenic.
Footnote: Context and Experimental Evidence
The experimental evidence for the breakdown products of individual amino acids came from feeding experiments, so that it might be argued that the context of starvation I assert is incorrect, especially given the contemporary fad for ketogenic diets and the like. However as regards evolutionary and clinical importance, I would argue that starvation is what matters.
Further reading
There is more information about gluconeogenesis in starvation in my answer to this SE Question.
There is a useful answer by @Don_S to another SE question concerning the use of glucose and ketone bodies by the brain.
Section 30.3 of Berg et al. 5e (unfortunately no longer available on NCBI Bookshelf)  deals with amino acid breakdown and the use of glucose or ketone bodies during starvation.


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What kind of fish is this white blue-stained fish?

This fish has been spotted at the Great Barrier Reef near Cairns (Queensland).
I put a big effort to find it via Google but never could encounter anything similar.
I have also made an attempt to find this fish here with no luck.

I don't know whether this helps, but that looks like a parrot fish.  I had a look online and also didn't find anything with that distinctive pattern. The closest I could find was Scarus ghobban (common names include blue-barred and blue-trim parrotfish), which is highly variable but the blue edges on the fins seem constant.
According to the sources linked above this fish can be seen in areas with sandy bottoms, so that seems consistent with your photograph.
Reference pictures:


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How does bacteriorhodopsin differ from the rhodopsin present in mammalian eyes?
In my high school textbook, it is written that they are similar. So, I was just curious to know about this.
Thank you.

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Although they are similar in both bacteriorhodopsins  and rhodopsins being retinal-binding proteins, the similarity in their amino acid sequence is very limited.
The key difference between them is that rhodopsin is a G-protein-coupled receptor, and this is not the case with bacteriorhodopsin. A quick Google search on Bacteriorhodopsin vs Rhodopsin will send you to a Wikipedia article that says:

Bacteriorhodopsin belongs to the microbial rhodopsins. They have similarities to vertebrate rhodopsins, the pigments that sense light in the retina. Rhodopsins also contain retinal; however, the functions of rhodopsin and bacteriorhodopsin are different, and there is limited similarity in their amino acid sequences. Both rhodopsin and bacteriorhodopsin belong to the 7TM receptor family of proteins, but rhodopsin is a G protein-coupled receptor and bacteriorhodopsin is not.

A very good paper if you would like to know more about the two is by H. Gobind Khorana on the Two light-transducing membrane proteins.


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What kind of bonds are there between a Transcription Factor and its DNA binding site?
I want to know what kind of bonds are there between a Transcription Factor and its DNA binding site when the complex is created. This information will be used to determine the method for a molecular Dynamics simulation, which intends to predict/calculate the binding energy/Gibbs free energy.

You might take a look at this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425445/ ("MM energy functions, on the other hand, are composed of independent, physicochemical energy terms that capture van der Waals and Coulombic interactions, solvation effects, and other atomic interaction energies")

Thanks for answering.  I would like some more specific information but I found other useful information


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Why does flicking a finger generate so much more force than extending it quickly?
Flicking a finger (holding it back with e.g. the thumb while building up "pressure" against the thumb, then releasing) is much more powerful than just uncurling the finger quickly.
I tried to do the same with other body parts, like flexing my arm and holding it back with my hand as I tried to straighten it, but the force from releasing that doesn't seem to be more powerful than simply punching out the arm flexed to extended without holding it back in any way.
Are fingers special?
What causes the body to be able to generate extra power like this?
It makes me think of shooting rubber bands.

No, the fingers are not special. Well, they're a miracle, actually, like the entire body is, but no more special than the foot or arm or anything else.

Your body in this case is generating more "power" by having something to push against.
When flicking your finger, your finger is pushing against your thumb and that pressure you feel is the force of both your finger against your thumb and your thumb against your finger. This is important as you can only apply so much force to a mass before it gives out and moves. Your thumb has much more mass than air so you can build up a lot of force on your thumb before releasing your finger and sent it accelerating. However, when extending your finger in the open air, it is only pushing against that, and air quite obviously has little mass to build off of.
You can experience this in another way; pushing against the wall creates builds up more force than shoving the air. If you were to somehow instantaneously make the wall disappear, your arms would extend faster than you can shove.
Using your hands to hold back your arm is correct, but the force you generate in that method is too little compared to the mass of an entire arm. Think about the mass:force ratio between a finger and the force between a flick, and an arm and the force holding back. (Edit:) Also, when letting your arm go, your hand stays stuck to the arm for a much longer period than your thumb against the tip of your finger.

You've not explained how it works anatomically, nor is your answer very scientific at all. I still don't understand what the mechanics behind the flick are .

@theonlygusti - This answer is correct, and quite scientific. It involves physics: friction, force, mass, etc. If you cannot understand this answer, one delving into the molecular phenomena (actin-myosin coupling and uncoupling building up more force) will be of no value to you at all.

@MrMineHeads - Thank you for a nice (and correct) explanation and first answer. Welcome and +1!

@anongoodnurse what does "build up force" mean?

@theonlygusti What I meant by a "build up of force" is that you can push much harder against your thumb than you can extending your finger because extending your finger has no opposite (very little) force pushing back (Newton's 3rd law). At that point, the only way your finger can gain velocity is by your muscles contracting quickly. Compared to pushing against your thumb where your muscles are much better at exerting their potential, the force your muscles in your forearms is smaller. If you'd like I can draw a rough FBD of exactly what is going on, but I feel like the explanation is robust.

Where is the force stored? Is my tendon being stretched like elastic? What's an FBD?

I tried to do the same with other body parts, like flexing my arm and holding it back with my hand as I tried to straighten it, but the force from releasing that doesn't seem to be more powerful than simply punching out the arm flexed to extended without holding it back in any way.

