text:
Could Racemic Epinephrine be used to Treat Anaphylaxis?
To be clear, this question is not a personal health question nor a question seeking health advice, it is only a theoretical question born of a curiosity for the pharmacology and biochemistry of adrenalin/epinephrine... I have never in my life had any kind of allergic reaction and your answer bears no effect on my health or anyone else's health.  The answer will only serve to help a fictional story be as scientifically accurate as possible.
My question is: In theory, is racepinephrine (the active ingredient in Asthmanefrin) compatible as an emergency replacement for epinephrine to combat anaphylaxis?
As a side question, what effect if any, does benzyl alcohol have on epinephrine?
Thank you for your time I certainly appreciate it!


text:
Will a mother praying mantis stay with the egg sack?
We caught a pregnant praying mantis (without knowing it was pregnant). It made an egg sack on the underside of a cardboard bridge in its container.
It is in Pasadena, California. It kind of looks like the one in this link, except that it is paler green color (kind of tan brown/green). In the past I have seen some with red eyes, but I think this one had eyes that were black. I'm not sure if the eye color changes in the light, though.
Not knowing how to care for babies, we left the container outside in the shade with an open lid (so that the mother can climb out any time she wants, and so can the babies when they hatch). The mother climbed out immediately but remained on the outside wall of the container (near the egg sack) for hours.  However, the mother is no longer there.  Is it normal for a mother to abandon the egg sack?  Can we expect the mother to return?

Do you know what species of mantis — this matters because some species do provide care but most don't ...

@tyersome : I had responded to your question, and now I find that someone removed it from the comments and put my response in the question itself (which makes sense, except you may not notice it). I likely also forgot to @ you in my comment, so I am doing that now (in case my added info is helpful).

source: Stack Exchange

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

sort: votes


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What is this insect that I found under my bed

Found it under a hotel bed in Las Vegas, what is it?

That is a cockroach nymph. Don't worry, not a bedbug.

Added info about the city. Thanks Karl for the info, I started looking when I noticed a lot of what looked like bites on my legs and some on my arms and it reminded me of the time when I had a bedbug problem about 10 years ago. Couldn't find any in the beds though.

A size scale would be very helpful here

looks like fragmented body part of a cockroach

It is a Madagascar hissing  cockroach. They are native to Africa, particularly Madagascar. In the U.S. these roaches only invade homes when accidentally brought in via imported furniture or food, although some people do keep them as pets.
https://en.m.wikipedia.org/wiki/Madagascar_hissing_cockroach

-1. I don't think you're correct. Please provide additional support for your answer. I agree that the OP's specimen is a roach, but the appearance and size of the OP's specimen do not match a madagascar hissing roach. Further, finding a single, random MHR in Las Vegas is unlikely. Please update your answer with additional pieces of information that more definitively match your ID. Thanks.

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


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Plant respiration produces carbon dioxide, so why are plants regarded as decreasing its atmospheric concentration?
In the absence of sunlight, plants give out the greenhouse gas, carbon dioxide. So why is it said that plants increase the concentration of atmospheric oxygen? Do they not increase the concentration of carbon dioxide and use the oxygen produced in photosynthesis.

Possible duplicate of Confusion regarding photosynthesis and respiration in plants

@tyersome that answer says "At night there is, of course, no photosynthesis and respiration will dominate and the plant will be a net producer of CO2 and a net consumer of O2." And I want to know if this is not a source of pollution.

possible duplicate of https://biology.stackexchange.com/questions/39253/how-long-can-a-plant-generate-oxygen-from-its-own-carbon-dioxide-produced-durin?rq=1

the plant grows and gains mass too, using $CO_2$.  I could be completely wrong, but perhaps during the growth phase a plant would photosynthesise more than it respires (because it’s gaining mass) which means there is a net loss in atmospheric $CO_2$ per plant.

Think! What are plants’ stems and leaves made of? Where does the carbon for that come from? So what is the net balance?

There are two factors here.  First is that you have to look at the plant's net production over time.  Say for instance (I'm just making up numbers here) that during the day the plant takes in 88 g of CO2 and uses photosynthesis to convert it to 64 g of O2 that's released into the air, and 24 g of C that is incorporated into the plant.  Then during the night it uses 12 g of the stored C for respiration (combining it with 44 g of O2 from the air), leaving a net daily production of 12 g C that goes into plant growth, and 44 g of O2 in the air.
Second problem is perhaps better classed as either linguistic confusion (to be polite) or ignorance.  CO2 is not "pollution": it is a normal part - more accurately, a fundamental part - of the carbon cycle https://earthobservatory.nasa.gov/features/CarbonCycle on which almost all life depends.  The problem is not plants (or animals) releasing CO2: it's humans digging up lots of fossil carbon and burning it, thus increasing atmospheric CO2 concentrations beyond the levels to which the ecosystem has adapted.
Now that you've changed the question, it's even more important to read the basic description of the carbon cycle at the link.  (Honestly, wasn't this covered in your high school biology class?)  Again, the bottom line is that plants produce a net surplus of O2, which animals consume along with the plants, so that the cycle remains balanced.

The tag you used on the question shows you know about photosynthesis, but it seems you don't fully recognize its significance.  Yes, plants use oxygen and release CO2 all the time for energy use, but they absorb much more CO2 (and release much more O2) while storing energy during the daytime than that 24-hour energy usage undoes.
While plants release CO2 as well as absorb it, they do much more of the latter.  By one scientific estimate, of all the the CO2 plants remove for photosynthesis, they release 40% of it back into the atmosphere.  But that means that 60% of that CO2 absorption is never released back into the atmosphere by the plants.  So, overall, the net change is that plants remove CO2 from the atmosphere (unlike animal metabolism and combustion which only add CO2 and remove none).
All those plant stems, branches, and trunks you can see are built out of CO2 that the plant will never release back into the atmosphere.  The only CO2 the plants release is CO2 that they previously absorbed from the atmosphere.

Do they not increase the CO2 proportion?

No, because the CO2 they emit came from the atmosphere to begin with.  And the carbon they don't release as CO2 stays as carbon compounds that make up the plant.
The issue with CO2 is not plants taking CO2 from the air and re-releasing it.  That doesn't cause a steady increase in atmospheric CO2.
Taking CO2 that has been sequestered in the ground for hundreds of millions of years and adding it all to the atmosphere in a geologic eyeblink of time, that's a problem.

Plants start to grow first, from tiny size (from seed in higher plants), and from there, any size in later stages they achieve to have, they achieve it only by first absorbing all the Carbon they need, from air first.
So huge part of plant's later dried weight is actually made from carbon. And all that carbon was incorporated into it's body through continuous photosynthesis - so it was "sucked" from CO2 in the air around the growing plant.
Importantly:
Unlike us, plant can not normally absorb carbohydrates (sugars, fat etc - we eat them, plants don't) in order to use them for metabolism and respiration (ie breathing). For this they can use only carbohydrates they themselves already created first from CO2, through photosynthesis.
Even when they can not use photosynthesis anymore (because of age or in the dark) - they use for respiration only that carbon which they stored in the body before by catching it from air.
And as long as the plant continues to grow and have access to any light it continues to absorb much more CO2 than it releases through respiration. So in balance it keeps absorbing CO2 and releasing oxygen in net balance.
As an mental exercise: It would be different if You would take, let say same house pot plant and place it into a completely dark room for a long time. That plant there is without light, while it already has body which it created previously through photosynthesis, it now can not capture any light and any carbon any more, yet it would still need to be continually breathing. So as this particular plant in the dark, have no source of energy for photosynthesis, and it still is breathing, so in this particular case it would produce CO2.
Practically something resembling such theoretical example happens with significance only, when we store plant body-parts like fruits and vegetables (or potatoes) for a long time. Fruits, vegetables and potatoes (often stored in the dark) breath and not photosynthesize.
The cycles between a day and night are also bringing plants for short time into the dark and as such they have negative balance (net producing CO2) for a short while, but it is insignificant from the whole day perspective (overal they consume much more CO2 than they produce it)
Interestingly, there also exist very rare species of parasitic plants (they are parasites of other plants) which are not having their own photosynthesis - in this case they have no chlorophyll and suck sugars out of other plants - and yes, they only breath and yes, they only produce CO2, so they would be probably the only plants which are net producers of carbon dioxide.

Welcome to Biology.SE! Your answer is helpful, but it is much more likely to receive a favorable response if you edit it to include supporting references (primary literature is best though probably not needed for a question at this level). ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thanks!

Thank You. I saw quite nice answers already, so I just took it easy and and thought about possible weaknesses in them to relay the message and tried reiterating from different point of view, which would help to absorb it. So, I just didn't thing about sources, as You sad, it feels kind of very basic. But I will try next time.


text:
ELISA troubleshooting
Hi,
Why does my elisa plate wells gives a brown color after adding the stop solution. I am giving a 4*5 minutes wash after each step. TMB gives it a proper blue color but when I add the stop solution (0.16M H2SO4), the color turns to brown. I am using all the reagents new. Any help will be appreciated.

