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Focusing on flowering plants, are there reasonable explanations why pentaploids would be more fertile than triploids?
For the genus Rhododendron, triploids are sometimes fertile but pentaploids appear to be often fertile. Once Rhododendron seedlings gets above the triploid level, aneuploids not near euploid appear to become more viable at least in greenhouse situations. What mechanisms best explain this increase in fertility of odd ploidy and viability of aneuploids as ploidy levels increase?


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What is the effect of antibiotic chloramphenicol on bacterial size?
When low amounts of antibiotics like Chloramphenicol is added in a bacterial culture, the steady-state growth rate decreases but what happens to the steady-state size? Can anybody please refer me to any paper that comments about the effect of these antibiotics on the size of bacteria (or yeast)?

There's this, but it's about a protist.

Thanks @canadianer for the prompt reply. It will be very helpful if I could get some references for bacteria/yeast as well.

Please can somebody help urgently? Thanks

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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There are 6 classifications of CFTR mutations. Is a causal relationship to the sweat test known?
Cystic fibrosis (CF) is caused by mutations in the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR).
The CFTR mutations are classified in 6 classes.
The sweat test is used to screen for CF. With the following boundaries:

<= 29 mmol/L = CF is very unlikely
30 – 59 mmol/L = intermediate possibility
=> 60 mmol/L = CF is likely

Can I make assumptions from the sweat test in which category a patient may belong? Or can I even make assumptions about a specific mutation?

The results of the sweat test are due related to the total abundance of functional CFTR protein in the plasma membrane, so different classes of mutation that similarly reduce the total amount of functional CFTR would have similar sweat test results.

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How to interpret Percent identity matrix created by Clustal Omega?
I did a multiple sequence alignment using Clustal omega. checked similarity for 3 protein sequences : aspartyl aminopeptidase [Homo sapiens], aminopeptidase P (APP) [Plasmodium falciparum 3D7], yeast aminopeptidase (S000001586)APE1. I got Percent identity matrix as
Percent Identity  Matrix - created by Clustal2.1
 1: PF3D7_1454400              100.00   16.18   20.35
 2: gi|5902181|gb|AAD01211.2|   16.18  100.00   29.66
 3: S000001586                  20.35   29.66  100.00

My doubts:

I would like to know how to interpret this matrix result
Coming back to sequence alignments results, when I click on 'Show colors', the alignment summary is colored in 4 colors - red, green, blue and pink. Can anyone help me in decoding the color reference of alignment summary?

Thanks

        Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2  16.18    100.00     29.66
Gene-3  20.35     29.66    100.00

Gene-1 and Gene-1 have 100% similarity (and all the other diagonal elements). Gene-1 and Gene-2 have 16.15% similarity, and so on. Therefore the matrix is symmetric M(i,j) = M(j,i).
You can also show just the upper triangular part of this matrix and that would be sufficient.
        Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2           100.00     29.66
Gene-3                     100.00

The colours basically denote the type (molecular nature) of residue. Have a look at this.

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What kind of spider is this? (Photo included)

We found this guy on the ceiling inside today. We live by Lake Erie in Ohio so we see a lot of large spiders, but this one looks different than most we encounter. It's was about the size of a quarter (~ 25 mm), and the abdomen was iridescent.

Not a spider person but I did find this useful summary of commonly encountered Pennsylvania spiders, a few of which are similar-looking.

It looks to me like a false widow spider, Steatoda grossa. It would be helpful if you could find one in their web so I could see what its web looks like.

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What is the DNA sequence of an apple?
I read that the genome for Malus Domestica was mapped, but I can't find a sequence anywhere.
If this is a stupid question, I would appreciate if you would please tell me where I am wrong in this!

Googled "malus domestica genome sequence". First result was this paper, which includes this genome bank entry (which is also the second search result)

@Luigi Thanks, but I don't know how to make sense of the genome bank entry

If all you want is to download the sequence of all the chromosomes, look at the haplotype assembly. Download the first file (psuedomolecules) and unzip it. Then you'll have the sequence of each chromosome in FASTA format.

https://www.rosaceae.org/species/malus/malus_x_domestica/genome_v1.0
You can see the data in the URL above. The details are described in this article.
As others said, NCBI seems useful.
Go to this site.
Chose chromosome you want to see and click genebank or refsequence corresponding to the chromosome in the table (Assembly Unit: Primary Assembly).
You can see overview of the sequence.
Find FASTA in the page showing the overview and click FASTA. Then the sequence data will be downloaded.

Thank you, I had a look at the above link, but I'm still not seeing the DNA nucleotide sequence.

The sequence data is shown like https://www.rosaceae.org/gb/gbrowse/malus_x_domestica/ You might be able to extract sequences from this. But I have not used this particular site. At least, you can see the conting sequences indicated in red by clicking the red areas like https://www.rosaceae.org/gb/malus_details?id=1311210

Thanks for your help. I used the DNA database at http://www.ncbi.nlm.nih.gov/ to find the answer

Here is the apple genome on NCBI.
http://www.ncbi.nlm.nih.gov/genome/?term=Apple

How many lines of nucleotide sequences are there?

Are all sequence lines necessary?


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What were fed to the rodents in Calhoun's experiments?
From, (https://en.wikipedia.org/wiki/Behavioral_sink) (https://en.wikipedia.org/wiki/John_B._Calhoun) (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1644264/)(https://www.gwern.net/docs/sociology/1962-calhoun.pdf)
As I see, Calhoun does not say what they fed to the rodents. I suspect that they might be foods without all the essential nutrients in enough amounts.
I suspect that answer to this question is not published, but may be found by staff in the institutes where Calhoun worked.
There is a nutrient that can deсrease slowly over generations, omega-3 fatty acids: see google's translation from https://znatok-ne.livejournal.com/86130.html :

During the period of intensive brain formation during fetal development, the human fetus receives DHA from the mother's body. In this case, the placenta selectively absorbs maternal DHA and transfers this PUFA to the fetus. For example, the transfer rate of DHA across the placenta is three times higher than that of ARA (Lauritzen et al., 2001). Due to the intensive and selective transfer through the placenta, the content of DHA in the mother's blood plasma is reduced by half (Broadhurst et al., 2002). We found a similar phenomenon in fish: during the gestation of eggs, which have an extremely high level of DHA accumulation, the content of this acid in the muscles of the fish almost halved (Sushchik et al., 2007). During the period of breastfeeding, the mother's stores of DHA also continue to be depleted, as this PUFA passes into breast milk (Lauritzen et al., 2001). DHA from the blood is selectively absorbed precisely by the cells of the brain, as well as the nervous system and organs of vision (Bazan,. The cells of these organs are able to retain the "captured" DHA for an extremely long time, ensuring its constant concentration. For example, in order to reduce the content of DHA in the brain and retina in rodents need to be kept on a DHA-free diet for two generations (Bazan, 2009).It is believed that the same effective conservation of DHA is characteristic of the human brain (Lauritzen et al., 2001).However, according to some estimates, in the human brain as a result metabolism consumes 2-8% of DHA daily, and these losses must be replenished by the body (McNamara, Carlson, 2006).

What leads you to suspect that?

@JiminyCricket. it is not published together with the 2 linked articles. i have searched https://eprints.lse.ac.uk/22514/1/2308Ramadams.pdf for "criti" and "food" and i have not seen anything about critiquing about the food.

I don't see any reason to think they were fed anything other than the standard rodent chow used in the labs at the time; the second link notes "hard pellets of food" which is the typical form of this feed.
If this food were short of essential nutrients you would expect that all lab rodents, regardless of housing condition, have the same deficiencies. It seems very unlikely to me that this would be overlooked across all studies of lab rodents. In any event, as all animals in the experiment were fed the same food, it's unclear how the results of population density could be explained by some sort of nutritional deficiency, since those results are about different behaviors at different densities while the same food is used for all.

"it's unclear how the results of population density could be explained by some sort of nutritional deficiency, since those results are about different behaviors at different densities while the same food is used for all" - i have added explanation about it to the question.

@qdinar Okay, except your argument has nothing to do with population density.


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Garden Mushroom Identification

Could someone please identify this mushroom?
Found in a garden situated in a mild Western European country.

Looks like shaggy ink cap, Coprinus comatus, to me.
Blacksmith37's answer suggests that shaggy mane is the usual common name. I hadn't heard that name until I looked at the Wikipedia page. In the U.K. it is shaggy ink cap, inkytop, inkhorn or lawyer's wig.
Update
This is a good general source of information. Also comatus (Latin) means hairy.

I think the more common name is Shaggy Mane , related to "inkies" and "micas". It is too old to eat when it gets pink, then black liquid. In the Midwest US they come up early spring and fall in the same spots. .... Sorry,I meant to imply that was the name in the US. It is a good beginner mushroom ; hard to confuse with anything poison.

Re: "too old to eat" (or rather, the implied inverse). The standard disclaimer applies: Never rely on identification from random people on the internet to determine if a mushroom is safe to eat. Also, never consume any mushroom you're not 100% sure is edible.

^^ from the wikipedia article on the mushroom: "The mushroom can sometimes be confused with the magpie fungus which is poisonous."

So... Does the goo actually act as a stable pigment?

@TheNate No - in fact the inkcap fungus is unusual, in that if it is harvested, or after it has shed its spores, the whole "cap" turns into black goo and auto-digests itself! But they are good to eat if they are picked young and eaten as soon as possible after picking.