The answer above is spot on. But let me respond (in kind, i.e. like the answer above) to this aspect of your question, hoping you can relate it to the answer above.
The arm question is exactly like the finger question; you're just looking at it kind of in the wrong way.
If you bend your elbow, say, to 90° at a distance of 1 inch from a pane of glass, then try to extend your arm as forcefully as you can with someone holding your arm back at the wrist, if they suddenly let go, your arm may well have enough force built up to break the glass. (This depends somewhat on the strength of your triceps, not an overly strong muscle in non-athletes.)
However, bend your elbow, say, to 90° at a distance of 1 inch from a pane of glass, then extend your arm as forcefully as you can into the glass, It probably won't break, because you can't build up enough force in your triceps over the course of that inch without resistance.
This is exactly analogous to the finger example explained above, except for the size and appearance of the fingers. It is analogous even to the extent that we do not use our finger extensors against resistance very often, much like our triceps.
You can apply this to any muscle-joint group in the body. The outcome will be roughly the same.
I do hope that helps explain the answer to your question.

Even holding my arm 1 inch away from the surface I still feel like it is the same power (sometimes even feels less) to hold it back than just punch it out

It's absolutely not the case, even if you feel or believe it is. The same exact positions (not you swinging a punch), one with force built up, one without, will give you completely different outcomes.


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Will modern-day insects grow to massive size in a high-oxygen environment?
It's a reasonably well-known fact that insects grew to massive sizes due to the excessive concentration of oxygen in the prehistoric-Earth's atmosphere.
If one were to try to recreate this high-oxygen environment in a lab setting, would insects reared within grow to massive size?

Yep! In the group I work in we have a little pet project doing things like that. Different environmental conditions totally change insect’s body sizes. Getting up to truly massive sizes is a bit more tricky, but it works pretty well.

@CalendarJ it would be excellent if you draft this up as an answer with a bit more detail. Thanks!

While @CalendarJ comments "Yep!" above, a quick search suggests that experimental hyperoxia typically only increases insect body sizes slightly. Everything below is from VandenBrooks et al. 2012 (of course there could be other sources that contradict this!)

A few beetles have been reported to reach larger sizes when reared in hyperoxia, but most of the species examined reach similar body sizes in 40% oxygen as in normoxia (Harrison et al. 2009).

and:

Here we investigated the impacts of Paleozoic oxygen levels (12–31%) on the development of Blatella germanica cockroaches. Body size decreased strongly in hypoxia, but was only mildly affected by hyperoxia.

and this figure:

These results show that male cockroaches grow much larger under present-day (normoxic; 21% oxygen, highlighted box) and elevated (hyperoxic; >= 24% oxygen) levels than under low (anoxic; 12%) conditions, but the hyperoxia-grown roaches are only a bit larger than normoxia-grown ones. (Similar results for females not shown.)

VandenBrooks, John M., Elyse E. Munoz, Michael D. Weed, Colleen F. Ford, Michael A. Harrison, and Jon F. Harrison. “Impacts of Paleo-Oxygen Levels on the Size, Development, Reproduction, and Tracheal Systems of Blatella Germanica.” Evolutionary Biology 39, no. 1 (March 1, 2012): 83–93. https://doi.org/10.1007/s11692-011-9138-3.

I think you perhaps have a misconception.  Body size is mainly controlled by genetics, thus we have species of "bugs" that are very small, others from closely-related lineages that are much larger.  Take for instance flies, which come in sizes from fruit flies through house flies up to horseflies.  They're all pretty similar (under magnification) to a non-specialist, yet it seems unlikely that raising a fruit fly in an oxygen-rich environment would make it grow to the size of a house fly, let alone a horse fly.
It doesn't take much thought to come up with many similar examples, such as beetles and butterflies, with species that come in a range of sizes.  It seems obvious that they've evolved a size which fits their evolutionary niche, and if they grew too large, they would be unlikely to survive.
Oxygen concentration is one of the factors that puts limits on the size of insects, but to get real size increases, you need to evolve new species that take advantage of increased oxygen, not just grow your 1st generation offspring.

Yes, this basically summarizes the answer I was seeking in this question; whether or not the difference in size of Paleozoic insects was caused by a genetic difference.

The latest documentary I watched about the Meganeura (a giant Dragonfly from Pre-Cambrian) seems to confirm your intuition.
Based on experiments by John VandenBrooks at Midwestern University, with bugs in conditions A with less oxygen than current Earth atmosphere, and a 31% oxygen atmosphere in conditions B:
The bugs from group B were roughly twice as big. It was a bit frightening. (I don't know if there's a paper that shows the size difference statistics for several individuals.)
Here's the documentary for French TV "Science Grand Format":

there is a lightweight interview of the scientist at 06:15
experiments on cockroaches at 06:50
they show the bugs different sizes at 7:45.

Do you have a citation/link to the documentary that you could provide?

@CalendarJ have added sources. Althought the scientist is interviewed and explain his results, I have not checked his research papers.


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What is the difference between differentiation and phenotype switching?
I am trying to model bone remodeling process and I wonder what is the difference between phenotype switching and differentiation. I am relatively inexperienced in biology. Please explain me with examples related to this context. Thanks in advance.

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Differentiation is a process which occurs in multiple steps. A precursor cell for example a mesenchymal stem cell can proliferate (divide/multiple).  The stem cell can commit to become a progenitor cell (osteoprogenitor cell) which can still proliferate but has acquired the possibility to differentiate to a different cell type. In some cases or when specific conditions are met,the progenitor can differentiate to a pre-osteoblast and finally to a mature osteoblast.
The differentiation process require the activation of a specific transcription program and leads to large changes in the cell like morphology, size, and function. Once differentiated, the cell cannot proliferate anymore and loss the capacity to divide.
Phenotype switching can be broadly defined as any change in the phenotype like morphological change, expression of specific biomarkers, etc. In the context of differentiation phenotype switching refers to the acquisition of a specific differentiation marker usually a transcription marker like Runx2. While they might not be a large morphological change, the fact that the cell express this transcription factor indicates it is switching phenotypes and starting differentiation.
In summary: differentiation is process which occurs in multiple distinct steps. Differentiated states are characterized by a specific morphology, acquisition of key bio markers (usually transcription factors), loss of the capacity to proliferate, and a cellular specific function. Phenotype switching refers to the time frame when a cell changes from one phenotype to another; when it acquires or loss a defined morphological state or key markers.