The full oxidation of TMB ( 3,5,3’,5’-tetramethylbenzidine) is 2-electron process.  The first step (one electron oxidation) gives the blue product, which is then further oxidized to a yellow product (2nd electron) that is stable in acid.  At high concentrations this might appear brown.
You might also not be fully quenching, leading to a mixture of blue and yellow products (should be more greenish though).  In this case add more stop solution.
TMB chemistry:
Josephy, P. David, Thomas Eling, and Ronald P. Mason. "The horseradish peroxidase-catalyzed oxidation of 3, 5, 3', 5'-tetramethylbenzidine. Free radical and charge-transfer complex intermediates." Journal of Biological Chemistry 257.7 (1982): 3669-3675.


text:
Can a young voice have physical causes?
I have noticed that some older adults (40+ range) can have voices that sound much younger than their actual age (i.e. an adult sounds like an adolescent).
My question is: could any physical aspects play a part? For instance the size of the throat, the tongue or something else? I am assuming that there are no external factors that are influencing this (smoking, exposure to chemicals, physical trauma, etc).

every aspect of an organism has a physical cause, there is nothing about an organism that is not ultimately physical.

In general, a grown up man will have a voice with a lower pitch than when he was an adolescent (Cleveland Clinic). The pitch height basically depends on the length of the vocal cords. According to Wikipedia:

Adult male voices are usually lower-pitched and have larger folds. The
  male vocal folds...are between 17 mm and 25 mm in length. The female
  vocal folds are between 12.5 mm and 17.5 mm in length.

So, the shorter the cords, the higher the pitch. There are other anatomical structures in the throat, mouth and nose that may contribute to more adolescent-like voice. To know what exactly is the cause in a particular man, an examination by an ear, nose and throat (ENT) specialist would be probably required. Additionally, a voice specialist could have a good insight even without physical examination.
There can be reasons associated with self-image that make one to consciously or subconsciously insist in speaking with a voice unusual for his age. Sometimes you can see this in singing competitions, when a young man introduces himself with a child-like voice but then sings as a grown-up man.


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What is the name of this plant which is located in Hyderabad city of Telangana State,India?
I found this plant in Hyderabad city of Telangana State,India.Many people of Hyderabad city have planted this flowering plant.I don't know the name of this plant.If it's flower treated as a circle,the flower has diameter of nearly 6cm length.Can any one tell me what is the name of this plant?

From the twisted overlapping appearance of the petals it is a member of the Apocynaceae family.  So I searched for "Apocyanaceae india" and found images consistent with your picture.  Good chance it is Allamanda blanchetii or Purple Allamanda.  Here is a picture comparable to yours (source/CC0).

Here's a bit about the plant and Wikipedia has a short page.


text:
Which bacteria takes the longest to double?
Currently I am writing a lab report on the enumeration of bacteria.
E.coli takes about 30 mins to double. That is going from 1 bacteria to 2 bacteria.
I want to know which bacteria takes the longest to double? Do some bacteria take a day to double?
Thank you for the help.

3000 years plus seems a little longer than 15 hours.

There is no answer to your question
The doubling time of a bacterium is dependent on the conditions: primarily on the temperature and the availability of nutrients, but other factors can apply. Because of this, the doubling time of any particular bacterial strain cannot be considered in the abstract, thus to give a single number  we can consider the optimum doubling time for a strain instead - i.e. how fast it will double under the perfect (for it) temperature and nutritional conditions. For the E. coli strain you worked with, this is likely 37 degrees and in a rich media such as Lysogeny Broth. But for the staggeringly vast array of bacteria out there, we simply don't know what the optimum conditions are much less have actually measured growth under them. In fact, there are many bacteria which are known about, but currently uncultured so we haven't even begun to understand their growth dynamics.
So even the simplified question of longest optimal doubling time cannot be answered because we don't have the data for so, so many bacteria. The question of the maximum time between divisions is even less clear: there are bacteria that live under conditions of extreme nutritional limitation that can take thousands of years to double, and strains that can exist as spores for at least 100,000 years and maybe even tens of millions. Do we consider their doubling time to be a 100,000 years? 25 million years? Without specifying the conditions under which the doubling takes place, the question is poorly defined.


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Predatory animal tracking methods
As far as I know, humans are the only animals that use visual references to track prey that is not immediately visible to them.
Do any other animals do this?
I'm not referring to stalking prey that the predator already has in sight, like many big cats do, and not tracking prey, that is out of sight, by scent or other means, before switching to visual before the final attack.
Are there any other animals that primarily use visual information, such as tracks, shed fur, broken foliage, disturbed earth, etc., to follow or approach a prey animal that they can't already see?

This is a really interesting question. Based on what I'm reading online the answer is no, not as far as we know. Bears, mountain lions, and other species have been noted to follow tracks but this is commonly thought to be due to following the smell an animal leaves behind, not the visual cue itself. This similar question on Quora has a discussion of this phenomenon.
As is pointed out in that discussion, the best candidate for this would likely be birds, particularly corvids. This article discusses a study in which ravens could not only tell when someone was looking at them, but could remember areas in which they'd previously been observed (i.e., they can tell when someone is 'spying' on them). This is a bit different than what you're asking here, but you can imagine that an animal that was capable of this level of cognition might also be able to connect seeing footprints --> find human if they were incentivized to do so (possibly by the potential to gain food or other resources). However, it doesn't look like that has been specifically studied.

-1. Please avoid citing Quora as a source -- Quora answers are rarely cited, not peer reviewed, and often FALSE. It's really a low quality site. We try to hold higher standards here on Bio.SE by requesting that all answers provide reputable support. (For the record, MentlaFloss is not really a whole lot better than Quora in terms of quality). These types of sources are best fit for sites like reddit. Here, please elevate your citation game as we are striving to compile expert answers to questions for biology researchers, academics, and students. see our site [tour].

noted. I included this one only because the primary response to the question in Quora was knowledgeable and answered by an Ms in a relevant field. But I will avoid this in the future.


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How to include multiple DNAs into a crystal structure
I have a crystal structure (PDB 3OS1)that shows the interaction of PFV intasome with a substate DNA. I would like to replace the existing DNA in the intasome as well in the substrate with a longer sequences. What is the easiest way to do it. Thank you.

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). You are also more likely to need to get a positive response if you provide more detail and background about what your are trying to accomplish — I'm not clear on whether you are trying manipulate actual crystals or a structure file. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site and then edit your question accordingly. Thanks!

Could you clarify? Why do you expect the protein to have the same structure with a different substrate DNA? And even if it is a reasonable assumption, you are going to have to edit the coordinates of the existing bases with those for different ones. Furthermore how do you imagine you can model additional bases? Your request for “the easiest way” to do it suggests you don’t realize what is involved. Do you?


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Study on Introns?
I am curious whether there has been a study done on the effects of removing introns. Specifically, what happens if you genetically edit a eukaryote genome to no longer contain introns? Or maybe just a specific gene where the introns don't overlap with exons depending on splicing. Has any such study been conducted?

Have you read up on the roles that introns play in eukaryotes?  To start you could look at a related question on this site and then follow "Related" links from there. What can you conclude from that information?  In general, we encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources).  ——— You may also wish to consult the help pages starting with [Ask] questions effectively on this site and then edit your question accordingly. Thanks!

The answer is yes of course, and you can find papers on the topic by a simple internet search.


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Found this insect in my bedroom. What is it?
I found this bug in my bedroom yesterday. I was afraid that it was a tick so I got rid of it after taking some photos.
The bug was found in Denmark and was about half a nail in size.
 Can somebody recognize it?

Photos with a less cluttered background may help; from what I can see though, I'm thinking a beetle belonging to the superfamily Scarabaeoidea (dung beetles and chafers -- I think we can eliminate stag beetles) but would like a closer view of the front of the animal (that we can't zoom in for any of the photos is a handicap).  Once we get those photos someone else will have a better chance of going deeper (it won't be me; I don't know the Danish fauna of the group I think we see here).

Thank you, @ArthurJFrost. I think that the background gives a perspective on the size of the beetle because it is not much bigger than the paint spatter. Do you still think the the pictures should be cropped?
I can't take more pictures of the beetle so if you don't think that anyone can determine the fauna from these photos, then leave your comment as an answer.


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What is the scientific name of this parrot?
I found this parrot at Nehru Zoological Park which is located in Hyderabad city of India.It's head to tail length is between 30cm-35cm.Can anybody tell me the scientific name of this parrot?

Looks like a male plum-headed parakeet (Psittacula cyanocephala)
wiki: the plum-headed parakeet


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Poly-symbiosis? What's the name for this?
A mutually beneficial relationship between two species is called symbiosis.
If multiple symbiotic relationships exist with a single common (dominant) species, is this called 'farming'?