By the way, don't eat this mushroom and consume alcohol. There is a substance in the mushroom (marketed as drug under the name Antabus) causing a prolonged hangover.


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What is this plant with some seeds around its leaf?
I am in India, This plant is growing on floor with very less soil
on it. I took 3 pictures of the same plant, It just rained yesterday.
I didn't see any insects around this plant. here is it:

Third picture is this: http://i.imgur.com/vxxCJos.jpg

It is Andrographis paniculata also know as Kalmegh or Kalamegha

It has close resemblance to Mexican Tea Plant also.


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Medical term for "holding urine for a long time"
Sometimes I get/feel pain in my stomach because of holding urine for long time. Is there any medical terminology describing: "holding urine for a long time", or pain associated with this activity?

Holding in feces for a long time is called "stool withholding". I don't know if there's an equivalent term for urine. In future, consider posting such questions to http://health.stackexchange.com instead. Why do you hold your urine in? Are you a schoolteacher or a bus driver? It's not the wisest move to hold your urine in for a long time; it carries risks.

A swollen organ may be described as distended if the swelling is symptomatic of a medical disfunction.
The purpose of most bladders is to collect and retain a fluid; if that fluid needs to be discharged periodically, and is not able to do so, then there is usually pain as a result of the distension.
Inability to urinate is known as ischuria or urinary retention, and could be the result of obstruction to the urethra, could be a failure of the bladder to fully contract during urination, or could many other possible causes.


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Picture of spider for identification
Would like to get spiders identified . Specimens can be sent for detailed examination if required .

Spider seen on floor inside house - at Phoenix USA

White off color spider on twigs and flowers of oleander tree with white flower in backyard of house at phoenix USA  - seen dropping off on disturbance and camoflouging with. White flowers. Picture can be magnified spider sitting on green stalk  below brownish dried flowers.

It is advisable to post one question(here specimen) a post.

The first is a male Theridiid, probably Parasteatoda tepidariorum (see below)

https://bugguide.net/node/view/1320395/bgimage.
The second is one of the "flower spiders" in the Misumena/Misumenops/Misumenoides/etc. group of Crab Spiders.  It would take a better photo to get closer than that, since this is a young female and isn't showing the color marks that make it easier to ID.  There's a hint of patterning on the abdomen, but it isn't clear enough to ring any bells with me.  In a comment below, I'll include a link to the Bug Guide page for these spiders so you can look at it - the relatively useful marks for field observation are the greenish bands (if any) on the sides of the cephalothorax, the 'mask' (if any) over the eyes, and the pattern (if any) on the abdomen.  Also, the reddish 'racing stripes' on the sides of the abdomen of fully adult females can be helpful in working out which spider it is.  I suspect that for most of us, most of the time, "Flower Spider" is going to be good enough.

Here's the link.  I'm not inclined to favor any particular species, offhand, without a better look at the abdominal pattern that appears to exist.  https://bugguide.net/node/view/1957/tree  My best guess is that it's likely to be somewhere between Mecaphesa (unlikely) and Misumessus.

The trouble with these (and many other) spiders is that it usually takes a good look with a dissecting microscope to get a confident ID.  You could send it to someone for such a check, but I'm no longer current with active spider folks, and I can't suggest anyone offhand.  What you could do is to do a search on "thomisidae" "research" or "taxonomy" and see what pops up.  Check recent papers for the authors' names, and write off to one or more to see if they would help.  Good luck!

White one: Flower crab spider white, They can be all white or have purple or even pretty red stripes along the sides, kinda cool.

Thanks.  Kinda cool  .  Further I would like to know its scientific name . Else if someone can suggest the contact to send the specimen to know it's scientific name .


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What type of beetle is this?
I found this beetle in my yard. Wondering what type it is.


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Microorganisms in Louis Pasteur's experiment of beans
Louis Pasteur's experiment proves that microorganisms do not grow from non-living matter, he discovered that microbes can cause food spoilage.
So, where do microorganisms come from? Do they come from the environment?

So, where do microorganisms come from? Do they come from the environment?

Yes!
There is no spontaneous generations. Microorganisms (virus, bacteria, unicellular eukaryote, small multicellular eukaryotes) just like macroorganisms (big-enough to be seen by the naked eye multicellular eukaryotes) are not recreated out of nothing. Abiogenesis happened a long time ago and as far as we know, it is not happening today.
This means that if there is a micro-organism somewhere, it must have come from the environment. It did not pop up out of nowhere.

That is the biggest question to be answered in biology, as of today we do not know where microorganisms originated from. What is known is that they outnumber us by combined weight and population. There are some interesting theories of their origin, one is called "panspermia" which proposes that life might have seeded the Earth from other planets. And considering that some bacteria are capable of surviving extreme levels of radiation        (D. radiodurans), it is not unreasonable to think they could have achieved interplanetary travel via space rocks.

The question is not about the origin of organisms, but rather how it is that microorganisms become present in food to spoil it.

This is one of the questions "So, where do microorganisms come from?"

and that question is immediately followed by a more specific form of that general question: "Do they come from the environment?".  That shows the question is about the presence of microorganisms at the time of Pasteur's experiment, not hundreds of millions of years earlier when they originated.


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Caterpillar identification: Peru

Could you please help me identify this caterpillar (Amazon rainforest, Peru)?
Is it a species of Megalopygidae???

Did you take this picture? If so, could you provide more information about where it was found (e.g., on the ground, on a tree, etc.).

Yes - On the trunc of a living tree - During the day - Tamshiyacu Tahuayo Regional Conservation Area.

It resembles a Puss mouth or flannel moth caterpillar. The adult moth is beautiful and the bristles of the caterpillar are very irritating.. It does indeed belong to the Megalopygidae

It is an pink flannelmoth because there is no other insect which ressembles it

Usually pinkflannelmoths have orange coloured centers

The proposition that something is something because it looks like it is completely falacious. I could say that a person is an ape because they look alike. Perhaps it is an undiscovered species?

But with just one photo from the top view you can't expect the answer right

I do agree with your there


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How does the synaptic cleft exist?
I'm not asking why the synaptic cleft exists, i.e. what function it holds, rather how.
So I know that the neurotransmitter diffuses across it, it is 20-40 nm wide and contains basal lamina (in NMJs at least), but I cannot find any allusion as to what causes the gap; how the two membranes don't just touch, and how so consistent a distance is created across neurons.
Google has so far failed me on this one, though perhaps I am not searching well enough, any help would be greatly appreciated.

There are membrane proteins that act as structural components of the gap (i.e. the synapses aren't just floating there, they are anchored to each other via membrane proteins).
https://en.wikipedia.org/wiki/Neuroligin
https://en.wikipedia.org/wiki/Neurexin
The most common examples are neurexin (expressed on the pre-synaptic terminal) and neuroligin (expressed on the post-synaptic terminal). Not surprisingly, these proteins are involved in synapse formation in the developping brain, as well as the adult brain (in plastic processes where new synapses are formed). To a first approximation, as synapses are growing, their membrane proteins bind their partners and become anchored. This also leads to intracellular signalling and further maturation of the synapse. That's how synapses know where to attach.

Thank you very much this is a great answer and just what I was looking for :)


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Procedure for doing western blot
I am writing a step by step guide for doing a western blot for a class.  It is intended for any  one with basic Biology lab skills.  I am hoping people will review my draft and give feedback on how to improve it.  Be as critical as you like about any aspect of it, I need it to be clear and concise as well as accurate.  Any tips appreciated.
https://docs.google.com/document/d/1Lpprwn4s127cb0D5TQezpurbjdF9hqJZQC0H7PIovE0/edit?usp=sharing

Welcome to Biology S.E.! If you need any assistance, please visit The Help Center.

You don't mention using a rocking platform in your blocking step. It's important or else all this particulate will sediment. Also this isn't really a question


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Primer design for HLA locus
i have designed primers for HLA locus DPA1(exon 2 region) based on Real-Time PCR (qPCR) Primer Design guidelines. primer will start from intron regions to cover full exonic region.
F-CAGCAACAGAGAATGTCAGC
R-CCCTGAAGCAGCAATTGATG
to check for amplification of only a single region  i have used in silico PCR UCSC but it shows multiple region from chr6.
pls kindly help me with solving this.
thanks

Well the obvious solution is to redesign new primers that anneal elsewhere in the introns. Is it other HLA genes that are being amplified? Presumably you've hit a conserved region.

When designing rtPCR primers always check the extensive and well validated  taqman library for the ABI system, the primers for the region you want are already well characterized:
http://www.lifetechnologies.com/order/genome-database/details/gene-expression/Hs01072897_m1#more-information-section


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Why is amyloplast produced by some plant cells but not other cells?
For example I know it is produced in Potato's and fruits and its purpose is to synthesize glucose in to starch through polymerization. But why is it only present in some cells? Is it only present in cells with higher glucose content?

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Just a guess: fruits/seeds need starch for the nutrition of the seedling. For tubers I guess it is better to differentiate chloroplasts to amyloplasts in regions where there is no light exposure (chloroplasts won't be able to carry out photosynthesis). This differentiation is controlled by plant hormones and light exposure also has a role.