Both differentiation and phenotype switching are terms which are used in intense research areas. Their definition will get revised in the next decade for sure. The definitions I have highlighted are what you will classically find in most publications but in reality it is difficult to define specific steps in a differentiation process because it is usually a continuous process.  Phenotype switching is even worse to define as it assumes that once classified to a category a cell does not have a dynamic phenotype: a cell which proliferate change phenotype as it goes through the cell cycle.

Thank you very much for the response. Differentiated cells lose the ability to proliferate. Does that mean they don't divide forever? Do they die?

Technically yes they should not divide. Theoretically, these cells could accumulate genomic mutation (UV, chemical environment, etc) and become cancerous but I'm unsure if this has been convincingly shown in the literature.
Yes differentiated cells can die by different mechanisms including apoptosis and necrosis, and be replaced by others cells. A good example would be neuronal cells.


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Is this aquatic plant duckweed or something else?

This plant has been growing in my pond for quite a time now. It multiplies in large numbers rapidly.
 Some told me it is duckweed or is it something else?

Can you please [edit] to add additional information as specified in the "species-identification" tag (hover over or click the tag to see details). In particular, measurements of the leaf diameter might be very helpful. Thanks!

That looks very much like a duckweed.
The multiple roots rule out most genera within this group and so this is probably a Spirodela.
The apparently relatively large size and red undersides are consistent with this being Spirodela polyrhiza.

Picture by Christian Fischer available under Creative Commons Attribution-Share Alike 3.0 Unported.

Not duck weed. It is Salvinia species very easy to grow ( invasive). I believe it is illegal to introduce in some US states. Koi /carp will eat duck weed.There are a few similar species of salvinia , unfortunately references will give the same name for different plants. My book ( Aquarium Plants ; Barry Jones, Tetra press) calls it auriculata which I believe is wrong. Auriculata is also called giant salvinia and looks different ( see comments @ tyersome ). I have grown Auriculata but not the salvinia that you have.

This is not correct — Salvinia species look completely different, for example they have hairs on the leaf surface and their "roots" look completely different — see for example here: https://www.cabi.org/isc/datasheet/48444.

I have edited to what I believe is correct.


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What kind of skull is this-I found it on the beach in Cape May
I am hoping someone can help identify this skull! We found it on the beach in Cape May. The skull size is about 4 inch in length. Thank you.

www.boneid.net provides a great searchable database of identified bones

Eyes at sides, have incisors and molars. This is a herbivore and not a sea mammal. According to the large incisors and placement of the teeth, I think it's a rodent.

Harun, Do you know what kind of rodent it might be?

Possibly a gopher.


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Why is sorbitol used in buffers?
Many protocols in my lab use sorbitol in buffers.  For instance, in co-immunoprecipitation, we include it at a final concentration of 200 mM in our lysis buffer. I'm not entirely sure why though.  I believe it might be as a crowding agent. But even if this is the reason, I'm not entirely sure what this means.  Could someone explain?

Generally, sorbitol is one of those 'old tricks' in the book which is thrown into cultures or buffers for several reasons. Here are a few that I have heard of:

Bacterial cultures (e.g. E.coli BL21) that are optimised to express (produce) protein, because sorbitol is thought to increase the expression of soluble protein. I have even heard of people (who work with very difficult proteins) that add to a final of 0.6M sorbitol in their culture media (note that the cultures grow very slowly).
In buffers intended for proteins, as it is thought to increase the solubility (i.e. avoid aggregation), similar to other sugar such as glycerol or osmolytes such as betaine.
Sorbitol is considered (chemically)  to be relatively inert, and many will therefore prefer to add sorbitol over e.g. glycerol or sucrose as a stabalizating agens when they work with proteins.
When you work with glycoproteins, you are generally depending on the addition of some sugar to stabilise the protein of interest - both during isolation, purification and analysis/testing.

The last point here could answer you question, as immunoglobulins are glycoproteins, you are generally depending on a high concentration of some sugar - such as sorbitol - to work with these proteins (i.e. antigens and antibodies) in e.g. immunoprecipitation.
I don't believe that sorbitol is a crowding agent - as this would perhaps facilitate aggregation, the opposite of the intended purpose. Adding crowding agents it typically done in protein crystallography with the addition of various PEGs to 'get the' proteins to form crystals. Instead, I think that sorbitol may (somehow) interfere with the proteins solvation shell - in the same way that is speculated for osmolytes (e.g. betaine or various sugars); however, this is something that I dont know much about and should be investigated.


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What is a "Valid Species"?
I read in a reference book on Google Books (Biology of Termites: a Modern Synthesis, eds. Bignell, Roisin, and Lo) that the termite Heterotermes perfidus found on the South Atlantic island of St Helena is a "valid species":

Gay states definitively that "there is no doubt now, however, that H. perfidus is a valid species ..." (p. 537)

I don't understand what "valid species" means.

"Valid" in this case is just emphasizing that the Heterotermes perfidus on this island are a different (real) species, and not just a variation of their closest relatives. You need not get bogged down with how we determine species, or define species. It just means that this taxon (named group) exists as a separate species: a "valid" species, based on differences that some taxonomist deemed important enough to describe and give a name. Others may disagree, and write a paper to synonomize it (sink it into another existing species), but that is part of the messy business of taxonomy.

Many thanks, that is most helpful.

This will vary from discipline to discipline. In paleontology valid species means a population that can be show to be morphologically distinctive in a way that cannot be better explained as sexual dimorphism or a growth distribution. In a living species it may rely on genetic (breeding) isolation.
Basically a "valid" species is meant to show it as distinct from a provisional species or subspecies. Generally the null assumption is that two populations are the same species unless evidence can be presented to show otherwise.The author is saying they have presented such evidence and this really is a distinct species.