A mutually beneficial relationship between two species is not called symbiosis, but is rather called "mutualism." The benefit is measured in terms of fitness; a combination of survival and reproduction. Symbiosis is the degree to which species are "together," which is used in terms of physical proximity or degree of dependency. Pathogens, for instance, have a symbiotic relationship with their hosts and physiologically depend on their hosts by feeding on them. Mutualism and symbiosis are often conflated, and should not be.
Let's dissect: "If multiple symbiotic relationships exist with a single common (dominant) species, is this called 'farming'?" It seems like you mean, if members of the same species increase each other's fitness. Reciprocal fitness benefits between species is called mutualism, and within species is cooperation. There are important differences between mutualism and cooperation from evolutionary points of view and they have vastly different intellectual histories. None of this is really called "farming," except for some ant-insect mutualisms, where ants raise and protect aphids for a reward (honeydew; i.e., plant sugars secreted by some insects).

I think that you are refering specifically to mutualism, check this diagram from Wikipedia . https://en.m.wikipedia.org/wiki/Symbiosis?wprov=sfla1
I suggest you to  edit your question adding mutualism or mutualistic symbiosis, furthermore, I would add the tags "Ecology" "ecological-communities" and "mutualism".
I haven't heard of that term or comparison, personally I would use "multiple mutualistic symbiosis between A and B,C,D,etc...
I can't help anymore, I hope that those changes in your question will help you to find a proper answer.
Héctor.

The term "holobiont" refers to a community of mutualistic organisms that function together as a unit. A human and the many species of gut bacteria that digests their food are the typical example of a holobiont. The term is mostly used to describe microbial life in and around a larger host organism, but coral reefs and the communities of fish, crabs, etc. they support are also cited, so domesticated plants and animals and human farmers could potentially be thought of collectively as a farm holobiont.


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Which cultivated plants produce most nectar for pollinators?
Pollinators are important for many crop types (e.g. wikipedia list), but I am wondering how important the crops are to feed the pollinator. Obviously, some of the crop plants provide much more food than others, and the plants that depend on pollinators for their reproduction will be likely to attract the pollinators with pollen, nectar, or both. But I am not sure that I can use the dependance on pollinator as an accurate estmator of the quantity of nectar that is actually available for pollinator.
I can think of the rapeseed as being very rich in nectar, but are there other "nectar rich" flowers ? For instance, what about sunflower, potatoes, peas ,sugar beet, mustard, flax, lucern, clover, maize, wheat...
To sum up, I would like to have a list of the most common European cultivated plants that produce a reasonalble amount of nectar accessible to insect pollinators. (rem : I've asked a similar question about pollen, and maybe the answer is the same, but as far as I understood some plants have more pollen and some plants have more nectar.)

That doesn't answer your question directly but it's worth noticing that – independently of their nutritional value – crops are a problem for pollinators since monoculture is an all-or-nothing regime.  By which I mean : a few weeks when food is plentiful yet totally absent during the rest of the year.  Characteristics of the supply during the all-you-can-eat weeks is only a side topic. Hence the insistance on biodiversity in agricultural settings.

thank you for your remark. I understand that the a large quantity at one date is not enough to sustain a population of pollinators, but I can find data about the flowering period and the landscape diversity. I find it more difficult to find data about pollen/nectar production during the flowering period (if any).

What about trees? in apple producing regions in the US, they have to bring over hundreds of bee hives to pollinate the trees, there was info on it in a program about monocultures.

trees are indeed part of the whole picture, but I've tried not to be too broad. And I already have some info about trees (in monoculture or in diversified hedges

Lacy phacelia or purple tansy (Phacelia tanacetifolia), which can be
planted any time of year due to its short growing season. After
flowering, it is plowed into the ground to enrich the soil with
humus
All types of clovers: excellent nectar plants that plowed after
flowering and enrich the soil with nitrogen, or scythe them and use
as feed for animals
Sunflowers: after flowering, they greatly enhance the structure of
soil and enrich it with hummus
Rapeseed and poppy
Buckwheat: planted it in summer and when it fades, the seeds and
ground into flour

Scroll to page 13 (Appendix II). Here you will find a list of all significant nectar-producing plants in Europe
Scroll to page 21 for average nectar production (mg sugar/day/flower) of important agricultural crop flowers
Melliferous potential of twenty-seven plant families determined from the N data sets recorded in thirty-eight papers ranked by decreasing median values - scroll to page 5 under Table 1)
The google keywords you are looking for are along the lines of: "melliferous potential of agricultural crops in europe" and variants of this

https://www.prairienursery.com/resources-and-guides/plants-and-gardening/planting-for-pollinators.php
This link should answer your doubts concerning such plants. Asking for a list concerning whole Europe feels something a little bit out of reach considering how diverse the environment is there, this link concerns mainly the UK, albeit you have to consider that a wide gamut of species concerns various different territories with similar climate, thus many plants listed there can be found easily elsewhere.

thank you for your answer. This is an interesting link but I am looking for this kind of data in the case of the main (in terms of area coverage) crop plants.


text:
Can different proteins be produced during translation of a single mRNA in eukaryotes?
Is there a translational mechanism that eukaryotes can use to produce different proteins from a single transcribed mRNA?

Yes; you may like to look up post-translational modifications. (https://en.wikipedia.org/wiki/Post-translational_modification)

I have suggested an edit to the title — if that is not correctly summarizing your question can you please clarify what you want to know.  Please also edit your question to specify whether you are interested in the phenomenon of polycistronic mRNAs as suggested by @user1136, which is also a reasonable interpretation of your question as it is currently written.

@tyersome — You are being too restrictive In asking if the poster is referring to polycistronic mRNAs. The question is ok as it is, except it may well have been asked before. I’m not in a position to check.

@David — I'm sorry, would you mind explaining what you mean by "too restrictive"?  I was trying to ask for clarification about the poster's intent, but I'm gathering it reads differently ...

@tyersome — There’s no reason to restrict an answer to one type or mechanism, especially as the poster doesn’t know the answer, and an answer would be more generally useful that covered polycistronic viral RNAs, alternative initiation, read-through, frameshift and post-translational proteolysis. I’m travelling at the moment, but if nobody finds the duplicate I feel exists, I’ll answer it comprehensively myself next week.

thanks for the input! I wanted to know if there is a way to get two or more proteins from one mRNA. I did not know of any eukaryotic polycistronic mRNA, and was looking to see if there is such a case. If not, if there is any way to alter translation to obtain multiple proteins

Possible duplicate of Can a single strand of mRNA form different polypeptide chains?

There are multiple mechanisms that are known to lead to translation of substantially (or entirely) different proteins from a single mRNA. While these mechanisms are more typically seen in viruses, I'm focusing on examples documented within the endogenous transcriptome of eukaryotes.
Alternative translation initiation
One process that can lead to different proteins being translated from the same mRNA in eukaryotes is the use of alternative translation initiation sites.1,2 Translation typically starts with a [pre-initiation complex](https://en.wikipedia.org/wiki/43S_preinitiation_complex) recognizing the 5' cap and loading onto the mRNA. This complex scans until it finds an appropriate start site. The choice of start site depends on the how well the ribonucleotide sequence matches the [Kozak consensus sequence](https://en.wikipedia.org/wiki/Kozak_consensus_sequence).3 If the region around the first AUG is not a good match for that consensus then a process known as [leaky scanning](https://en.wikipedia.org/wiki/Leaky_scanning) occurs and the pre-initiation complex can continue along the mRNA until a "good" start site is found.
While this can result in proteins with different functions, they will typically still have large regions of amino acid sequence in common. One example of this is in a kinase known as MK2, which is "a key regulator of transcription, migration, death signaling and post-transcriptional gene regulation".4
Polycistronic mRNAs
While more common in prokaryotes, in some cases eukaryotes also have polycistronic transcripts5,6.  These transcripts encode multiple separate proteins (i.e. from independent open reading frames). The examples that I have found for mammals are all bicistronic (operons with two genes): LASS1-GDF1, SNRPN-SNURF, MTPN-LUZP6 and MFRP-C1QTNF5. You can search for those gene pairs, but there doesn't seem to be a huge amount of information available and in many cases one of the genes is almost completely uncharacterized. Eukaryotic operons (aka polycistronic mRNAs) are ubiquitous in trypanosomes, appear to be very common in nematodes (round worms), and are also frequently seen in Drosophila (a fly).6
Translational read-through
[Translational readthrough](https://en.wikipedia.org/wiki/Stop_codon#Translational_readthrough) aka. stop codon suppression occurs when an in frame stop codon is ignored either stochastically or under specific conditions and translation continues beyond that point. This leads to a C-terminal extension of the protein which in some cases has been shown to have functional implications7,8. An example of this is the [PSI+] prion in yeast, which promotes translational readthrough throughout the yeast transcriptome by inactivating a factor involved in translation termination.7
Translational frameshifts
This is well covered in the answer by @acvill.
References:
1: Kochetov, A. V. (2008). Alternative translation start sites and hidden coding potential of eukaryotic mRNAs. Bioessays, 30(7), 683-691.
2: Wan, J., & Qian, S. B. (2013). TISdb: a database for alternative translation initiation in mammalian cells. Nucleic acids research, 42(D1), D845-D850.
3: Acevedo, J. M., Hoermann, B., Schlimbach, T., & Teleman, A. A. (2018). Changes in global translation elongation or initiation rates shape the proteome via the Kozak sequence. Scientific reports, 8(1), 4018.
4: Trulley, P., Snieckute, G., Bekker-Jensen, D., Menon, M. B., Freund, R., Kotlyarov, A., ... & Gaestel, M. (2019). Alternative Translation Initiation Generates a Functionally Distinct Isoform of the Stress-Activated Protein Kinase MK2. Cell reports, 27(10), 2859-2870.
5: Tautz, D. (2008). Polycistronic peptide coding genes in eukaryotes—how widespread are they?. Briefings in Functional Genomics and Proteomics, 8(1), 68-74.
6: Blumenthal, T. (2004). Operons in eukaryotes. Briefings in Functional Genomics, 3(3), 199-211.
7: Schueren, F., & Thoms, S. (2016). Functional translational readthrough: a systems biology perspective. PLoS genetics, 12(8), e1006196.
8: Loughran, G., Jungreis, I., Tzani, I., Power, M., Dmitriev, R. I., Ivanov, I. P., ... & Atkins, J. F. (2018). Stop codon readthrough generates a C-terminally extended variant of the human vitamin D receptor with reduced calcitriol response. Journal of Biological Chemistry, 293(12), 4434-4444.