Amyloplasts are non pigmented organelles responsible for plant sugar storage, release and gravity perception (or tropism). This being the case they are commonly found in root caps (for gravity) and storage sites like tubers, fruits and grains.
So due to cell differentiation, it is not possible for these plastid organelles to be present in all cells the same way chloroplasts (another type of plastid) is not present in the stem (with the exception of small plants and succulents) and most of the root cells (Reece Urry et al, 2011).
Reference
Reece J.B., Urry L.A., Cain M.L., Wasserman S.A. et al (2011). “Campbell Biology 9th ed” Pearson Education, Inc., publishing as Pearson Benjamin Cummings, 1301 Sansome St., San Francisco, CA 94111.


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Optical density machine name
What is the name of the machine used to measure optical density? We used it in a lab but I can't remember what they called it.

densitometer? turbidometer? spectrometer? spectrophotometer? There are many such devices and some details on the type of experiment may help here.

Hmm I think it was the spectrometer. That sounds right. We where measuring the growth of cell cultures.

I'd bet the farm that it's a spectrophotometer.

Optical Density is synonymous with absorbance which is based on the principle of absorption of light. The machine that is used to measure absorbance is called a spectrophotometer. Spectrometer does not indicate that light absorbance is being measured. A spectrometer can measure any spectrum; for e.g. Mass Spectrometer measures the spectrum of molecular mass (to be precice mass per charge).
Cell density can be also measured by the level of light scattering; turbidimeters or nephelometers are used for these kind of measurements.
PS: You should pay more attention in your class :P

Also called a spec, for short.

When you use a spectrophotometer to measure culture density you are actually measuring turbidity/light scattering, not absorbance.


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Species ID from Hungary

I found it on the wall, it was calm for 15 minutes. Central Europe, Hungary. Never seen anything like this. I have two more pictures.

This appears to be a Gastropacha Quercifolia, the Lappet Moth.

It is found in Europe and Northern and Eastern Asia.
The wingspan is 50–90 mm. The females are larger than the males. The moth flies from June to July depending on the location. Source


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In (human) zygote cell differentiation, do we know how the cells coordinating the process know their current position?
I've seen this question asked in a mature person -- e.g. lip cells will create more lip cells -- but how about in the developing zygote.   I've seen neighboring cells help determine the type of the new cell. Do we know how they know where they are located, and how many cells of a certain type have already been made, making "lips" complete, or teeth, etc.  So in summary:
1) how do the cells in the growing zygote know "where they are", assuming they need to, to determine what cells to build where for the body?
2) how do the cells know, when the cells of that type building a bone or lips or teeth, etc, are done, since obviously many participate in the process. ?

Can't put up a detailed answer right now, but this link might help for you and anyone else who wants to answer. http://www.popsci.com/body-electrician-whos-rewiring-bodies

This answer may interest you.

There's a protein called Bicoid in fruit flies (see https://en.wikipedia.org/wiki/Bicoid_%28gene%29) that determines the head/tail axis. I remember from biology class that there's a similar protein that determines the up/down axis as well, although I forget its name.
There's almost certainly something similar in humans.


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What causes leaves to be hydrophobic?
In my garden, I'm growing broccoli. I was spraying it with water the other day, and I noticed that water bounced off the leaves. When I just misted it instead of a full-on spray, the water beads collected, but stayed as beads instead of spreading out. Some of them bounced off, but some accumulated. So what makes that happen? I know the leaf is hydrophobic, but I haven't found by searching Google if there's a coating of some type on the leaf or if it's something else that's making it hydrophobic.

This is due to presence of a hydrophobic chemical called as cutin present at the the aerial surfaces of plants.

Cutin is one of two waxy polymers that are the main components of the plant cuticle, which covers all aerial surfaces of plants. The other major cuticle polymer is cutan, which is much more readily preserved in the fossil record,.[1] Cutin consists of omega hydroxy acids and their derivatives, which are interlinked via ester bonds, forming a polyester polymer of indeterminate size.

Source: https://en.wikipedia.org/wiki/Cutin

While your information on Cutin is correct, the effect described by the OP is due to extracuticular wax, not cutin itself. It is actually quite fascinating how long the nature and microstructure of these waxes and their relation to hydropobic surface effects was ignored. It's worth checking out the webpage of the research group working on the Lotus Effect: http://www.lotus-salvinia.de/index.php/de-de/ .


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Digestion of milk in humans
The intial step in the digestion of milk in humans is carried out by which of the following enzymes?
A) lipase.
B) trypsin.
C) rennin.
D) pepsin.
I'm confused between the C and D option. as it's not specified whether they're asking about adult humans only or humans in general (where infancy also included), which between pepsin or rennin will be the answer for this question?
I know that in infants the milk digestion is initiated by rennin and in case of adults due to its absence it's carried out by pepsin. Which is the correct option for that question?

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

Short answer
My best bet is D)
Background
A) seems incorrect as lipases break down fats. However, one has to realize there quite some fat in milk (up to 3.5% in untreated milk). Digestive lipases in man are secreted by the pancreas into the duodenum.
B) Might be a correct answer, as trypsin is released in the small intestine and...

[Trypsinized] peptide products are further hydrolyzed into
  amino acids via other proteases, rendering them available for
  absorption into the blood stream. Tryptic digestion is a necessary
  [first] step in protein absorption as proteins are generally too large
  to be absorbed through the lining of the small intestine.

C) Chymosin, known also as rennin, is a proteolytic enzyme synthesized by chief cells in the stomach. Its role is thought to be in digestion is to curdle or coagulate milk in the stomach, a process important in young animals. If milk were not coagulated, it would rapidly flow through the stomach, impairing protein digestion. So this is a enzyme in the stomach and active earliest in the digestive system (answers A and B concern enzymes in the duodenum, which is later down in the digestive tract). However, in humans there is only a chymosin pseudogene present, and since the answer specifically deals with humans, answer C) is incorrect.
D) Pepsin is

...[] one of three principal proteases in the human digestive system, the other two being chymotrypsin and trypsin. [These] enzymes [...] break down dietary proteins into [...] amino acids, which can be readily absorbed by the small intestine. Pepsin [mainly] cleav[es] peptide bonds between hydrophobic and [..] aromatic amino acids [...The other two proteases have different targets].
Pepsin's proenzyme, pepsinogen, is released [...] in the
  stomach [...], and upon mixing with the [...]
  gastric juice, [it is] activate[d] to [...] pepsin.

Here we have the adult equivalent of rennin, also active early in the digestive tract, namely the stomach. So D) is the enzyme present in humans (as opposed to C) and active already in the stomach (as opposed to later in the duodenum in answers A and B). So D is the answer.

https://www.physicsforums.com/index.php?threads/908437/  please do check this link.I agree with your short answer but the reason why pepsin seems to be contrary to what I learnt from the link that I quoted.Have a look at that link and come back here again to let me know your views on that :)

I did. https://www.physicsforums.com/index.php?threads/908437/. Did you?

you say chymosin is present in human infants. But chymosin wiki says humans don't have chymosin.they have chymosin pseudogene. So pepsin is the answer be it be human infants or humans is what I had learnt.

also see this please https://www.ncbi.nlm.nih.gov/pubmed/1455182 this supports my claim of no rennin in humans (infants and adults)

@user129402 - gotcha. This is on humans and they lack the chymsoin gene. Nice thinking!

@AliceD we should also remember that there are many proteins in milk other than casein, which are digested first by pepsin.

von Ebner's glands secrete lingual lipase. Perhaps option $A$) is a good idea?

Additionally, @notherHomosapien's answer here [  https://biology.stackexchange.com/questions/57531/what-inactivates-pepsin-in-infants ] indicates that humans do produce rennin (at least during infancy). Meh, this is confusing....I think I'm going to have to ask this as a separate question. I like how you took apart the question option-by-option in your answer. Good answer! O:)


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Why does abnormal mitosis takes place in the cells of tapetum?
I know that the tapetal cells present in the anther are binucleate. I also know this means that after karyokinesis the cell does not divide itself and instead form a syncytium.  This occurs due  to abnormal mitosis, but I don't find a reason for abnormal mitosis to occur.
What is the reason for abnormal mitosis to occur?


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Does "eating less" stimulate cell starvation?
2016 Nobel Prize in physiology or medicine was given for the study of autophagy.
Judging from the description, a healthy cell responds to starvation (and other types of stress) with autophagy.
Does starving of the organism for short amount of time (around a day) cause cell starvation? And, can we say that starving for short amount of time stimulates autophagy?

@MartinKlvana around a day


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Photosynthesis and thermosynthesis(?) in plants/organism
A while back I thought to myself: if plants could absorb the entire(or most of) light spectrum as opposed to a narrow range, would it be better/absorb more energy/etc. Recently i read that was not the case because any higher on the spectrum and it could knock electrons loose(or something like that) and any lower and it would generate heat instead. Also the article said that plants focus on specific wavelengths for photosynthesis, hence the colors.
If heat is the main issue, then is it possible to turn the heat energy into usable chemical energy? Potentially allowing plants to absorb a much larger range on the light spectrum? And if the plant could absorb heat as well, would it be cool/cold to the touch?

Theoretically it should be possible for an organism to use hat to produce a chemical that it can then use to make useable energy however at present we know of none that do this. If it is possible though it would allow for life in the warm, dark oceans of Europa and if life is not there already it would make it pretty easy to introduce life permanently to a planet like the moon Europa. However in deep sea vents types of anaerobic respiration are most effective and on the surface light is and so if any organisms ever did use thermosynthesis on earth they were probably outcompete do by other forms of energy production and forced to extinction.