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How many different chemical substances are there (on the average) in a human cell?
How many different chemical substances are there (on the average) in a human cell?
I saw of an estimation of ~ 1 billion (10^9) in sci-pop books.
Is there any reliable estimation rooted in the scientific community?
There is this question, but it does not have any answer. It only states that modern researches use (model) only a very limited number of chemicals within a cell. But what is the estimation of the real complexity of a problem.

Why do you care? This is Guinness Book of records stuff, that went out of science two centuries ago.

For the scope of the question, it will largely depend what elements should be considered. All chemical substances would include atoms, molecules, basic chemical substances (for example amino acid, nucleic acid), supra molecular substances (peptide, protein, DNA molecule), and complexes. When considered from this point of view, any pair of amino acid or nuclei acids is a new entity. With all the possible building blocks that makes a huge combinatorial list. So the answer will largely depends at which "level" of details the question should be asked.

I think that the sci-pop books will be as reasonable as any other estimation.


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Can any one explain me the structural difference between Proteins and Peptides?
I have read in books that Proteins and Peptides are fundamental components of cells which carryout important biological functions.Can any one explain me the structural difference between Proteins and Peptides?

Welcome to SE Biology. Have you tried to research this yourself? You should do this before posting — I am sure you will find an answer. If not, [edit] stating what you have found and why you are still unclear on the topic. See our help on asking good questions.

Dear users of Biology Stack Exchange,I have been banned from asking new questions in Biology SE by the system.It's showing that "you have reached your question limit" and "sorry,we are no longer accepting questions from this account".That's why I'm editing my questions.Your up votes may help me in getting out of this ban.So,please upvote my questions if you like them.I didn't know about question ban previously till I had got imposed and no one told me about that ban.I would have improved my questions if I knew that.So,please help me in getting out of this ban with your upvotes to my questions.

Dear David and theforestecologist ◆,I'm unable to ask questions on Biology SE.Whenever i click on "Ask" option it's showing that "sorry,we are no longer accepting questions from this account" and it's telling that I need to edit my questions.I'm editing my questions for the second time after the question ban had imposed on me but the ban remaining as it is. Today i need to post a question and it's telling i should wait 6 months for posting that!! It's 'horrible' and facing this ban is 'too hard for me'.Please,can anyone help me in getting out of this ban? I will be thankful for that.

You need to ask about this on meta, if it will allow you. Then one of the mods will explain the situation to you. @theforestecologist is better placed than me as he is a moderator (the diamond indicates this) but you need the ampersand to alert anyone to a post. He should see the one I have included.

David and @theforestecologist ◆, i have already asked a moderator of Biology SE about this question ban nearly 25 days ago.He told me to improve the questions i have asked previously.I'm doing that and I'm also asking other people to help me in getting out of this question ban.

OK, the "homework questions..." is a close option that is often used when one thinks the question shows insufficient research. If you look at the Help on asking questions, it says "search, and research". This question is really basic in relation to the definition of this site as being for "for biology researchers, academics, and students", so you would be expected to search on the internet on sites like Wikipedia or NCBI bookshelf.

In terms of structure: both are composed of amino acids.
A peptide is when at least two amino acid are linked together.
A protein is composed of multiple amino acids and have a secondary, tertiary and even quaternary structure.
In terms of function: larger molecules have more complex functions.
Peptides can act as a intracellular or extracellular ligands which will activate a signal.
Proteins have a large array of functions (enzymatic, structural, receptors etc)
This article explains in more details the differences in proteins structure and functions:https://en.wikibooks.org/wiki/Structural_Biochemistry/Proteins

pls include pictures :)


text:
What species is this fast-moving spider?
This is a frame from a recent recording:

Location
Forest in Central Europe at around 1pm.
Abiotic factors at the time of recording

Temperature = 23°C
Humidity = 38%
Wind = 6 km/h

Description

Approximate size = ~3 cm including limbs
Semi-transparent limbs and cephalothorax, opaque abdomen
The abdomen presents a pattern which reminds me of the coat pattern in giraffe G. camelopardalis tippelskirchii
its general morphology makes me think it might be part of Pholcidae family but I'm not entirely sure because the height of the abdomen seems a bit too bulbous on the Y axis
web structure rather irregular

Observed behavior
Very short reaction time (dropped a piece of leaf on top of its web), very fast moving spider. I can't provide a better estimation for the speed, but here's is the 3rd frame after the one above (on the previous two frames it just very slightly flexes its limbs):

And one frame later it's already gone.
Internet search

Google image search: no results using the first image you see in this post
Google text search: different sentences like "long-legged transparent forest spider" only returned the usual daddy long legs you can find at home in urban areas.
Finally I tried https://spiderid.com/spiders/ selecting white and brown but none of the displayed spiders matches anything that resembles the frame above.

Any help will be much appreciated. I guess the pattern on the abdomen is key to identify this species but I haven't had a lot of luck while looking for abdominal spider patterns.

Go to iNaturalist and type in "spiders" as well as your country, then go to the species tab and scroll down until you find it.

It looks like a male Linyphiid, most probably a Frontinellina frutetorum

Source: https://ednieuw.home.xs4all.nl/Spiders/Linyphiidae/Linyphiidae.htm
Thanks to John Robinson and Ed Nieuwenhuys who helped get a probable match for this spider.