I have found the question that this is a duplicate of. May I suggest about how your answer could have been improved. Its strong point is the references it gives, but as most readers will not follow them up or may not have access to all the papers, you could — in my opinion — improve the explanation in your commentary. Just saying "alternative translation" does not make it clear to the uninformed what you mean. The answer to the original by @WYSWYG is not perfect (IMHO), but he gets it right by referring to alternative initiation and mentioning sites. And he also mentions read-through.

@David — Thank you very much for all your valuable feedback and tireless work on maintaining standards on this site.  Do you think it would be better to close this question as a duplicate?  If you think is worthwhile to keep this question I'm happy to work on implementing your suggestions in my answer ...

I had voted this as a duplicate (the text of my comment is autogenerated when one does that) but nobody else has seconded that — perhaps because the original is not specific to eukaryotes. My advice is to go ahead and improve your answer, explaining the basic Kozak mechanism in eukaryotes and how it has emerged that this is a simplification in many cases. If the question is ever closed as a duplicate I don't think you will loose your points, and you could always delete your answer and repost it on the original.

@David — Thank you for your encouragement! I finally found the time to put some more effort into this and while I'm not really satisfied I'm done for today. I welcome any further feedback you are willing to provide.

That's fine. I do have a list of all the di- and tri-cistronic transcripts in Drosophila in supplementary material to a paper I published, but that would be a bit OTT.

Separate from the alternative translation start site mechanism that tyersome describes is programmed translational frameshifting.  This is independent of alternative splicing or post-translational modifications, and happens when a ribosome switches reading frames while a protein is already being translated.  Typically, this phenomenon is associated with viral translation, and allows viruses to encode many proteins on relatively short genomes.  Take HIV as an example: the polyprotein gag-pol requires efficient −1 frameshifting for expression of the individual gag and pol gene products.
In eukaryotes, examples are more sparse.  Check out this review from 2012 --

... examples of mammalian genes that utilize −1 frameshifting are the mouse embryonic carcinoma differentiation regulated (EDR) gene and its human ortholog PEG10. A slippery sequence of G GGA AAC, in combination with a pseudoknot, mediates highly efficient −1 frameshifting, similar to viral frameshifting motifs (Clark et al., 2007). Recently, a programmed ribosomal −1 frameshift has been identified in the adenomatous polyposis coli (APC) mRNA in Caenorhabditis elegans that is mediated by a slippery sequence A AAA AAA or A AAA AAC (Baranov et al., 2011). The functional relevance of this frameshift is uncertain.

Frameshifting events are often mediated by conserved RNA secondary structures, like pseudoknots and stem-loops.  For some specific examples of the types of structures involved in frameshifting, see the following publications:
Identification of a New Antizyme mRNA +1 Frameshifting Stimulatory Pseudoknot in a Subset of Diverse Invertebrates and its Apparent Absence in Intermediate Species
Structural probing and mutagenic analysis of the stem-loop required for Escherichia coli dnaX ribosomal frameshifting: programmed efficiency of 50%
−1 Frameshifting at a CGA AAG Hexanucleotide Site Is Required for Transposition of Insertion Sequence IS1222

Some more recent examples of (potential) programmed translational frameshifts in eukaryotes:
Search for potential reading frameshifts in cds from Arabidopsis thaliana and other genomes
Preprint: Extensive programmed ribosomal frameshifting in human as revealed by a massively parallel reporter assay

+1: This is a helpful addition, but your last two links are eubacterial rather than eukaryotic  examples.  Did you find any non-viral examples that have been shown to have functional significance in eukaryotes?

Updated my answer to include more recent examples of programmed frameshifts in eukaryotes.  Thanks, tyresome


text:
Does sleeping fewer hours than needed cause common cold?
Does sleeping fewer hours than needed cause the common cold? If so, how?

The question can be interpreted ambiguously: 1) literal meaning, sleep deprivation causes common cold, or 2) sleep deprivation causes "common cold"-like symptoms. (1) has been answered with weakened immune system and virus, though it'd be interesting to see if someone can explore on case (2), moreover if it's not caused by external source.

Technically speaking, no. Common cold is caused by a virus. Practically speaking, as the answers show, lack of sleep makes you more vulnerable to any virus.

Generally the answer to “does X cause cold” is “no, unless X is rhinovirus”. In particular, cold doesn't cause cold...

There have been some studies directly linking sleep deprivation to increased risk of catching a cold  ("Behaviorally Assessed Sleep and Susceptibility to the Common Cold Sleep". 2015;38:1353–9.).
Colds are caused by a family of viruses. There is pretty solid evidence that sleep deprivation has a significant weakening effect on your immune system. Given a weakened immune system, it would be more likely that you would catch a cold if you are exposed to one of the cold-causing viruses.

Though it would be not just colds, but any infectious disease.

@jamessqf Sure, but that wasn't the question. The first reference looks specifically at the common cold, the second reference looks at the general issue of weakened immune system.

It's a matter of correctness, I think.  If the question is simply whether sleep deprivation causes colds, then the answer is no.  Rhinoviruses cause colds.

@jamesqf And next time a rabid dog bite does not cause rabies, the virus does?

It is a similar thing as with https://biology.stackexchange.com/questions/5445/why-does-the-cold-make-us-sick?r=SearchResults Even a small child knows that a virus causes the disease. The point is whether cold temperature of nose and throat or sleep deprivation do or do not open the way for the virus to overcome the immunity becase in a typical city in the right season there is no lack of the virus. Just saying - not a disease is caused  by a virus so everything else must be a myth is just wrong. One should adk, would I be sick if I didn't get cold or if I slept more?

@jamesqf What actual point are you trying to make? The answer explicitly says "Colds are caused by a family of viruses" and refers to "cold-causing viruses". It explicitly says that lack of sleep weakens the immune system and that this makes it more likely to catch a cold. OK, it doesn't explicitly say that a weakened immune system also makes it more likely that you'll catch any other infectious disease, but isn't it obvious enough that it doesn't need to be said? Are you just upset that the answer doesn't include the one-word summary, "no"?

@Vladimir F: You might get rabies from a dog bite, but you are (in the US) much more likely to get it from raccoons, bats, and other wild animals: https://www.cdc.gov/rabies/exposure/animals/index.html  Conversely, only a miniscule fraction of people bitten by dogs get rabies, because almost all dogs are given rabies vaccines.  So dog bites do not cause rabies, getting bitten by any mammal with the disease does.  Likewise, lack of sleep does not CAUSE colds, it may weaken the immune system and make you more susceptible to infection by ANY virus - perhaps even rabies.

I think everyone agrees that "causes the cold" is imprecise language, and "causes increased chance of catching a cold" is a more precise but also pedantic way to say it. There's no point in arguing semantics any further.

@jamesqf: We can use Aristotle's causes here. The Rhino virus is the material cause; sleep deprivation is the formal cause. In general, many things happen for a combination of causes.

@jamesqf If you want to be super semantic about it, the entire set of spacetime within the OP's past Cauchy horizon caused his cold.

A new study published in this week's journal SLEEP finds that people who sleep less than six hours are more likely to catch a cold. Researchers tracked 164 healthy men and women for a week at a time, monitoring how much they slept and exposing them to the rhinovirus, also known as, the common cold.
Aric Prather, lead author of the study, and his colleagues found that those who slept less than five hours were 4.5 times more likely to have a cold than those who slept seven hours.
Only 18% of those who slept six or more hours got a cold, while 39% of those who slept less than six hours got the virus.
According to the Centers for Disease Control and Prevention, most adults average two to three colds a year and kids have even more.
Prather pointed out that when we don't sleep enough, it may impact our immune systems in a variety of ways -- from how the cells act to enabling our inflammation pathways.