Welcome to Bio. Could you add sources to your answer?


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Is the flesh of a fruit selected for the benefit of the sprouting seed or to attract the frugivorous seed disperser animal?
In a question about the low protein content in fruits, one answer suggests the energy, carbohydrate, and protein content in a fruit evolved to entice animal seed dispersers, not foster the sprouting seed.
Another answer suggests plants are made mostly of cellulose, hence why the fruit has more carbohydrates than protein. The implication here is that the content of the fruit is optimized for the benefit of the sprouting seed, which is constructing a plant, not an animal.
Both of the answers to this other question: Plant a whole fruit or only seeds? suggest fruit is all about dispersal.
Which is the correct explanation?
It seems like it would be an easy answer to prove experimentally: plant two seeds in nutrient-poor soil, one with its fruit whole, another with its fruit mostly eaten (or even entirely passed through an animal's digestive tract). Then see which seeds thrive better.
Obviously fruits cultivated for human consumption have had their evolutionary course commandeered for benefit of the frugivore. And to a lesser extent probably many plants have a symbiotic relationship with their seed dispersers. But is that relationship an enhancement of the primary evolutionary purpose, or an suppression?

worth noting it is a lot easier for a plant to make carbohydrates than proteins, that alone should make it mostly made of carbohydrates.

While I know you didn't mean this, it's worth clarifying there is no purpose in evolution, the fruit is what it is because that's how the various evolutionary processes such as natural selection and random drift have shaped it.
That said there isn't a known evolutionary mechanism for a fruit evolving in any other way than to benefit itself.  The only way I can think of in which the second option you suggest, that the plant does it explicitly to help the animal survive could be true, is if the animal surviving helps the plant in some way.  For example it is well known that some trees produce sugar water for ants to eat, and in exchange, the ants will attack herbivores that try to eat the plant.
Otherwise, the sugar is there to help the tree's offspring, but not how you think.  The plant's baby doesn't literally use the sugar in the fruit for itself.  Instead the plant offers the sugar to entice an animal to eat the seed.  The seed will then be deposited by the animal in pile of undigested nutrients in a place far away from the parent plant.  If the plant just dropped the seed below itself, it would have to compete with it's own child for sunlight, water, etc.  So instead the fruit offers the sugar to an animal to get the seed dispersed.  In this way, the plant must offer a benefit to an animal for it's own selfish interest.  But the seed itself will only use the nutrients on the inside of the shell casing, even if the fruit is never eaten and still surrounds the seed.

OP already understands all this (besides some imprecise terminology they could improve about "purpose"): they clearly are not suggesting that the fruit is anything but selfish, they're asking about whether the selection is for attracting distributors or feeding the new plant.

oh. lol. well, it's to attract pollinators, I've never heard it suggested anywhere the fruit is for the plant's offspring to use, that's typically considered the part only inside the protective shell.  It's called the endosperm: https://en.wikipedia.org/wiki/Endosperm


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What is synaptic bias?
In non linear model of a neuron there was a mention about bias (Bₖ) which was the summation of the synaptic weights.
I want to understand what synaptic bias is and their application/use in neuronal modelling.

Often artificial neurons are created with conventions that zero is "rest" and 1 is "threshold". The unit starts at 0, and when it reaches 1 it will send an input to all of its targets and be reset back to 0.
This isn't exactly how real biological neurons work, but its a reasonable approximation in some contexts (and can do real world computations).
Most of the inputs to a unit are variable, so you add some voltage to the neuron based on the synaptic weight. For example, one input with a weight of ".2" would move the cell 1/5th of the way to threshold by itself.
When people talk about a bias input, they are referring to an extra "always-on" input with a small synaptic weight. This can maintain a rest greater than 0 in a leaky integrate-and-fire cell; this allows for some more biologically relevant forms of inhibition (negative synaptic weights) to have an influence on the unit, by offsetting the bias input and pushing the voltage back to 0.
More often, I am familiar with using a bias input in networks that are not leaky. These networks just integrate until they reach threshold (although they may or may not get negative inputs). For these networks (or for a leaky network where the bias current is substantial relative to the leak), adding a bias input ensures that the network won't stochastically "fall asleep" due to a period of low activity. If the bias current is equivalent to ".02" units per cycle, for example, you would guarantee that the cell would fire once every 50 cycles with no other input.
There are some real excitable tissues that show similar behavior, but not due to a real bias input. Rather, there are intrinsic channels that slowly depolarize a cell. Some examples are in cardiac myocytes and the sinoatrial node making up the heart's "natural pacemaker", as well as in brain circuitry that controls breathing. The bias input is sort of a "made up" construct that is functionally, but not mechanistically, correlated with real biology.


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What is the difference between spidroin-1 and spidroin-2?
So I'm doing a research project for my school and I'm trying to decide on the exact nature of the project. My current plan is to try to genetically engineer E. coli or Yeast to produce spider silk protiens. However when trying to find an appropriate gene for my project I learned that the common house spider's silk has two different spidroin protiens. Just by a simple google search I can't tell the difference. So, what is the difference between spidroin-1 and spidroin-2

I've looked into literature on this. Wow, there is a lot of research on this. Here's a quick summary:
Functionally they are very similar. Both are fibrous proteins. Together they constitute spider silk. Sp-1 and Sp-2 are two different genes, often present in multiple copies in the genome, depending on which spider species you consider. They differ in amino acid content and are post-translationally modified differently. Sp-2, for instance, is heavily modified. There also exist different transcriptional isoforms of these proteins. It seems quite complex.
There are also different types of silk. You may be referring to major ampullate silk, which is only one of six different types of silk fibres spun by the spiders of the genus Nephila. Only this one contains major ampullate spidroin-1 (MaSp1) and major ampullate spidroin-2 (MaSp2).
Excerpt from one paper on the subject, which lists some differences:

MaSp1 and MaSp2 are large proteins of about 250 to 350 kDa that share
  a general domain architecture. Both proteins contain a large, central, repetitive domain that
  consists of approximately 100 tandem copies of a 30 to 40 amino acid
  repeat sequence. The consensus repeat sequences for both MaSp1 and
  MaSp2 are glycine-rich and end in poly-alanine motifs (usually four to
  seven residues long). For MaSp1, the consensus repeat includes (GGX)n
  motifs (where X = A, L, Q, or Y) and very low proline content. In
  contrast, the MaSp2 consensus repeat has significant proline content
  and characteristic motifs such as GPG and QQ.
  The repetitive domains of different spidroins display a relatively
  high level of amino acid sequence variation that has been implicated
  in providing the elasticity and toughness that is characteristic of
  the different fibers.

It is possible that different amounts of Sp-1 and Sp-2 are combined to tune the elasticity and toughness of the silk. I have no idea whether the mechanical properties of silk are changed by the spider to suit the context (e.g. elasticity in windy conditions, or whether the content changes seasonally in response to temperature differences). That would make for a cool research hypothesis.

Wow that was much more intense than I was expecting. I'd make my project about the mechanical differences but I don't have access to the appropriate machines.


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Recessive is Dominant to Dominant?
If a gene has for instance three alleles, p, q, and r, then could p be dominant to q, q be dominant to r, but r be dominant to p? Can a gene that is recessive to one allele not be dominant to another allele that is dominant to the second? If it can, what are some examples of traits that do this?

I'm not sure, if it's possible. See what "dominance" really means here (first answer). https://biology.stackexchange.com/questions/44475/can-difference-in-the-expression-potential-of-alleles-lead-to-dominance

To some extent, it depends on what you mean by "dominance". If you take a phenotypic definition of dominance, then the answer is (technically) yes, you could imagine such a gene system.
That is, imagining alleles p, q, and r, and three phenotypes P, Q, and R, with the following homozygous behavior:

pp ➞ P
qq ➞ Q
rr ➞ R

Then you could theoretically imagine the following heterozygous behavior:

pq ➞ P
qr ➞ Q
pr ➞ R

In that sense, p is dominant to q, q is dominant to r, and r is dominant to p.

The problem arises in trying to figure out the underlying biochemical rationale for such a system.
In the typical cases where we talk about dominant and recessive alleles, we're talking about a single axis of functionality, particularly an all-or-nothing case: The dominant gene has activity, and the recessive gene doesn't. If you have one or two dominant alleles, you have activity and thus the dominant phenotype, and if you have no dominant alleles you have no activity and thus the recessive phenotype.
It doesn't have to be all or nothing. That's where incomplete dominance comes in. If you have two dominant alleles you have a lot of activity. If you have one dominant allele you have less activity If you have no dominant alleles, you have no activity.
In some cases, dominance is not gain of activity, but rather loss. This is termed a "dominant negative". The normal, recessive allele has a certain activity, and the dominant negative allele can come in and shut off that activity. A frequent mechanism of action for a dominant negative is to non-productively out-compete the recessive allele for binding sites.
Such a single-axis explanation of dominance can't contain your proposed system. However, there are systems where there are multiple axes of activity. The ABO blood group system is a good example. Here you have three alleles, a, b and o. a codes for A activity. b codes for B activity, and o is inactive for both. Thus you have both a and b being dominant to o, but neither is dominant to each other, resulting in an AB blood group when both are present.
However, as long as we're just adding activity, we still can't realize your cyclical dominance system - we'll be stuck with co-dominance.
Totally hypothetical system:
To support your cyclical dominance system, we can possibly combine multiple activity a dominant negative. Here's one possible system that I came up with.
The allele p induces activity A, but is a dominant negative (that is, actively suppresses) toward activity B. The allele q induces B, but is inactive toward A. The allele r is inactive toward B, but is a dominant negative toward activity A So we have the following:

pp ➞ A ➞ P
qq ➞ B ➞ Q
rr ➞ O ➞ R
pq ➞ A ➞ P (q tries to have activity B, but is suppressed by p)
qr ➞ B ➞ Q
pr ➞ O ➞ R (p tries to have activity A, but is suppressed by r)

Is there a set of genes which has such a system? I'm not aware of any. Notice that to get such a cyclical dominance, you need to not only have multiple activities but also dominant negatives - and in the correct correspondences. If such a system exists, it would be very unlikely.