Pawelek;
Unfortunately, I'm not very experienced at European spiders, but I suspect you're looking in the wrong place.  First of all, this appears to be an adult male spider (large ball-like structures at the ends of the pedipalps, in front of the 'face'), so the body pattern is probably going to be a bit different from the one you see on the females.  Male patterns are often an afterthought in identification references, unfortunately.
Secondly, this doesn't look much like a Pholcid to me - I'm getting more of a Linyphiid impression, from the shape of the abdomen, the visible patterns on cephalothorax and abdomen, and the filmy sheet it's hanging under.
I wish I could be of more help than this - but perhaps Ed Nieuwenhuys can help.  Here's a link to his site; if you look down toward the bottom, there's a contact link you could send him a photo and this question:
https://ednieuw.home.xs4all.nl/Spiders/spidhome.htm

Hi, Pawelek - for some reason, the answer dropped the "Hi," I had put before your name, and it refused to let me add it in later.  Most odd and unfriendly!  At any rate, please don't think I would simply start right in in that brusque fashion.  I'm a grouch, but not an unfriendly one!

Stack Exchange discourages "hi" and such salutation on the post though.

John, I wrote to Ed and he confirmed it is a linyphiid as you suggested. He said it looks like a Frontinellina frutetorum. If you modify your answer to reflect this I'll be happy to mark it as accepted. Thanks for the help!

Hi, Pawelek;  That's a nice offer, but I would feel a bit dishonest if I modified my post to give a suggested species that I don't, in fact, know.  I'm glad Ed gave you a probable ID!

I suggested so because I wouldn't have been able to get such a close match if you hadn't pointed me to Ed's site :) (for which I'm thankful). I'll answer it then for the sake of not letting the question "hanging" after having managed to get a probable match.


text:
Tools I can use to find similar genes
What tools are available to estimate the function and purpose of a gene ? I think the right approach is to find similar sequences of genes that we know the function of.
All the information I have on a gene is (for example):
KXN84633.1

and
>lcl|Query_208731:23119-24312
CTACAGACATATCCCATCCAGAAGAAATCTTTATCTATCGAATACCTTCGCGATAACGCGTATCTACGCG
CTCGAACAGGCCAAATAGCTGCAATGTTAAGGCTGAGGGATAGTATTTCCAAAAACCTATCCCGGCATTT
TGAGGTACATTTACTTTCTTCCGTATCTGGCCTGACTAAAAATCCTGCGTAGTCTCAAGGGTTTACATAT
ACTCATACGCCTATAATAACAGCTAGCGATTGCGAAGGCGCAGGCGAAGCATTTCGCATATCACCTATCC
AACCTACCACCCCCTCTCTCTCAAAAACTGACGCAAGTTCAGACGCAAATACCCCTATAGAGTTCTTTTC
ACGTCCTGCATATCTCACAGTCTCGCATCAACTTCATCTAGAATCCTTCACCACGGCTCTCTCTCGCGTG
TATACCCTTTCACCATGTTTTCGTGCGGAACGATCTATGACTGGACGACATCTGGCCGAGTTCTGGATGC
TTGAGGCCGAGTGGAACCTTGCAACGCGTTGCGATAGCTTAGAAGAAATTTGTGCCTTTGTGGAAGGCTT
AATTCGGACGTCGGTAGATCATGAGTCGCAGGATGTCAAGGCTCTGTGGGCGGAGAAAGGAGCGGAAGTA
GAGGAATTCAAGATGTTTCGTGCCGCATTTGACAACGCTCAGCCTTGGAGGCGATTAACATACTCGGATG
CAGTCGAGGCGTTGAGCACGGCTTATGTCAACGGACATCCTTTCGAATTCAAACCTGTCTGGGGCGAATC
ACTCTCGAGCGAACATGAACGTTGGCTGGCAGAGGTGTACGTTGGTGGACCAGTGTTCGTGACAGACTAC
CCTATCAAACTTAAACCGTTTTATATGCGGGTCAACGAAGATGGGAAAACCGTTGCGTGTTTCGATTTGA
TTGTACCTCATGCTGGTGAACTTGTGGGTGGAAGTGTGAGGGAGGAGAGATGGGATGTCCTCTCAAAACG
GATGGCAGAGCATGGATTGTTGCCTCACCCTGACCAGAATGAGGGTGCCCCAACTGATTCGACATATGAA
TGGTATCTGGATTTACGCAAGTATGGTGGAGCGCCGCATGCAGGGTTTGGTCTTGGGTTTGAAAGGCTGG
TGAGCTGGGTTGGAGGGATTGACAATGTGCGAGAATGCATCGGCATGCCTCGGTGGACTGGGAGAATGAT
TATG
>lcl|Query_208731:22646-23071
ATGCTCCTTCGCAGGTTATACTCGACTGCTGCACATCCTGCCAGGTTCAAACTACCGCCGACAATCAAAC
AGGTGCTTTCAGCTAATGGCAGCGAAAGTTCAGCGACATCAGTGACTGGCTGGATTAAATCTATCCGTAA
ACAGAAAAACATAACCTTCGCTGTAGTCAGTGATGGTACAACACCAGAGGGCCTGCAAGCAGTTGTGTCA
AAAGAACAGGGTACTTCCCCAGAAATGTTGAAAAGGTCAGTTCATCTCTCACAGCTCGAAACCGGAACAC
TCACCAATTGAAGACTTACGAACGGTACAGCAGTGCGGCTCACAGGAAATCTAATTCAGTCTCCTGGCCG
AGGTCAAGAATGGGAGCTTGTCATTCAAGAAGGTGACAAGAACGCTATCGAAATCCTCGGCGACTGTGAT
ATTGAC
>lcl|Query_208731:c22559-22323
ATATCACATTCAACATCCAGGGTAATGACATCGCCATGTCGCTAGACAGCGTCGACAATGACTTCCAAGA
AACACTCGTTCCCATCTCCACTGGAATCTCTCTGGAACTCGATCTTATCAAACCCCGTCAACCGCAAGAG
CAAGAGTCCAAACTAGCAATCTGTCTTCACCCCTGGTCTCGACTCGGAGGACGCAAAAGCGACCCGTGCG
GTGTCTTATTCCACGAGCTCAGGTCGA
>lcl|Query_208731:c23949-23902
CACGAACACTGGTCCACCAACGTACACCTCTGCCAGCCAACGTTCATG

obviously I am new to this :)

This sounds like a homework question, although your previous posts perhaps suggest otherwise. In any case, you should give us a bit of background. Where did you get what looks like an accession number (that I can't find on the internet) and these sequences (which I can) — why the Query annotation? Have you searched the internet for methods to compare an unknown sequence with known ones. We can tell you, but our homework policy would have you try yourself first.