I take it the baseline for control was around 13% had a cold?

How has the cold virus survived for so long? Is it able to lie dormant within a host until their immune system is weaker than normal? More people seem to get a cold in the winter.

@PaulMcCarthy Generally diseases likes colds survive by circling through large populations, and mutating quickly enough that you don't have much resistance to it by the time it comes back around to you.

@azurefrog Yes but more people appear to get a cold in Winter. If the virus was just circulating, roughly the same numbers of people would have a cold all year round.

authors: Vladimir F Героям слава


text:
Embryonic cells, when can you detect them in vivo? (In order to do whole genome sequencing)
I was wondering, when is it possible to extract cells (humans or mice) in order to sequence them and detect diseases.
Extra: Urine of the embryo in humans is excreted in the 16th week, so I guess that then it's possible to extract some embryo cells.
EDIT
In other words, when is it possible to grab enough DNA to know the full genome of the embryo without damaging it?
In order to sequence it and avoid most genetic diseases and regulate the weekly abortion limits.
Thanks

In vivo or in vitro?

Sorry, in vivo, now I'll edit.

So you are discounting human non-invasive pre-natal testing, on the grounds that it uses cell-free DNA?

@swbarnes2  it depends,  I am especially thinking in the abortions and genetic diseases.

So, when are there enough cells to grab enough DNA and fully genotype the embryo?, Then you could know most genetic diseases. My question would be answered.

By "fully genotype" what exactly do you mean?  Are you talking about a large panel like 23andMe, or a whole genome sequence?

My fault, I didn't  mean genotype, I wanted to say sequencing. Sorry!

Are you asking about detecting cells or having enough material to do whole genome sequencing?

@swbarnes2 about having enough material of the embryo to do whole genome sequencing

As usual, the answer is "it depends what you mean". There is a large existing field (prenatal genetic diagnostic testing) which trying to diagnose genetic diseases in fetuses using different technologies. These technologies are described more in points 2 and 3 below, whereas point 1 is a somewhat academic statement about the technical capabilities of genomic technology in pure research settings which are currently not really relevant for medical applications.
I can think of 3 different answers to the question as originally posed:

With currently available sequencing technology you can never know
the full genome sequence of a human well enough to see all the potentially damaging variants. The "finished" human reference genome in
fact has gaps and errors that are constantly being corrected. For
more information about what "finished" means, see here. Only one assembly of a telomere-to-telomere human chromosome exists as far as I know, and that's only the X chromosome. Even accepting that this best available technology is good enough, it also relies on things like the ability to isolate lots of high-molecular-weight DNA, which makes it very tough to do on the amount of cells you could get from a newborn without highly invasive procedures such as e.g. sampling fetal tissue in vivo. My guess is that even amniocentesis would be very hard to get good HMW DNA from.
With currently available sequencing technology you can however test
very early provided you used IVF, at least as early as the 100-cell stage
(probably earlier). This is a chancier method that will miss a lot
of information but gives you good enough info to diagnose
aneuploidies or other very obvious variants.
Alternately, you can screen cell-free fetal DNA as early as 7
weeks (or possibly earlier). However this does not involve
isolating cells so it is potentially not what you are thinking
about. It is somewhat better information than preimplantation
screening, but rather worse information than you can get from whole
cells.

Likely none of those are exactly the answer you want, but it's also a less simple question than it appears at first: a) getting cells is hard and probably not necessary for the current tech, and b) the tech isn't actually as good as generally advertised.

Thanks!, It is a good and really complete answer. Hopefully in the future we will be able of doing a more complete sequence of the embryos or fetus and avoid those diseases developed during the development. Do you know any source (blog, researcher wordpress...) that talk about this area? Or the scientific name of this field? Thanks!! Héctor

@Héctor - see edit. I think you are interested in prenatal genetic diagnostics. I have added a link to the answer, which you can also see here: https://www.acog.org/Patients/FAQs/Prenatal-Genetic-Diagnostic-Tests?IsMobileSet=false

Oops, meant to also link to this article: https://obgyn.onlinelibrary.wiley.com/doi/full/10.1002/pd.5520 and there is a journal "Prenatal Diagnostics" that you may find useful: https://obgyn.onlinelibrary.wiley.com/journal/10970223


text:
Why/how does exposure to noise cause cochlear hair-cell loss?
I am trying to understand why listening to loud music - e.g. concerts or earphones at high volume damages hearing.
According to the National Institute on Deafness the cause is physical.

Most NIHL is caused by the damage and eventual death of these hair
  cells. Unlike bird and amphibian hair cells, human hair cells don’t
  grow back. They are gone for good.

But I don't understand why/how would noise - which should basically lead to higher amplitude waves in the basilar membrane, induce damage and death of these hair cells?

There are a number of pathophysiological mechanisms that are thought to underlie noise-induced hearing loss:

Mechanical damage to the delicate cells and supporting structures of the organ of Corti;
Reduced blood flow to the inner ear;
Intense metabolic activity, which increases mitochondrial free radical formation.

Reactive oxygen species (ROS) are highly reactive. They are essential for mitochondrial function to generate energy. However, too many of them damage cellular lipids, proteins, and DNA, and upregulate apoptotic pathways. The observed impaired blood flow to the cochlea can enhance the toxic effects of ROS. Mechanical damage to the delicate hairs and membranes of the hair cells reduces their ability to converge acoustical energy into potential differences.
References
- Le Prell et al., Hear Res (2007); 226(1-2): 22–43
- Kurabvi et al., Hear Res (2017); 349: 129-37


text:
Why do red muscle fibres have more mitochondria than white muscle fibre but less ATP than White muscle fibres?
This is a question given in my Anatomy book and I am really confused because logically the substance which have more mitochondria should have more ATP as mitochondria is the power house of cell.But the question contrast the logic.

It would be good to see some figures to support the assertion in the question. What is really needed is ATP/ADP ratios. I appreciate that you trust your book, but anatomy isn’t biochemistry.

This is because of the difference in mitochondrial protein expression of red and white muscle fibres. There is difference in posttranslational modification, which leads to functional difference as red muscle contraction is slow, and white muscle contraction is rapid.
Metabolic control in mitochondria contributes in speed of activity and cellular energy production. So, these differences effect the cellular energy levels in both white and red muscle fibres.
Following factors also contribute to the ATP production:
White muscle mitochondria have higher proton leak.
Red muscle contain high palmitic acid and oleic acid, but white muscle possess more phosphate ions.
Collagen and elastic fibers are largely distributed in red muscle mitochondria, whereas high titin levels and densely packed sarcomeres are present in white muscles. Whereas high levels of long sarcomeres are present in red muscles.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118618/
https://www.hindawi.com/journals/bmri/2018/5816875/

MacIntosh, Brian R.; Gardiner, Phillip F.; McComas, Alan J. (2006). Skeletal Muscle: Form and Function. Human Kinetics. ISBN 978-0-7360-4517-9.
[https://en.m.wikipedia.org/wiki/Myocyte?wprov=sfla1 ][1]
[1]: https://en.m.wikipedia.org/wiki/Myocyte?wprov=sfla1
Good question,  I guess that high production could be linked to higher relative consume of ATP which could depend of necessity of energy and ATPase effectivity/ concentration of ATPase.
I suggest you to investigate the reference cited above.

Please do not post text as images. It discriminates against those sight impediments and need to use screen readers.


text:
Can I sterilize the equipment for experiments without an autoclave?
If I don't have access to an autoclave, can I sterilize my equipment in a regular pot. If so, what time is needed at about 110°C (I measured inside) for a proper sterilization?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

It certainly can be done. Tyndallisation may as discussed on labmate may work well for your situation. If not, there are many other viable alternatives suggested.

**Tyndallisation:
  **
  Developed partway through the 19th century by English physicist, John Tyndall, the eponymous Tyndallisation was a commonly used
  technique by the microbiologists of the 1800s. Tyndall experimented
  with boiling beef broths to develop a method to sterilise liquids in a
  safe and comprehensive manner.
His research led him to the basic principles for Tyndallisation, a process by which medias are subjected to relatively short boils at a
  regular atmospheric pressure. This relatively straightforward method
  is still suitable for small labs, or research facilities which only
  require sterilised equipment part of the time.
It is not recommended to attempt to sterilise closed glass containers using this method, without lining them with cotton and
  capping them with foil – allowing for air to escape without being
  subjected to contaminants.
The process involves boiling fluids for 10-15 minutes before leaving to cool to room temperature and leaving it to sit for 24
  hours. Repeat this process another three or four times, by which time
  sterilisation should have occurred.
Naturally this method has reduced in popularity due to the requirement to continue the process for up to five days to achieve
  sterilisation.


text:
What are these bugs skittering about the kitchen sink?
I found a bunch of these around a kitchen sink in an apartment building in Toronto, Canada, in late October, 2019.
The bugs vary in size, but are all very tiny, less than one millimeter (the photos were taken with a macro lens, and still barely captured them).
They move very fast when they detect light changes, and hide in the crevices around the sink.
They die very easily when squashed.
Edit: Managed to shoot a larger, more photogenic specimen.