Dominance by silencing the other allele
The mechanisms by which dominance work are still very much unknown. One type of mechanism that will be of particular interest to this question is the modifier of dominance where the protein product of an allele silence the expression of the other allele in order to cause dominance relationship.
Is the pattern you describe possible?
In such system, I can imagine a case where allele A1 would silence A2 which would silence A3 which would silence A1. I can't think of any reason such a pattern should not exist. However, I am not aware of evidence of such pattern.
The interesting case of SI in Arabidopsis thaliana
This type of dominance (dominance through silencing the other allele) has been reported in the self-incomtability locus of Arabidospsis theliana (Durand et al. 2014). At this specific locus there are 6 alleles but they have a very hierchical relationship where A1 silences all other alleles, A2 silences all alleles but A1, A3 silences all other alleles but A1 and A2 etc..
Related posts

Evolution of dominance of alleles
What determines if a gene is dominant or recessive?


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How does an octopus eye react in free fall?
according to Wikipedia:

Attached to the brain are two special organs, called statocysts, that allow the octopus to sense the orientation of its body relative to horizontal. An autonomic response keeps the octopus's eyes oriented so the pupil slit is always horizontal.

so how would an octopus' eye react on the ISS (assuming the octopus has an aquarium or something it can live in)? In which direction would the eye be parallel to?

Statocysts are composed of a spherical structure with smaller granule statoliths inside; the orientation of these granules is recepted by cilia receptor cells. So in a situation like the ISS, statoliths would be randomly floating around, being recepted by cila receptor cells. At some times, the distribution of statoliths may be concentrated on one side, triggering random changes in the direction of the eye. So in this situation, the direction of the eye may be constantly changing.

did you make this account just to answer this question?

No, when I was deciding the title for the account, I looked at the window and saw my neighbor's ham radio.

late follow up question, would this cause harm, pain, or confusion to the octopus?


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Why do depleted blood veins seem to appear near the surface (or skin) more frequently than blood vessels and arteries?
I could be wrong, but it seems like blue veins generally exist closer to the surface of the body rather than red blood vessels and arteries. And I'm also wondering if this is evolutionary because during an injury, the outside gets damaged first, and I am just speculating that it's more important for muscle tissue to keep gaining blood from less damaged blood vessels than removing already depleted blood that simply bleeds anyway out due to the injury.
Or, if this is simply a trick of the color, that blue veins are just dramatically more noticeable and the first hypothesis is completely wrong.

Short Answer:
The veins you see are special veins right at the surface; major arteries are typically much deeper in the tissue.
Longer Answer:
Great question. Usually veins and arteries come in more or less one-to-one pairings, traveling side-by-side (often nerves accompany them as well). Both types of vessels tend to be fairly deep, because, as you note, damage to blood vessels can be quite problematic.
However, superficial veins, the ones you can typically see right under the surface of the skin, are different. They don't have a direct artery pairing, and they are not the only venous drainage from the areas distal to them.
Instead, superficial veins have a known purpose in temperature regulation. When core temperature is high, the superficial veins are relatively dilated to allow temperature exchange between the blood and outside. When core temperature is low, the superficial veins constrict to cause the blood to flow deeper and retain heat.
A nice side benefit to these superficial veins is that, because they aren't completely necessary for circulation, they can be harvested as surrogate vessels to divert around a blocked artery, like in coronary artery bypass grafting. The saphenous vein from the leg is often used. Superficial veins can also be removed for cosmetic reasons.

References
Webb-Peploe, M. M., & Shepherd, J. T. (1968). Responses of the superficial limb veins of the dog to changes in temperature. Circulation research, 22(6), 737-746.

Nice syrightforward easily understood explanation for those not adept in the physiology or biology.


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Does global sperm count decline also mean lower testosterone?
So I read about the sperm count decline in men in rich countries.
I wonder if this is accompanied by other changes for example in testosterone levels or in other hormones linked with the reproductive system ?
Also other measures such as semen volume ?
Example report on this issue
https://www.sciencedaily.com/releases/2017/07/170726110954.htm
Also, the report shows a steady decline - will this continue and what would be the bottoming out of this trend ?

With an aging population, thanks to better medical science lower average testosterone and sperm is to be expected. If the study is not accounting for this it is pointless.

Obesity is an important confounder here as well.

Adding another question.

Levine, H., Jørgensen, N., Martino-Andrade, A., Mendiola, J., Weksler-Derri, D., Mindlis, I., ... & Swan, S. H. (2017). Temporal trends in sperm count: a systematic review and meta-regression analysis. Human Reproduction Update, 23(6), 646-659. is the actual citation for the study.

I think I'm half way to finding an answer
https://www.sciencedaily.com/releases/2018/03/180318144836.htm


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Where does mycelium growing in wood get oxygen?
As per title, where does mycelium, growing in wood, get its oxygen? I mean when the mycelium is spreading into wood, say an old log, beneath the surface.
As an example, say I put mushroom dowels into a log, and seal it over with wax - standard way of doing it. Where is the sealed off mycelium getting it's oxygen ?

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

Thanks, yeah fair enough. I didn't really know where to start on this question, I did some googling but didn't find anything. This stack exchange question turns up on the first page of google search so I think maybe not many people have discussed this point online.

they need an aerobic environment, they absorb oxygen from water or from there air. mycelium are cells and have a cytoplasmic membrane, which can absorb oxygen the same as other eukariotes.

When you insert mushroom dowels into a log and seal the holes with wax, the mycelium doesn't suffocate because the log itself is permeable to air.
Wood has a natural structure in such a way that it can exchange small amount of gas (Specially oxygen).
The mycelium absorbs oxygen from the tiny air pockets present within the log’s fibers, bark, and other openings. That is really enough for the mycelium's growth.
If you are not aware the log cultivation you can check: Grow mushrooms on Logs

Great answer thanks


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Is tyrosine hydrophobic or hydrophilic?
I’ve seen tyrosine classified as a hydrophobic amino acid due to its aromatic ring in some textbooks and as hydrophilic due to its hydroxyl group in other textbooks.
How does tyrosine actually function in a peptide under physiological conditions (aqueous polar medium and pH~7)?

I am sorry. That was just opinion... :)

https://biology.stackexchange.com/questions/71272/reading-an-amino-acid-physicochemical-properties-diagram/71275#71275

The answer to this question emerges from an examination of the structure of tyrosine — or, more strictly, the tyrosyl residue, which is how it exists in proteins, the concern of the question:

It has both hydrophobic and hydrophilic features and can exhibit both
  behaviours depending on the circumstances.

The ring is aromatic and hydrophobic, but the hydroxyl substituent is hydrophilic.
It is important not to try to fit things into rigid classifications that may not be appropriate for them. Indeed, one should ask how useful a particular classification is in any circumstance, and be aware of its limitations.
The classic illustration of the importance of these dual properties of tyrosine is in Perutz’s description of the differences between the oxy- and deoxy- structures of haemoglobin, where oxygenation of the haem cause the movement of tyrosine from the hydrophobic interior of the protein to the hydrophilic surface. This movement is associated with breaking of ionic bonds between the subunits in the overall change in quaternary structure:

(This is a modified version of Fig. 3 of the original, produced many years ago for teaching purposes. The wiggly line is a cartoon representation of the polypeptide chain of the α-subunit of haemoglobin between His-F8 and the C-terminal Arg residue. For clarity, the preceding region is not shown but its continuation indicated by an arrow head.)

Hi, @David. I was wondering why the arrows in the figure were so curly and convoluted? What's this meant to represent?

@Jam — The arrrow heads just indicate the continuation of the polypeptide chain. The wigglyness is just meant to indicate the omplexity of the structure, with the key point being the helices in which the tyrosine is embedded move. I was a believer in giving students diagrams that they could reasonably attempt to reproduce in a written examination question, rather than using elaborate computer representations where this was impossible. For this forum, the latter type of diagram would be better, I admit.

Tyrosine (Tyr or Y, 4-hydroxyphenilalanin) is usually reffered as polar amino acid because its hydroxyl groupe (polar is rather hydrophilic),  but there is a catch with the benzen ring and stacking pi-pi interactions.

So many authors just put this aa in the "middle". But the other parth of your question is much more complicated.

First of all you need to know that amino acids can behave as zwitterionts. Basicly this is state where is chared amino groupes and karboxyl groupes in amino acid equaly. This state descriped the isoelectric point which is value Ph where is amino acid occure as zwitter ion. The isoelectric point od Tyr is 5.66  Ph. So in 7 Ph it will be charged anyway.