I'm just a software developer having a little dabble to see what I can get to. It is indeed a button mushroom gene.

I personally do not find the second part with the queries helpful without greater context.
The first part appears to be an accession number (more information on these can be found here: https://www.ncbi.nlm.nih.gov/Sequin/acc.html). By going to NCBI (https://www.ncbi.nlm.nih.gov/) and searching that accession number, you can get a lot of information quickly and easily.  Searching this particular number shows it to be a Asparagine-tRNA ligase from the fungal genus Leucoagaricus (https://www.ncbi.nlm.nih.gov/protein/KXN84633.1/).
If you simply have a DNA or protein sequence and no accession number, you can perform a BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi).  This will search your sequence against a massive database of annotated DNA or protein sequences. The specific type of BLAST to run and the ideal parameters will take some reading on your part to determine.  However, if you're just starting out, nucleotide BLAST for DNA sequences, protein BLAST for protein sequences, and default parameters will often suffice. This search will provide you with the best "hits" to the database which you can then follow up on to get an idea of the function of your original sequence.

thank you, that may do the trick.


text:
Do dead bivalves always float in water?
This 2014 Oct 14 article by Jolene Bouchon avouches:

How do you know if your bivalves are alive? Immediately get rid of anything with broken or damaged shells. Clams and mussels shells should be slightly open, and should shut quickly when you tap on them. If they're closed, don't shut, or float in water, they're dead. Introduce them to the trash. Oyster shells, on the other hand, should be closed tightly. And, as with all fish and shellfish, your bivalves should have a fresh, oceany smell with no hint of fishiness or ammonia.

Screenshot below hails from 0:15.
Jasper White avouched the opposite on Epicurious.com

When submerging the steamers in the water, watch for any that float—this means that they're already dead and should be discarded. (Note that when preparing mussels, the opposite is true: They clamp shut tightly, trapping air in the shell, and therefore should float when alive. Discard any that sink.)

So who's correct, and why?

You may have better luck on the cooking stack.

Do they close is a better predictor.
before cooking tap the bivalve if they remain open do not cook or eat them.  Unresponsive bivalves of any kind not safe to eat are dead and there is no way to tell for how long. Whether they open during cooking is meaningless for mussels they can stay locked tight even if healthy and freshly killed.  Smell is also a good predictor never eat shellfish that smell off.
The differences between wild and farmed mussels makes this even less useful, wild mussels may be filled with sand making them heavy even if dead. Of course if a mussel is comes pre-cooked only smell is useful.
float vs sink is not really useful since it relies on how tightly sealed a bivalve is and whether it trapped air when it closed. A air seal is not a guarantee with many bivalves, mussels included, nor is trapped air. It is just not a useful metric.


text:
Effectiveness of feces as a fertilzer
How effective is feces such as cows, chicken or horses for fertilizing the earth of a garden in order to grow crops.

What crops are we exactly talking about and what feces are we exactly talking about? It mostly depends on those plants' chemical needs and the chemicals in the feces of those animals (and the chemicals present in the soil where that plant is located, and even the current growth stage of the plant).

I am thinking about staple food crops such as carrots, potatoes, cucumbers or yams.

How do you measure effectiveness?  Consider that people have been doing it for probably thousands of years, and still do so today.  Or walk around a cow pasture and notice how the grass grows far more lushly around each cowflop.  Or read throught the 30K or so hits on Google Scholar: https://scholar.google.com/scholar?hl=en&as_sdt=0%2C29&q=effectiveness+of+manure+as+garden+fertilizer&btnG=

It depends largely on the crop there are many papers about it.  You will have an easier time searching for manure instead of feces. https://tropicalsoybean.com/sites/default/files/Comparative%20effectiveness%20of%20cattle%20manure,%20poultry%20manure_Ghosh,%202004.pdf and https://scholar.google.com/scholar?hl=en&as_sdt=0,31&q=effectiveness+of+manure+as+fertilizer

Thank you, I will read into this further.

Horse manure allows the propagation of the plants etc that horses eat as they do not process the seeds.


text:
Can anyone identify whether or not these are bird or rodent mites?
I found these on my patio furniture directly under a bird's nest that has hatchlings. Surrounding landscape is ivy so we do have raccoons and mice in the area.

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

As you'll notice from the answers to my linked posts, "a clear detailed shot is needed to ID this specimen confidently... In most cases identification of Mesostigmata to family or lower can be accomplished only if the specimen is an adult female."


text:
A little help understanding DNA supercoiling
I am studying molecular biology from Lewin's Genes XII and got confused in the supercoiling topic. Since then I read from several other sources and so far understood the following. However, I can't seem to connect the dots. A bit of help in connecting the dots would be greatly appreciated.
So these are the stuff that I understand so far

Supercoiling is coiling of already coiled double helix
Positive supercoiling overwound the DNA (increase the number of turns thus decreasing the number of base pair per turn making it more twisted)
Negative supercoiling underwounds the DNA
Linking number is the sum of twist and writhe, twist is basically number of turns and writhe refers to the number of supercoil. It remains constant as long as phosphodiester bonds are not broken
unwinding DNA at replication fork results in positive supercoil downstream

Now coming to the confusion

In the diagram we can see that negative supercoiling has taken place. Twist value has gone up and to compensate that (to keep the linking number constant as no phosphodiester bond has broken in this case of cccDNA) six negative supercoils have been introduced.
All the books clearly mention that negative supercoil is something that underwounds the DNA resulting in less turns with more base pair per turn. But in this case it is clearly seen that the number of turns have increased (from 36 to 42) and to compensate that -6 supercoil is introduced. So here negative supercoil has resulted in over wounding instead of underwounding
similarly, from the linking number equation > Lk = Tw + Wr, If there is positive supercoiling (i.e., Wr is positive) the Tw (twist value) will go down to keep linking number constant. So, the statement saying positive supercoil wound overwound the DNA is not matching at all. shouldn't positive supercoil increase the Tw as well (I understand mathematically it is not possible because then linking number would change, but all I'm saying is that I fail to connect the concept that says positive supercoil overwounds the DNA (more twisted) with what I see in the equation i.e., twist number drops and only writhe goes up.