Thankfully they are not cockroaches or bedbugs, but I cannot tell what they are from the pictures.

@KarlKjer Thanks for ruling those two out! I posted some better pictures, do they help narrow it down?

Yes, they define them.

Those are springtails, order Collembola. Looks like they are in the family Entomobryidae. They are completely harmless. They don't bite, or spread disease. They often find their way into potted plants in people's homes. I'm not surprised that they are in your sink. Their small size makes them subject to desiccation.
https://en.wikipedia.org/wiki/Springtail https://en.wikipedia.org/wiki/Entomobryidae


text:
Why is Carbon Dioxide a Greenhouse Gas whereas Ammonia is not?
Why are some gases Greenhouse gases while some are not?
I did search this on the net but didn't get any clearcut/credible answers.
What exactly is the property that is common among Ozone, Water Vapour, CFC and Methane?

There is "no" ammonia in earth atmosphere ; maybe a concern on some other planet.

I'm voting to close this question as off-topic because it belongs on the earth science stack

@John - I would suggest Physics as the most appropriate for the precise physical mechanisms involved in the Greenhouse Effect, ie the ways molecules absorb and emit EMR and why different molecules respond differently. Other factors, like relative quantities and processes that cycle particular elements and compounds through the atmosphere would be in the realm of Earth Science. Chemistry... even though it has some relevance I'm not sure it would be the best.

@KenFabian climatics, weather, and climate change are all solidly within earth science. earth science =/= geology.  also the earth science stack already has questions and answers about this.

This is better suited for the Chemistry site, but there are two reasons.  1) The gas allows visible light to pass, but blocks infrared.  (Which has to do with the nature of the bonds between atoms &c.) 2) It exists in the atmosphere in sufficient quantity to have an effect, which ammonia doesn't: https://www.livescience.com/57305-ammonia-detected-in-atmosphere.html  It's quite reactive, so ammonia that's released from e.g. fertilizers or urine doesn't stay around long.

less good for chemistry, but a good fit for earth science stack, which covers climatology.

@John: I meant better for Chemistry to answer the question of whether ammonia (or any gas) does block infrared wavelengths, and if so, why it does.  To be an effective GHG, it has to block outgoing IR while letting visible wavelengths in, and IF it does, there has to be enough in the atmosphere to have a significant effect.


text:
Confirmation of organoid's character with the respective organ
How can we verify that the Organoid formed from culturing stem cells shows the exact characteristics of the organ it is developed for?

Verification of organoids is done by detecting the cellular proteins for particular tissue type using Immunofluorescence.
For verifying intestinal organoid, apical membrane markers  (villin or alkaline phosphatase) and basolateral markers (E-cadhehrin) are detected by immunofluorescence. Transporters present in intestinal membranes are also displayed on organoids.  The peptide transporter PEPT1 and the glucose transporter SGLT1 are located on apical membrane, and the glucose transporter GLUT2 is present on basolateral membrane. So, these proteins can also be used as markers for verifying intestinal cells.
Via:

https://www.nature.com/articles/srep16831
https://www.ncbi.nlm.nih.gov/pubmed/19329995


text:
Is a lion a bony fish?
If you ask Wikidata "Does the species lion (Q140) have a parent taxon line up to the Osteichthyes (Q27207, bony fishes)?", it answers yes:
SELECT ?item1
 WHERE {
  wd:Q140 wdt:P171* ?item1.
  ?item1 wdt:P171 wd:Q27207.
 }

Here's a direct link.
Now, I assume that this must be wrong at some level (I'm no biologist, so please correct me if I'm wrong), so I tried to find the error.
This query displays that path more explicitly, starting with mammals:

Mammals (Q7377) have Tetrapoda (Q19159) as a parent taxon.
Tetrapoda (Q19159) have Tetrapodomorph (Q1209254) as a parent taxon.
Tetrapodomorph (Q1209254) have Rhipidistia (Q150598) as a parent taxon.
Rhipidistia (Q150598) have Sarcopterygii (Q160830) as a parent taxon.
Sarcopterygii (Q160830) have Osteichthyes (Q27207) as a parent taxon.

The third point seems strange, because Rhipidistia are described as a taxon of fish, which would mean that all mammals are fish.
Maybe this comes from the fact that tetrapods (and therefore mammals) evolved from Sarcopterygii 390 million years ago, as described here.
Is "having evolved from" considered a parent taxon in biology? If not, which of the five statements above is wrong?

Hi Cheeesus and welcome to Bio.SE! As you guessed, lions are unsurprisingly categorically not bony fish. I think you should be clear about what exactly the parent taxons are. To me it looks like they are ancestors. So we may have evolved from species that were bony fish, but that does not make us bony fish.

@James, thank you. Yes, to me too it appears like the data in Wikidata confuses "parent taxon" in the evolutionary sense ("mammals evolved from bony fish") with "parent taxon" in a classification sense ("lions are a subtaxon of mammals").

If you take cladistics literally (instead of as a useful tool), then yes, lions - and humans - are just bony fishes, by the same logic that says birds are dinosaurs.  (But both are just bony fishes, so there :-))

Possible duplicate of Am I a lobe-finned fish?

related questions https://biology.stackexchange.com/questions/87725/how-does-taxonomy-work-the-case-of-the-avian-dinosaurs/87728#87728 and https://biology.stackexchange.com/questions/70874/are-humans-gnathostomates/70954#70954 you should really be searching for similar questions before oyu ask.

The path is correct. The safest reading is to say that the lion shares a set of characteristics with the lungfish. You can also say that lion and carps are bony vertebrates (Euteleostomes).
In evolutionary taxonomy, each taxon does not need to consist of a single ancestral node and all its descendants: it allows for groups to be excluded from their parent taxa (in other words, not "being part of" but, as you said, "having evolved from"). Thus, lungfishes are closer to the lions than they are from, e.g., sharks or trout. In other words (even if this is too simplistic to say so), their "common ancestor" is more "recent".
In the Linnaean taxonomic system, all fishes were in the same class. This corresponds to our "everyday life" classification of fishes but not to the most recents findings about the "common ancestors".
To make things clearer, you need to understand the concept of paraphyly. The bony fishes group is paraphyletic with respect to the tetrapoda. In other words, it consists of the group's last common ancestor and all descendants of that ancestor excluding the tetrapoda. "Bony fish" is therefore not a clade, but "Osteichthyes/Euteleostomes" is a clade (= a monophyletic group of the bony vertebrate with a common ancestor that looked like our "modern" fishes).

Thanks, but this should somehow be indicated when using the property "parent taxon". Lions and extant bony fish like clown fish both have Osteichthyes as an ancestral taxon, but you cannot really say "A lion is a bony fish", can you?

Oh, maybe I'm confusing Osteichthyes with Teleostei?

Yes, I think that this is where the confusion takes place. Teleostei is distinct from mammals, but they share a common parent taxon (Osteichthyes) from which they evolved.

Are there any extant Osteichthyes which are not Teleostei? I don't mean "extant species which have evolved from Osteichthyes", I mean species which are now considered a subtaxon of Osteichthyes.

you mean "modern" bony fishes that are not teleostei ? Yes, the lungfish, this is why I took it as an example.

Thank you so much. Paraphyly made things much clearer.

Nice Q. & A! I want to post a related Q on "clades". Here it would be: does that not still imply that dipnoi are closer to the tetrapod than birds (or mammals) (I refer to the Paraphyly diagram in wikipedia)

for me they are all at the same distance if you look at the length of the lines.


text:
Does Japan have an ageing population?
I often hear Japan has a declining/ageing population.
It seems to be the prime example for this kind of thought.
Yet after moving to Japan and after having been there for travel several times already. And in comparison with my native country Germany as well as Europe in general, I think this concept seems questionable.
While I hardly see any children outside in Germany and it's mainly parents with one child.
Everywhere I go in Japan I meet a lot of children. Especially in the greater Tokyo area, if I go to restaurants there's always a bunch of kids. And usually you see at least two children per parents, if not three.
I can understand that in general this concept might be true but might not be applicable for bigger cities.
Where does the concept come from? Is there any proof it's actually true?

This seems better asked on Skeptics.SE, and would require a notable claim. I don't see any biology in the question. Your comment on the one answer makes me even more skeptical that you are actually looking for a biology answer here.

Thank you, actually I want sure either if it's good here but it seemed the best fit. Skeptics sounds better though. I didn't find that one.