Quick summary chemistry: Tyrosin is polar amino acid which is hydrophilic or hydrophobic up to conditions.

For biological use tyrosine is good adept for phosphorylation and others modifications of -OH group on C4 benzens ring. But basicly is up to circumstances how tyrisyl in peptideds will behave.

@David your answer is excellent (and I upvoted it), and you're right that the OP was interested in the behavior in peptides, but your aside here is wrong. Free tyrosine is of great interest in biology and medicine. It's a metabolic intermediate in a number of important pathways, include catecholamine synthesis.

The comment made by @DanHall is correct, so I have withdrawn my original comment. The point I wanted to make was that in considering amino acid residues in proteins, the zwitterionic nature of the free amino acid is irrelevant. Some of the free amino acids (tyrosine happens to be an example) have other roles in the cell, and in those the zwitterionic nature ensures their solubility in the aqueous milieu. However their side chain is key to their function.


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What is the reason behind that sometimes when I see new thing I feel that I have already seen them?
I have googled it and I found that it is, because of good memory, but how it can be due to good memory as it didn't happen before. It happened to me many times, that I feel that the scene which is happening now, has already happened to me in my past. But it was a new scene in my life, so why does I feel like this? How is it possible that a same scene happens twice?. What is the reason behind it, that we feel something twice in our lives.

What you are talking about is a déjà vu, the feeling of familiarity even though the situation is not familiar at all. It is, in fact, a very common phenomenon. A high percentage of people report having had déjà vus. It is nevertheless hard to put a number to it, because the experiences and déjà vu definitions might be different. I have found numbers between 60 and 90% of the population.
The claim that this is a sign of a good memory is related to the view, that a déjà vu is not a false memory, because you actually realize that the situation should be unfamiliar to you (also mentioned here).
But how do déjà vus happen? There are several theories...
It seems clear that déjà vus are associated with activity in the temporal lobe (on the side of the brain). That's where memory is processed, especially episodic memory (things that happen - in contrast to learning a skill). People with epilepsy often report déjà vus right before a seizure that starts in the temporal lobe.
One theory, put forward in this paper, says that the memory and feeling of familiarity are processed in different areas and there is a false activation of the familiarity area during a déjà vu. The brain is not always working proberly, e.g. false sensations can happen, like hallucinations. So, the false activation of that familiarity center could give us the sense of familiarity in an unfamiliar situation.
Similar to this is the idea, that there might be a mismatch between perception and memory formation. When something we are experiencing right now is "leaking" into our memory due to false activation, we think that this has happened in the past. There is a problem with this explanation: despite having a strong feeling of familiarity during a déjà vu, people fail to give any context to when this previous event happened or which other events have preceded it. So, it doesn't seem to be perceived as a memory.
Another explanation could be a false combination of the experience with something that is loosely connected to it (like planning the trip, watching a movie with a similar scene, etc.). Our brain always tries to connect experiences. It might falsely identify something you've seen in pictures or read in a book as a real experience.
As you see, we still struggle to explain the phenomenon. It is caused by some error in the way our brain perceives a situation, writes or retrieves memory or processes familiarity. This error might be a wrong activation or wrong timing or the like.


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Evolution question on speciation? Really confusing!
Okay, my teacher assigned this homework question, but nothing like this was ever given in our textbook.
Suppose that a type of tree tends to speciate over 10 million years and a species of fly tends to speciate over 1 million years. In the event of a mass extinction, which of the following predictions would LIKELY be true?

A) It is impossible to determine how many niches or species the trees and flies would lead to over time.
B) The trees would fill more niches and create more species than the flies.
C) The flies would fill more niches and create more species than the trees.
D) They would both lead to the same number of species.

I am stuck between A, B, and D because A would have merit, as speciation period may not always correlate to have many changes occur, B may have merit because it could be showing a Gradual model of speciation, and D may have merit because they might both just end up as the one species described? Any help, not even an answer but guidance would be really great.

I appreciate that you have given which answers you think are the best possible and are now asking for help. Homework questions here can be a slippery slope, but I believe you have shown your due diligence and why you need help with it. Welcome to Stack Exchange Biology, by the way! If you have any issues or questions, please visit the help center!

Given that this is a homework question, the answer is C.  It is true that there isn't enough information given to answer this question, but there rarely is for homework questions.  The point is to keep the number of variables small so that a single best answer can be determined, not to perfectly reflect reality.  The only information you are given is the time taken for speciation to occur, which means that you should assume that all other variables don't matter in this case.  All other things being equal, the one that speciates faster will fill more niches.

The answer is C
Because it explicitly tells you the fly speciates faster than the tree (1my vs 10my). That means after the extinction event, all things being equal, the fly will speciate into more niches/species in the same amount of time. While other outcomes could occur, with the information given C is by far the most likely outcome.
This is no different than a physics question asking you which of two object will reach some arbitrary marker first give two different known velocities.

It's a very strange question and hard to know for sure what they are trying to ask. My thoughts would be that they mean, given the opportunity to speciate following a mass extinction which would be expected to produce the most species after some time. The answer would then be C, that number of fly species > number of tree species because they speciate at a higher rate this would be the "likely" outcome - however, any of the three predictions could occur in reality.
I rule out A becuase it's not a prediction, B would be the expectation if the rate was higher in trees, and D would be the expectation if the rates were the same. As long as you can justify the answer I see no reason for them to complain - part of the issue is the odd question, that's the teacher's/author's fault.

The information in the question, as given, is insufficient to provide any answer about niche filling. If the speciation rates are known, and differ (which is, I assume, given above as average waiting time to speciation), and extinction intensity is assumed equal for both groups ("fly" and "tree"), then "fly" is likely to leave more species, and neither (B) nor (D) can be correct. That leaves (A) and (C). There is no information about the rate of filling niches, so (A) must be correct. Note that this is especially true, if the information I list as assumptions is also not given.


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Why do naked mole rats live in colonies with a queen?
What was the evolutionary advantage in having queens? Is it because the ones that had queen like tendencies in the new environment had kids that cooperated better giving higher chance of survival of the colony? Do the worker naked mole rats have an evolutionary advantage in not reproducing because it allows them to devote more energy to the long journey to make one of their siblings the new queen?

Hello! Do you already have a good understanding in social evolution? If not, you will probably want to read this post first. The above post only talks about how genetic correlation between individuals can lead to social traits. It doesn't talk about behavioural correlation due to reciprocity for example. Make sure to read all that.

Then, well... I don't know what's causing social (or apparently social) behaviour in naked mole rats. Here is an article that will likely bring some light to the discussion


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Why are bats so resistant to getting disease from viruses?
I saw in the YouTube video COVID-19 that bats carry so many viruses, yet never or almost never get a disease by any of them. I'm looking for an evolutionary reason as well as a reason based on how their bodies work. However, when you're giving the reason based on how the bodies work, I want you to find some clever way to summarize the reason in a way that I can understand because I hardly know anything about biology.
Could the evolutionary reason be something like this? Bats live in large groups all the time and keep switching around their groupings. Viruses that infect bats evolved by natural selection to do everything they can to spread between bats and survive and not have every last bit of it fought off. Bats in turn evolved by natural selection to not let viruses take over their body more than just a tiny bit. So it was to the evolutionary advantage of both bats and viruses that infect them to form a compromise where the virus gets to invade their bodies to a very small extent but not too much.

Excellent review in the New Yorker, that discusses that very question, among other things.
https://www.newyorker.com/science/elements/from-bats-to-human-lungs-the-evolution-of-a-coronavirus
Here's what Carolyn Kormann writes:
"As the coronavirus family grows, different strains simultaneously co-infect individual bats, turning their little bodies into virus blenders, creating new strains of every sort, some more powerful than others. This process happens without making bats sick—a phenomenon that scientists have linked to bats’ singular ability, among mammals, to fly. The feat takes a severe toll, such that their immune systems have evolved a better way to repair cell damage and to fight off viruses without provoking further inflammation. But when these viruses leap into a new species—whether a pangolin or a civet or a human—the result can be severe, sometimes deadly, sickness."
Hope it helps…

I got the answer to my question in the article you linked. It said bats and viruses have been coevolving for a long time. I also got curious to find out how large flocks of bats can get so I YouTube searched "flock of bats" and got the YouTube video https://www.youtube.com/watch?v=PNPioS_roRE. They go into caves in such large numbers in an inclosed space easy for viruses to spread. Maybe the bats didn't evolve to strongly fight the viruses and instead the viruses evolved to not try to take over the body to such a huge extent in order to not be fought back so hard. It's kind of interesting to

think how they might have coevolved. They probably evolved a compromise where they're all like the common cold to bats. The different types of viruses are probably also in a mixed evolutionary stable strategy. Isn't it amazing that bats constantly live so close together in such large numbers in caves and carry so many viruses and are resistant to getting disease from any of them?

When the video was saying it was something to do with the fact that bats evolved to fly, I couldn't understand what it was saying. After I saw it again in https://www.npr.org/sections/goatsandsoda/2020/02/05/802938289/new-coronavirus-wont-be-the-last-outbreak-to-move-from-animal-to-human which was linked by https://www.npr.org/sections/goatsandsoda/2020/02/09/803543244/bats-carry-many-viruses-so-why-dont-they-get-sick, I quickly figured out what they were saying this time. Bats need to fly. They require a lot of energy to fly so the energy drain of viruses is less compared to the total amount

of energy they burn so they had weaker natural selection to fight off the viruses almost completely. Really they tolerate a larger amount of viral infection in their bodies but not that large an amount. The virus tries really hard not to be fought off completely and the bat evolved  to try really hard not to have the viruses invade to a really huge extent so they evolved a compromise where the viruses can invade to some extent but not too much.