After studying this topic a bit more I came to the conclusion that supercoiling itself does not overwound/underwound the DNA any further that it already is. Supercoiling just relieves the stress introduced after DNA gets further twisted in the first place, it relaxes the DNA by decreasing the twist back to normal (10.4bp per turn just like normal relaxed B-DNA) (in case of positive sueprcoiling and vice versa for negative) and the extra tension that made the DNA twisted in the first place now increases/decreases the writhe for positive and negative supercoiling respectively. The authors might have considered a DNA molecule with higher writhe value also a more wounded form of DNA that's why they used the term 'overwound'
Please correct me if I am wrong


text:
How many kangaroos would you have to add to a northern climate before they could start adapting to it?
If some enterprising billionaire wanted to introduce Kangaroos to a northern climate such as the northern boreal forest by Fort McMurray in Alberta, would it be possible for the Kangaroo's to survive and adapt to that climate creating a new super kangaroo (which will henceforth be known as the polar-roo)?
How many kangaroos would have to be dumped into the boreal forest before we would have enough to reach the critical mass that some of the kangaroos would be able to adapt and mutate to this new climate and conquer the north?

Welcome to Biology.SE! While interesting your question doesn't fit the criteria for questions on this site — specifically this question is extremely speculative and consequently no definitive answer is possible.  ——— Please take the time to go through the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

You seem uncertain of the plural of kangaroo. Stick with the oos — oo’s would be possessive.

Do we know that kangaroos wouldn't adapt perfectly well to a northern climate?  (Or let's say a cooler one, since Australia is in the southern hemisphere.)  It's not as though they have any chance to naturally experience such climes, or migrate to them.  There are kangaroos in Tasmania, which is about as far south as they could get without building boats.

Thanks for the suggestions! I have fixed the plurality of the kangaroos in my question.

there are (probably still) feral wallabies in the Peaks district http://www.roaches.org.uk/wallabies.html . Not boreal forest by any means, but at least northern hemisphere ...  (I definitely agree that answers to this Q are going to be opinion-based, though)


text:
Which are more beneficial: lyophilized or hydrolized collagen peptides?
Looking at two different manufacturing methods for collagen peptides: hydrolyzed vs lyophilized (freeze dried), I read that hydrolyzed results in a hydrophobic biolayer molecule collagen peptide.
Re: https://www.quora.com/What-is-the-difference-between-hydrolyzed-collagen-and-natural-collagen

There is a big difference between types of collagen or natural
  collagen available on the market. The main collagen sold is cheap
  hydroyzed collagen, which is produced by extreme heat. And the
  opposite end of the scale if lyophilized collagen which is freeze
  dried and more delicate expensive processing. The collagen known as
  natural collagen retains its triple helix and is an active collagen
  very similar to that of humans. This natural collagen is derived from
  fish skins of fresh water fish like silver carp.

Lyophilization process:  https://www.rdmag.com/article/2017/03/lyophilization-basics
While this may be quickly absorbed through the GI tract, thus "FASTEST ABSORBENT", does this hydrophobic biolayer hinder hydrolized collagen's ability to be broken down into amino acids - which is what we want out of them, right?  Or is it that lypholization retains its triple helix?
I'm not entirely clear on all the terminology, but essentially I would like to know which one is actually better and used by the body, rather than marketing "fastest absorbed by the body".
Additional reference:

US National Library of Medicine National Institutes of Health - lyophilization vs hydrolyzed collagen
Collagen Type I, salmon

If down-voting, please provide a reason.

Please do not continue reposting the same question. You should instead edit questions to preserve their history.

I changed  the question

Is anyone actually interested in answering the question?

"Hydrophobic bilayer" is not related to collagen supplements but to cell membranes, in this case, apparently to intestinal cell membranes. That part is confusing, so if you do not know where you have read it, I suggest to remove that.

I have found no evidence that lyophylization of collagen "retains its triple helix." And even if it does, this is not important for its effectiveness, because collagen needs to be digested (broken down) into individual amino acids or peptides before absorption, which means that any triple helix would be be gone at that point.

The first step in digestion consists of degradation of hydrolyzed
  collagen to form dipeptides and tripeptides or free amino acids.
  Several proteases (eg, pancreatic proteases, small intestinal
  brush-border proteases, peptidase) are involved in the degradation
  process (Clinical Inteventions In Aging, 2014).

The point of lyophylization colagen is not to improve its digestion or bioavailability, but to extend its shelf life.

Lyophilization enables longer shelf life, often as long as two-five
  years and makes it much easier to transport the product. In addition,
  products can be stored at room temperature  (rdmag.com).

You can also see that "hydrolyzed" and "lyophilized" do not exclude each other, because "Lyophilized Collagen Hydrolysate" is being sold.


text:
In Griffith's experiment, if both S and R strains are added, can the R strain be isolated from the blood of the mice?
In Griffith's experiment on transformation, when both the S strain and the R strain were injected into the blood of the mice, could the R strain be isolated from the blood of the dead mice?
I think it's not possible as R strains are deactivated by the immune system of the mouse, but Wikipedia says both R and S strains were isolated from the dead mice.

What is your question?

whether live r strain can be isolated from blood of the dead mice in griffith's experiment when injected with both virulent s strain and non virulent r strain

It would be nice if you could start sentences with a capital letter, and also use capital letters for people’s surnames. Question marks are needed after questions. If you did this it would show that you had made an effort in constructing your question and encourage us to answer it.