I hate to sound rude, but you could easily answer this yourself with even the most minimal look into well-tabulated demographic information, rather than highly non-representative observations. About 13% of Japan's population is 0-14 years old, the third lowest fraction in the world. (https://data.worldbank.org/indicator/SP.POP.0014.TO.ZS ; easy to find with Google)  The fraction of the population over age 65 is 28%, the highest in the world. (https://data.worldbank.org/indicator/SP.POP.65UP.TO.ZS?most_recent_value_desc=true) The population density is high, so you'll certainly see more kids than in many other countries, though not proportionally more. I will leave it as an exercise to look up the numbers for Tokyo itself.

Of course I looked up those numbers. But I'm not sure how they come into place. Are they really representative?

How about the corollary: how representative are your observations?


text:
Can all animals breathe manually?
Originally I was pondering about why we have the ability to breathe manually. I couldn't think of any tangible advantage, given that the body can develop mechanisms to regulate the rate of breathing when needed.
An uncited source (on reddit) said "any animal that can vocalise 'can' breathe manually." Is that true?
Secondly, do non vocal animals, for eg., some arthropods, not have any conscious control over their rate of breathing?

Are you talking about slowing breathing if they are trying to be stealthy, or vocal communication?

@James any form of manual/forceful inspiration/expiration. I interpreted the answer (on reddit) in the sense that being able to control breathing is a necessity to be able to speak/vocate; although I'm not very sure. Just wanted some more insight into the matter.

Could you link to the Reddit? This site works best when the questions are specific and answerable.

https://www.reddit.com/r/explainlikeimfive/comments/2b927k/eli5_can_animals_breathe_manually_or_are_they/

I think I see the problem. You need to properly define what breathing manually is. For example, a bird may have to control its breathing to sing, but may not willingly hold its breath per se. Would that count? Any dog owner knows dogs will restrict their panting as soon as they see a squirrel or equally chasable critter. Would that count?

Some mollusks have lungs and can use breath for nest building, defense and diving. They have 100 times less neurons than arthropods.
semi-aquatic insects can control air for going under-water, and some spiders, beetles and spittle-bugs can control bubbles. There are even shrimps that snap at water to produce bubbles.
Fish can hoover and squirt out targets using gulps, without even having lungs, build bubble nests and they also have a swim bladder that they can use to control buoyancy. Human lungs and fish swim-bladders are thought to have evolved from primitive fish that gulp air: https://mainichi.jp/english/articles/20160819/p2a/00m/0na/004000c
It illustrates early vertebrate control of breath-like mechanisms. It's sometimes their main mode of interacting with objects and prey.
Some reptiles hold their breath under water and use bubbles, i.e. iguanas, water anoles and crocodiles. Some reptiles can vocalize, i.e. gecko's : https://www.youtube.com/watch?v=0Q_1KW0Q-10
Scientists don't think that they have much conscious thought.
Amphibians can hold their breath for long periods to swim and use the throat to hoover prey, and most frogs can vocalize: https://youtu.be/y7F0ObBiHio
orang-utans can blow bubble gum, swimming birds and mammals can often do a lot of bubble stuff.
Perhaps the truth pivots on knowing what animal consciousness is, which is amply debated on the web.
Manual involves hands. Consciously and voluntarily involve thought, and those are the words used in biology.
Animal will and conscious reasoning is one of the most controversial topics in science, and scientists still argue both ways, because they CAN argue, and there is no agreed measure of consciousness.

showing invertebrates posses something does not preclude a group of vertebrate lacking it. Some insects also have wings and parental care. breathing control is not hard to evolve so it could easily evolve multiple times.


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What causes the shape of the dense structure in this "giant squid egg" sac?
The YouTube video Swimming Next To Giant Squid Egg shows a giant egg of a squid and/or an egg of a giant squid. Text in the video's description includes the text quoted below, which indicates that the "egg sac containing hundreds of thousands of baby squid."
Question: The egg sac is mostly transparent and contains an optically dense structure with a very striking shape. If I didn't know it had hundreds of thousands of individual organisms, I'd think there was a brain developing at the top and a body forming below it. Is this shape just random? Does it change over time? Does it represent motion of all the little squids swimming around? It looks to me like it could be a slow-motion murmuration for example.

screenshots from the video linked above; click each for a full size view or just watch the video.

MANDATORY ONSCREEN CREDIT - Ronald Raasch
A team of divers filmed a rare glimpse of a huge transparent egg sac containing hundreds of thousands of baby squid.
The stunning underwater video was filmed by Ronald Raasch, 48, as he was diving with two other team-members from the research vessel REV Ocean in the cold waters outside Ørsta, Norway.
On October 5, the team of divers was swimming back to shore after visiting a WWII shipwreck about 200 metres from the coast, when they had a once-in-a-lifetime encounter with a mysterious object.
Floating 17 metres below the surface and 15 metres above the ocean floor, was a giant transparent orb which the divers quickly identified as a 10-armed squid’s egg sac.


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What is the scientific consensus on whether humans were monogamous during the period of evolutionary adaptedness?
The book The Mating Mind by Geoffrey Miller asserts, as part of its thesis, that humans were not monogamous in the environment of evolutionary adaptedness.
I found the book vivid and persuasive, but I'm interested in what others in the field would say. Is this the scientific consensus among evolutionary psychologists?

"during the period of time wherein evolution shaped our minds" - there was one distinct period?

I'm voting to close this question as off-topic because its non-speculative aspects appear to be answerable by archaeology rather than biology.

@David Any sense of a better site on this network to ask this question?

Not really. There does not appear to be a SE list for archaeology. I just googled for archaeology list and there seem to be a large number, but which would be appropriate I have no idea.

There is no such thing as  "period of time wherein evolution shaped our minds". Our "mind" (whatever you mean by 'mind') is always evolving and has always been. It might not be enough to make your question on-topic but it would be already a good move toward it if you could just specify dates of interest.

I'm referring to the environment of evolutionary adaptedness; do you think this is a useful concept?

It might be worth expanding the question with some background.  For instance, are you asking whether there was a period when humans or pre-humans were "naturally" monogamous, and trying to discover when & how this changed?


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Identification of larva on cat fur
I found this larva (assuming it is a larva) when my cat jumped off my bed, I'm assuming she just picked it up outside. However, I'm not quite sure what it is or if it should be a concern she had it on her. When it moved, the tip of the "head" looked black and it did have "feet" like a caterpillar. If it helps, I live near middle TN and the approximate size was about an inch long. I took some pictures found below, if anyone has any information on it, thank you!

Made a small correction. Larvae is the Latin plural from the singular larva, which is what you are referring to.


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What are the chemicals in the gap at a synapse?
I am learning about (introductory level) biological psychology and the synapse structure came into mind. I do understand that neurotransmitters are transmitted between two neurons via the synapse structure.
What I found about neurotransmitters was that there are several types of them, including amino acid, and other stuff (I don't really know chemistry..). The problem is that, according to the following picture, neurotransmitters are transmitted across the gap. What are the chemicals in the gap at a synapse? There must be some medium that transmits neurotransmitters right?

My guess is that there is a special solution in which neurotransmitters are soluble. Any help will be appreciated. Thanks in advance!

Hello Zang.Welcome to Bio SE.Your question already been answered. Check it here: https://biology.stackexchange.com/questions/85719/what-material-fills-the-synaptic-cleft-is-it-water/85913#85913

@Science123 Thank you.


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How is incomplete dominance explained at the molecular level?
What happens at the molecular level between two alleles that demonstrate incomplete dominance? Do the proteins coded by each allele have different functions, or is there an interaction at the RNA level?

Allele could mean different things: it can be a point mutation, a whole new gene or even a whole chromosome. The molecular mechanisms involved obviously depend on which of those we are talking about.

@RogerVadim My understanding of "allele" would exclude "a whole new gene or even a whole chromosome". Did you have some examples in mind?

@Armand From the point of view of population genetics allele is a rather general term, just like mutation is not necessarily an SNP. Btw, I didn't mean new chromosome - but that chromosomes inherited from the two parents may have many differences between them. Here is from Gellespie: "Here we will use locus to refer to the place on a chromosome where
an allele resides. An allele is just the bit of DNA at that place."

@RogerVadim OK, I guess we'll agree to disagree.

@Armand In order to meaningfully disagree you need to suggest your definition of an allele :)

@RogerVadim Good point. It would be something like "homologous DNA at the corresponding locus on the homologous chromosome" .  I agree that the origin of "allele" in pre-molecular genetics makes a molecular definition somewhat problematic.

@Armand Homologous is a good point - I guess my phrasing about new gene was misleading - at least for diploid organisms. My main point is that allele could be a rather big piece of DNA (or even several pieces) with complex functioning on molecular level. I would change nothing from the point of view of pop. gen., in particular, in terms of discussing dominance, but it may correspond to many different molecular mechanisms.