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Why didn't humans evolve to reproduce identical twins all the time?
According to the selfish gene theory, it seems like because identical twins sometimes get produced, a mutation to a gene that says, "if you have an identical twin, be fully altruistic towards them" would get selected for when ever it happens to arise in an identical twin. After humans evolve to be fully altruistic towards identical twins, wouldn't a mutation to a gene that makes a woman more likely to produce identical twins also be selected for because if it happens to appear in a a child who has a non-identical sibling, that gene might be discontinued from reproduction by the partial selfishness of the sibling but if it appears in an identical twin, the other identical twin will preserve that gene with their altruism.

Can we even assume that it's possible for a gene to say "be altruistic to your twin"?  Certainly we don't see any sort of exclusive altruism between siblings.

What you describe could have happened under the right conditions. However, there are a few things you haven't considered.

Because humans are especially altricial, always having twins would double the cost of children on parents.
The benefit of sexual reproduction is immune diversity. So a population like this could be far more vulnerable to disease.

So as far as this thought experiment goes, genes can't be too selfish or they dramatically reduce their own fitness. It's something worth simulating computationally to see what happens.
References

Sexual reproduction as an adaptation to resist parasites (a review)

Although I didn't want to making the question very long to explain it, what I meant was that should be an evolutionary advantage for a mother to reproduce 2 identical twins only once than to get pregnant and reproduce one kid then get pregnant again and reproduce another kid when she only has enough food to feed 2 kids. I'm assuming the tendency for a mother to choose not to reproduce once she already has 2 kids means having identical twins won't cause her to reproduce more than 2 children.

2 children require twice the resources of one, during gestation those resources come directly from the mother, twins are more likely to have complications because of this higher demand on the mother's body. Twins are often underweight or premature and have higher occurrence of birth defects. https://www.ncbi.nlm.nih.gov/pubmed/11321243

Maybe it was an evolutionary disadvantage to produce two kids at the same time because when two kids get produced at the same time, by the time they're nearly finished getting reared, two children both have a high energy demand at the same time and the parents can't keep up with providing both of them such a high energy demand. Maybe the parents also were unable to simultaneously defend two babies against predators.

From jzx's answer, I thought of a possible answer to my own question. Maybe not producing identical twins all the time is a paradoxical evolutionary stable strategy for the following reason:
Until recently in evolutionary history, the population remained constant when parents only had enough food to feed 2 children. Siblings didn't evolve to be fully altruistic towards each other so if a parent had 3 children in case of the small chance of having enough food to feed 3, none of them would willing let themself starve to make sure the others survive, risking making only one survive, so the parents would have had an evolutionary advantage in only producing 2 children in the first place. Although definitely producing identical twins is an evolutionary advantage, a mutation that makes the chance of producing identical twins slightly higher than it already is is an evolutionary disadvantage because a woman with an increased chance of producing identical twins might have produced 1 child on her first pregnancy and identical twins on her second pregnancy, giving a total of 3 children and increasing the risk of only rearing 1.

If we produced identical twins all the time then we'd completely lose genetic diversity which would, I assume, overwhelmingly compromise our adaptive capabilities. Don't forget, those identical twins then need to reproduce with other identical twins of others families. Moreover, and this is the more obvious explanation, as a consequence deleterious recessive disorders would rapidly increase in rate.
For more, see
https://en.wikipedia.org/wiki/Inbreeding_depression
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109585
You might also like to study frequency dependent selection for why it is sometimes advantageous to have identical twins, albeit at a low rate.

I think that you may be confusing identical twinning with reproductively closed populations. Also, with the mix and match of chromosomes and crossover events during Meiosis, there will still be a good deal of diversity, even in populations that are relatively isolated. Even if two identical twin males mated with two identical twin females and produced the same number of offspring, it is highly unlikely that any of the offspring of different births would have an identical genetic make up.

I don't see a reason we'd lose genetic diversity because the identical twin of the spouse of somebody wouldn't be the same person as the spouse of their identical twin.

But by definition you restrict the diversity by at least a factor of 2. i.e. imagine you had two non-identical twins v two identical twins.


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Is there a term to designate the property for an enzyme of catalyzing several reactions from the same substrate?
LacZ (beta-galacosidase) catalyzes the hydrolysis of lactose into either galactose and glucose or allolactose.
Is there a term to designate such property for a single enzyme of catalysing several reactions from the same substrate (i.e. forming different alternative products)?

There is a problem with the nomenclature of enzymes that catalyse more than one reaction because they fall into (at least) two structural types. One can refer to both of them as:

multi-functional enzymes or multi-functional proteins

The latter term is used in a 1976 review of the topic.
However for precision it is necessary to employ terminology that distinguishes between them, especially as the term multi-functional has also been used to indicate the different physiological functions that a single enzyme activity can have (e.g. in this review of cysteine cathepsins).
The more common type — to which the lacZ gene product does not belong — can be considered as fusions of proteins containing separate catalytic activity. Examples include the AROM complex of the shikimate pathway of fungi and protists, and the fatty acid synthase complex of eukaryotes. The Wikipedia entry for fatty acid synthase uses the term:

multi-enzyme protein

The term, multi-enzyme complex, is often applied to such proteins (as above) but is also applied to complexes of individual enzymes, and so is not suitable as an unambigous descriptor for this type of enzyme.
In the case of the product of the lacZ gene there is a single catalytic site, with a single binding site for the substrate but an additional site to which the glucose produced by hydrolysis of the β-galactoside may or may not bind to produce allolactose. The authors of the linked paper describe this as:

an enzyme with bifunctional activity

This is a description, rather than a ‘snappy’ term, and even so requires further elaboration to remove all ambiguity:

an enzyme with a catalytic site possessing bifunctional activity

But this class of enzyme is relatively rare, which is why I suppose no ‘snappy’ term has (to my knowledge) arisen.


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Is T7 promotor leaky in DH5 alpha?
In my experiment I found that a GFP gene under T7 promotor in high copy number pTAC-2 vector is showing green fluorescence producing colonies of DH5 alpha under UV light. what could be the possible reason?

Shouldn't pTAC have the tac promoter and not T7?

You got a T7 phage contamination?

Did you eliminate autofluorescent activities?

Confirm your strain has DE3 or other mutated lacp? Best practice to include selection antibiotic for the lac cassette as well. Also @243 answer above. Finally Check agar for any supplements and run map on plasmid to confirm it is ptac

Consider the phenomenon of zygotic induction, as originally observed by Art Pardee, Francois Jacob, and Jacques Monod (sometimes called the "PaJaMo", or "PaJaMa" experiment): regulation of a repressed promoter can be affected by the copy number of the promoter in the cell. Put another way, if the copy number of the lac operator in the cell is high enough to bind or titrate all of the available lac repressor protein in the cell, then some of the lac promoters in the cell will be expressed.


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True or False: Endocytosis delivers vesicles directly to the cis face of the Golgi complex
Does anyone know the answer to this question, and also the explanation of to why this is True or False?
I know that Endocytosis is the process of uptake of materials into cells including microorganisms, solute particles, and food particles from the ECF. The Golgi Complex is the trafficking directory organelle of the cell which vesicles enter in the cis face and exit in the 'rougher' trans face. It adds tags to vesicles for target compartments. Proteins come from the rER wrapped in vesicles and directed to the Golgi Complex.
In my knowledge the membrane bound or secreted proteins are directed to the rER first, thus I am half certain that this question's answer is False.

I've added the [tag:homework] tag to your question, since that seems appropriate (even if the question you got was not meant as homework). However, I do think you're providing your own thoughts and tenative answer on the question, so I don't understand the close votes.


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stem cells divisions and normal cells division
I'm a beginner in biology, but I've read that stem cells replace the "worn out" cells or the dead cells. Well, I'm a bit confused - why do they do this?
Aren't there any cells nearby which are the same type as the worn out cells or the dead ones, that can divide and so on?


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Definition of Cis-eqtl
I have simple question, do cis-eQTLs use the SNPs that are within 1 Mb from the gene's TSS on the same chromosome ?

Kind of.
What you describe is a cis-eQTL, but the exact distance (1Mb in each direction, 1Mb total, ...) and the definition of the location of the gene (TSS, transcript borders, ...) depend on whoever calculates a cis-eQTLs and are not universal.
The 'cis' part just means the SNP is somehow near the gene, there is no defined limit on the distance.


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Why is there Turner syndrome if one of the X chrosomes is inactivated anyway?
In females one of the two X chromosomes will condensate and turn into Barr bodies. So chromosome abnormality-free women will only have a single transcriptionally-active chromosome. Then why can abnormalities like Turner's syndrome still occur in the  presence of a single active X chromosome?