I have a suggestion if possible read the Griffith's experiment from Benjamin Peirce..

S starin have capsule and cause infection.
R starin have no capsule and not cause infection.
According to griffith experiment S strain was killed by heat but R starin remain active, because S strain provide genatic information R strain. Then R strain use information to complete own structrure and reproduce itself.


text:
What is the biological advantage of bilaterity?
I was wondering why there were so many bilateral species (under the bilateria clade) in comparison with the cnidaria clade. I have two or so questions:

Am I (or are we) unaware of the diversity and population of the cnidaria clade, so I can't say that bilaterity seems to be prefered by the natural selection?
Is bilaterity an advantage only on earth and not in water (where I think most of the cnidaria clade is (jellyfishes)).
If the answer to the last question is true, why is bilaterity an advantage on earth and less an advantage in water, and why is the contrary true for "unilaterality" (I don't know what is the word to describes the cnidaria clade).

Thanks!

Welcome to Biology.SE! Interesting question and I look forward to seeing what answers you get, but unfortunately I suspect it may not be answerable. ——— Jellies have radial symmetry.  ——— You may want to take the time to check out the [tour] and then the help pages starting with [Ask] effectively questions on this site. Thanks!

keep in mind cnidaria are bilaterally symmetrical, they are just symmetrical in other ways as well. Then you have sea cucumbers which may have evolved bilateral symmetry twice independently.

Bilateria, as a clade (all animals, excluding sponges, cnidaria, comb-jellies, and placozoans) is monophyletic, and as such, originated from a single species that was bilaterally symmetrical. Sometimes the explanation for a particular trait involves ancestry, and if an innovation is advantageous, it tends to spread. Along with this group came advances in the central nervous system, and digestive systems. It is advantageous to put senses up front, in the head, with the mouth. Having a tube-like digestive system, with a mouth at one end, a gut in the middle, and an anus at the other end, turned out to be efficient. Cnidaria (and other non-bilaterians) are not nearly as diverse as bilaterians, and most bilaterians are marine. So the bilateral advantage holds both in water, and on land.


text:
Effects of mushrooms on their hosts
I learned that mushrooms are normally classified as either decomposers or symbiotes. I would like to know the differences between the two types and whether they are detrimental or beneficial to their host, often a tree.

where have you looked for answers so far?

I have read an article (https://sciencing.com/role-fungi-play-food-chains-13253.html) and their separate wikis.

They are saprophytes/ saprotrophs / parasitic / symbiont. Of type.

It probably makes sense to classify mushrooms (fungi) in two separate ways:

symbiotic vs. free-living: symbiotic organisms are those that live in close association with a host (etymologically sym="with", biosis="life"), free-living organisms don't.  So a mycorrhizal fungus that lives within or on the surface of a plant root is a symbiote; a fungus that lives in the soil is free-living.
mutualistic (benefiting from and benefiting a host) vs. parasitic (benefiting from but harming a host) vs. saprotrophic (consuming already-dead material; these are your "decomposers"). (Commensalism [benefiting from, but neither hurting nor harming, a host] is  a fourth possibility.) Mycorrhizal fungi are generally mutualistic. Fungi like chestnut blight or the genus of phythophthora, which includes the organism that causes potato blight, are pathogens; so are the myco-heterotrophs. Fungi such as wood-decay fungi are saprophytic.

To answer your question, species of fungi that are associated with trees may be either mutualistic (e.g. mycorrhizal fungi) or parasitic (e.g. chestnut blight).

Parasitic fungi might also be called pathogenic (i.e., disease-causing)
In popular speech, "symbiotic" is synonymous with "mutualistic" (i.e., organisms that benefit each other); in biology, however, it may refer to either a parasitic or a mutualistic organism. An individual symbiotic organism is often called a "symbiont".
In general, saprotrophs would be free-living (since they don't get their resources from a host, it doesn't really make sense for them to live on a host)
Individuals of a some fungal species can switch lifestyles/categories depending on their environment: these are called facultatively mutualistic/commensal/parasitic, e.g. see Redman et al. 2001.

Redman, Regina S., David D. Dunigan, and Rusty J. Rodriguez. “Fungal Symbiosis from Mutualism to Parasitism: Who Controls the Outcome, Host or Invader?” New Phytologist 151, no. 3 (2001): 705–16. https://doi.org/10.1046/j.0028-646x.2001.00210.x.


text:
gene manipulation books for beginners
Are there any introductory book to explain gene manipulation in yeast for non-biologist?
I had a look at this book and now I have some ideas. I like to read another book at the same level which is more applied/practical. I find this book chapter useful too, but I find it a bit more difficult to follow. Also video lectures are appreciated.

What do you mean by gene manipulation? Do you want protocols for yeast transformation?

For example, as I understood there is a plasmid which is a circular DNA. We introduce this plasmid to yeast so that the plasmid with its marker replace the desired gene. To achieve this we need to look at the flanking side of the gene to be deleted. So the plasmid must have these flanking parts. But how do I design the plasmid in for example snapgene software and how do I construct the plasmid say with PCR or other methods? After I make the plasmid then I can follow some protocol to do the transformation.

I think the information you are looking for would be contained in a genetic engineering book. not only for yeast but all eukaryotic and prokaryotes cells. I'm afraid that there will not be a book on that topic for a non-biologist but the topic is usually covered during Bachelor/Master studies.

I think that the information you are looking for could be covered on this website:https://www.addgene.org/protocols/
Not only has addgene a protocol section, it also has an education section for understanding the concepts of genetic/molecular cloning: https://www.addgene.org/mol-bio-reference/
The material is for biologist, but should be relatively easy to understand for you are starting.
They also have a nice ebook which should cover some of the topics you asked: https://info.addgene.org/download-addgenes-ebook-plasmids-101-3rd-edition
Hope that helps!