Pseudoautosomal region in mammals
On sexual chromosomes, we have a so-called PseudoAutosomal Region (PAR). The PAR is the region which still recombine with the Y chromosome (in males only) and is though to be important to allow separation of chromosomes during meiosis.
Pseudoautosomal region and dosage compensation
Because the PAR is diploid in males too, there is no need for a mechanism of dosage compensation and hence, in females, the PAR of the inactivated X-chromosome remain active.
Turner Syndrome
Turner syndrome is caused by an issue of dosage of functional elements found in the PAR. In people having Turner syndrome the PAR is haploid, while it remains diploid in both healthy males and healthy females.
Here is a small review paragraph from Sybert and McCauley (2004) that report the evidences suggesting that Down syndrome is caused by haploidy in the PAR. Please see the linked paper directly for further references.

Loss of interstitial or terminal long-arm material of the X chromosome (Xq) can result in short stature and primary or secondary ovarian failure.15 Deletions distal to Xq21 appear to have no effect on stature. In general, loss of the short arm (Xp) results in the full phenotype. Very distal Xp deletions are compatible with, but do not ensure, normal ovarian function. Loss of this region usually confers short stature and the typical skeletal changes, in part as a result of haploinsufficiency of the short stature–homeobox (SHOX) gene, located in the pseudoautosomal region of Y and Xp. The SHOX gene is probably not the only gene responsible for the skeletal features. Aneuploidy itself may contribute to growth failure. Loss of a region at Xp22.3 appears to be associated with the neurocognitive problems in Turner's syndrome. Loss of the testis-determining factor (SRY) gene locus on the short arm of the Y chromosome (e.g., 46,X,del(Yp)) also leads to the phenotype of Turner's syndrome, even without a 45,X cell population. A region on Xp11.4 has been proposed as critical for the development of lymphedema.

@Jagoe I did not know that +1 Do you happen to know what fraction of these 35% are from the PAR? If you happen to have a reference, I would happily add that to the answer. Thanks

@Jagoe Ok. Note that your link is broken


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Do seeds use cellular respiration when they are germinating?
Do seeds use cellular respiration when they are germinating?

What have you found while searching on the internet on your own? PS: Consider asking yourself why seeds have a high fat content.

Seeds have preserved energy and nutrients in the form of cotyledons that are used for germination because they can't harvest their own energy until they grow leaves for photosynthesis. But I don't know whether they use cellular respiration, I'm guessing they do?

Google: germination oxygen consumption

@Timothy yeah, and how do you think the stored energy is utilised? How is it converted from its physical form of fats/carbs to help its growth?

Those stored fats and sugars have to be burned to be utilized. Besides how ridiculous it would be to have a multicellular organism mature using only fermentation.

So seeds use their stored nutrients via cellular respiration? Thank you!

It would be helpful to provide citations to back your statement.


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Is aneuploidy/aneusomy only a problem for cell division?
One of my textbooks states that:

"recent studies suggest that aneuploidy can be seen in upwards of 10% of human brain cells without any noticeable effects"

I do know that trisomy 21 causes problems, specifically mental retardation by not allowing the brain to turn certain genes ON and OFF at certain protein levels, but I do not understand why plants are okay with aneuploidy?
Is it because plant cells are more "plastic" than animal cells that, they are okay with aneuploidy?
Because neurons never divide, do they never have to deal with aneuploidy?
Or is aneuploidy a problem of stress that results from failing to control gene expression?
or is it a problem strictly of mitosis?

I just want to understand WHY brain cells .... are okay with aneuploidy

Great question. The standard hypothesis has been that aneuploidy confers some kind of advantage to  the function of the organ (brain). After initial reports estimated a very high (>30% of brain cells) aneuploidy, it would be plausible that any potential negative effect would somehow have to be compensated. One hypothesis was that it increases the functional diversity of the neurons.
However, this notion is outdated. For instance, a recent study, which also nicely summarizes preceding literature, and has been published by Knouse et al. PNAS 2014 ( http://www.pnas.org/content/111/37/13409.full ), and has applied a more sensitive and accurate measurement, and also surveyed other tissues, found that the fraction of aneuploid cells in the brain is around 1-2%, and not higher than in most other tissues. One possible conclusion, which has also been drawn by the authors, is that for the brain aneuploidy is as much of a problem as for other organs, and that - given the low fraction of aneuploid cells, which is similar to other tissues - aneuploid cells in the brain do not contribute to some special organ-specific property. (Concerning your related questions to brain: the aneuploidy in brain is believed to result from cell division artifacts - also see paper mentioned above.)

I just want to understand WHY ... plant cells are okay with aneuploidy

Although plants appear more tolerant against aneuploidy than humans, aneuploidy can be quite harmful to them, and can easily lead to phenotypic aberrations. While the basis of the increased resistance of plants over humans isn't known, or at least hasn't been known at the time of the publication listed below, it appears linked to some genetic factors as different strains can have a different robustness - see Henry et al. , Genetics, 2010 ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998307/ )

Is aneuploidy/aneusomy only a problem for cell division?

No, aneuploidy can create further problems (e.g.: also see second paper). For instance, in plants, it can also change the activity of genes, or the spatial organization of chromosomes - as described in Huettel et al. Plos Genetics, 2008 ( http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000226 )


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If action potential is "all or nothing" then how are finely tuned signals sent from one neuron to another?
If the action potential is an "all or nothing" phenomenon, then how is one type of neurotransmitter secreted rather than another? Let's say, for example, if a neuron received an excitatory post synaptic potential that initiated a graded potential that initiated an action potential, what specific signaling cascade or mechanism would denote the release of one excitatory neurotransmitter (say nor-epinephrine) over another (say dopamine) ?

https://www.ncbi.nlm.nih.gov/books/NBK10818/

@JM97 That link is very misleading in the context of this question. See my answer.

how is one type of neurotransmitter secreted rather than another

Most neurons release a single major neurotransmitter. JM97 commented a link about cells releasing more than one, but that is talking about "extra" neurotransmitters are short peptides, different from the major neurotransmitters like glutamate, GABA, acetylcholine, dopamine, norepinephrine, etc - I think that link is very misleading in the context of your question. Those cells don't choose one or the other, they release their primary neurotransmitter plus the peptide.
However, there are lots of different neurons and lots of different TYPES of neurons, so some release one type of neurotransmitter, others release another. Typically this is denoted by refering to cells as "___ergic": GABAergic cells release GABA, glutamatergic cells release glutamate, etc. Those specific cell types express the proteins necessary to synthesize their neurotransmitters and transport them into synaptic vesicles, ready to release. The actual signalling cascade that results in vesicle release is pretty much the same across different neurons: the difference is in what is packaged into those synaptic vesicles.

if a neuron received an excitatory post synaptic potential that initiated a graded potential that initiated an action potential what specific signaling cascade or mechanism would denote the release of one excitatory neurotransmitter (say nor-epinephrine) over another (say dopamine) ?

Simple: if the action potential is fired by a noradrenergic cell, that cell will release norepinephrine on all of its targets. If the action potential is fired by a dopaminergic cell, that cell will release dopamine on all of its targets. They are different cells.
In contrast to outputs, which use a single primary neurotransmitter, individual cells can receive inputs from many types of neurotransmitter. So a dopaminergic cell could receive GABAergic inhibitory inputs and also receive glutamatergic excitatory inputs, but it will only release dopamine on its targets.
If you have a network, and you wanted that network to release more dopamine on average, you would increase the synaptic weights of the excitatory inputs to dopaminergic cells: that is, increase the amplitude of EPSPs in those cells (you could possibly also reduce the inhibition).
In the title of your question, you asked how "finely tuned signals" can be sent. Tuning of signals isn't just about which neurotransmitter is released, but rather which cells that neurotransmitter is released on to. Individual cells can both receive 1000s of inputs and send outputs to 1000s of other cells. The patterns of those connections and the patterns of active cells are what determine the "message" - this is called "encoding".


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How did the double circulatory system evolve from the single circulatory system
I already learned how the mammal circulatory system (double circulatory system) evolved from the reptilian circulatory system. How did natural selection evolve the reptilian circulatory system and the amphibian circulatory from the fish circulatory system (single circulatory system)? Did the reptilian circulatory system evolve from the amphibian circulatory system? If so, how? http://www.shmoop.com/animal-movement/animal-circulation.html shows what the fish, reptilian, and mammal circulatory system look like and https://universe-review.ca/I10-82-circulatory.jpg shows what the amphibian circulatory system looks like.


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Why did humans evolve the ability to feel such a high level of heat pain?
It's probably because our ancestors were frequently around 300°C metal which badly damages flesh in a fraction of a second because they made fires to cook. I don't see why that would cause natural selection to make that pain so extreme instead of only slight. It's so rare for somebody to die from getting a nasty burn from touching such a hot metal. Is it because those who didn't feel heat pain were frequently holding very hot metal objects and although each one touching made them only a tiny bit less likely to survive, the damage added up and eventually they would have held such hot metal objects so many times that they had a very high probability of dying?

You are thinking way to close in evolutionary history. 1) Early life likely arose in thermal springs or around volcanic vents in the oceans. It would be beneficial even for single celled organisms to have proteins that helped them detect or repair damage from heat. Those evolve a different function in multicellular organisms and is how you can detect heat. 2) We evolved in forests and brush land. During dry periods, lightning strikes set off forest fires. those that react and flee reproduce another day, those that don't, don't, but you could likely go back to the very first mammals for that.

Without antibiotics it absolutely is not rare to die from an infected burn wound.

Do we have burn specific receptors or does it just hurt because it damages the tissues as a physical damage could do? Are other apes less sensitive to burn pain? I think these questions should be answered first (and maybe you guys know the answer).