@RogerVadim Re: "allele could be a rather big piece of DNA (or even several pieces) with complex functioning on molecular level" It seems to me that an allele (being a gene) should be a single functional unit and should also exist at a single locus (i.e. be essentially in complete linkage disequilibrium with other alleles of the same gene). Once we start considering more complex molecular configurations, I don't think the term "allele" applies anymore. Is there a population genetics example with multiple pieces of DNA that you could describe?

@Armand recombination does not have to occur necessarily at the boundaries of genes. If a complex phenotipic trait is determined by a joint action of several genes, and these are separated due to recombination, this in itself could be mechanism for the incomplete dominance in question.

Molecular mechanisms of incomplete dominance (also called partial- or semi-dominance) vary.  As an example, let's look at snapdragons and morning glories, two flowering plants that both exhibit incomplete dominance relative to flower pigmentation.
Snapdragons (Antirrhinum majus) have multiple alleles at the nivea locus.  The wild-type nivea transcript (niv+) encodes a chalcone synthase involved in pigment biosynthesis, and a single copy of the niv+ allele is sufficient for wild-type pigmentation.  However, niv+ is semi-dominant with the mutant niv-525 allele, leading to reduced pigmentation in the heterozygote.  The original publication by Coen and Carpenter 1 describing this effect offers some possible molecular explanations:

Transcription factor sequestration.  The niv-525 allele could encode a defective enzyme.  This allele also contains an inverted duplication of a transcription factor binding domain required for enzyme expression.  The defective niv-525 allele therefore titrates away transcription factor from niv+, leading to less enzyme and therefore less pigment.

Transvection.  There is some physical interaction between alleles on homologous chromosomes, such that transcription of one or both alleles is activated or repressed in trans.  This could be realized as binding of the enhancer associated with the wild-type allele to the promoter of the defective allele.  Figure 9 of Gohl et al. 2 has a good explanatory graphic.

Anti-sense hybridization.  The inverted duplication on the niv-525 allele contains a TATA box.  Transcription initiated at this site would result in a transcript anti-sense to the wild-type mRNA.  Hybridization of the sense and anti-sense
RNAs creates dsRNA that is selectively degraded and/or inefficiently transported out of the nucleus, ultimately leading to less enzyme product.

Morning glories (Ipomoea purpurea) show similar genetics at the A locus, which also encodes a chalcone synthase.  However, unlike the snapdragon niv+ allele, a single copy of the wild-type a allele is not sufficient to produce wild-type pigmentation.  Therefore, incomplete dominance in morning glory results from a simple dosage-dependent mechanism, as described in Johzuka-Hisatomi et al. 3

References

Coen ES, Carpenter R. A semi-dominant allele, niv-525, acts in trans to inhibit expression of its wild-type homologue in Antirrhinum majus. EMBO J. 1988;7(4):877-883.
Gohl D, Müller M, Pirrotta V, Affolter M, Schedl P. Enhancer blocking and transvection at the Drosophila apterous locus. Genetics. 2008;178(1):127-143.
Johzuka-Hisatomi Y, Noguchi H, Iida S. The molecular basis of incomplete dominance at the A locus of CHS-D in the common morning glory, Ipomoea purpurea. J Plant Res. 2011;124(2):299-304.

Strictly speaking, incomplete dominance is an interaction between two alleles of the same gene not between two genes.
The most common cause of this is the dosage effect. For example, the product of CHS-D gene is an enzyme required for the synthesis of purple pigment anthocyanin in morning glory flowers. If a plant has two functional (A) alleles of this gene it produces enough pigment to have intensely purple flowers. The a allele has the loss-of-function mutation (isn't able to produce working enzyme) so homozygous a/a plants will lack purple pigment resulting in white flowers. But heterozygous A/a plants have half of the normal enzyme level and half of the pigment so the flowers are lighter purple (source).  Genes like this are said to be haploinsufficient. In cases of full dominance, one functional copy of the gene is enough to produce a "normal" phenotype (the gene is haplosufficient) or the gene is upregulated to bring the concentration of functional products to the required level (source).
There are other mechanisms for incomplete dominance. For example, in snapdragon flowers, the allele niv-571 at nivea locus can inhibit the expression of "normal" Niv+ allele in heterozygous plants (source).

Zlira, it seems you beat me to this answer by 30 seconds, with the same examples!

Could be missing something here, but incomplete dominance is more like an absence of interaction in both biological and statistical senses- e.g. the additive model is a case of incomplete dominance in which you model phenotypes by summing the effects of each allele independently. Dominance/recessivity is conversely best understood as an interaction (absence of independence) between alleles. As you say, dosage is a good mechanism for codominance, but dosage effects will be strongest in the absence of allelic interactions.

Dominance or Recessiveness is the characteristic of allele, not gene.
Particular gene contains data for producing specific protein.  Protein produced from one allele can effect protein synthesis of other one.   Protein formed from recessive allele can show dominance over the dominant allele, and this is known as Dominant negative.
The protein produced from one allele is faulty and prevents other allele's protein to work properly. Both the proteins interact with each other in particular cell.
Genetic trait for red hair is an example of dominant negative.   Gene MC1R is responsible for red hair. Protein produced by this gene converts red pigment into brown.  When this protein is faulty the red pigment is accumulated and hair appears red in colour. Usually red hair is recessive trait.  Two faulty MC1R gene results in read hair characteristic.  Both the proteins formed from MC1R gene need to bind so that red pigment converts into brown.  But when functioning product binds with faulty one, the protein becomes defective.  So this defective MC1R protein is responsible for showing dominance.
https://genetics.thetech.org/ask-a-geneticist/genotype-vs-phenotype

Thanks....The answer is not related to incomplete dominance.

It is actually answer to second half of the question..as incomplete dominance is explained in earlier answers.


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Help to identify larva found in sink?
I need some help in identifying this critter. It was found in southeast Georgia in a home I am renovating. There were several around the sink and toilet bowl.
Approximately 5 millimeters long. Stripes black/dark gray. Tapered end seems to be moving as though it was the head. Bulbous end has two extrusions like antennae?
Thanks in advance.

Found it!
Seems to actually be the pupae phase of the common drain fly - psychoda spp.
Looks like I'm going to be routing or replacing the pipes in that house.
Thanks.

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please edit your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Which culture media is suitable for cheek epithelial cells?
A month ago, I tried isolating cheek cells from saliva and the experiment was a success, however, I was wondering if it is possible to cultivate these cells in vitro. I'd say it's possible, but I wasn't able to find any publications about this topic online, even on PubMed (I found one, but it was outdated and the part with used media wasn't clear). Is it possible to use just DMEM media and if so, how long will the cells survive in the media, or are there any other alternatives?

There are different kinds of epithelial cell basal media. These are also usually supplemented by different factors. I cannot find a medium specific to oral mucosa and the composition of the basal medium is difficult to find. This paper says that DMEM supplemented with human serum or conditioned with fibroblast supports growth of conjunctival epithelial cells.


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Help me identify these creatures found in sink
The conical flask was kept in a sink for about 3 or 4 week, was waterfilled, and I have no idea if they grown after the flask was waterfilled or before the flask was waterfilled. We do not work with animals so these arenot any experimental material, but maybe they are soil borne if the conical flask contained soil sample (I do not have any idea what was kept in that flask before it was left in that sink)

They were not moving and they were sticked firmly on the glass wall. They had some constriction marks. Length apporox 0.2 to 0.5 cm, Width approx 0.1 to 0.3 cm. colour pale white to brown.

Maybe eggshell of something???

I think it's clearly a pupae.
They look like fruit fly pupae, which are very common.
The size also match the description (length of the fruit fly pupa is about 2.5 mm).

I think this will be a larva. Check this video. If it was in a sink, is very probably than will be a fly. But the specie only will be identified with a genome assay, or taxonomically once they out the pupa.

but mine were not moving

@AlwaysConfused Pupae don't move around in space. They move around inside but you may or may not see that movement. They look to me a lot like fruit fly pupae but I'm having trouble picturing the scale to know if that's likely true; in any case, if you keep watch over them you will likely find out soon.

Sorry, i mean larva not pupa. In one phase of the larva-fly transition, the larva stays inmobile, just after the fly out the eggshell. I thinked that was clearly at the final minutes of the video.


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Does more ATP present mean that a microbe can ferment more and decrease the pH?
I noticed that EMP produces 2 ATP and EDP produces 1 ATP. Does that mean that if more ATP is present that would give more energy for fermentation and lowering the pH of a system?

You need to explain clearly what you are talking about, avoiding abbreviations. Why do you think fermentation requires energy? What type of microorganism are you concerned about? What is the relevance of the pH? At the moment your question is incomprehensible.

I'm thinking about the oral community and if utilizing the Embden–Meyerhof–Parnas Pathway more than the Entner–Doudoroff pathway could result in a lower pH.

To repeat, why do you think fermentation requires energy? It produces it.

@David I guess he/she meant more fuel/substrate for fermentation, or more free energy to drive the process...

@O.rka An underlying question would be what is the limiting factor that would stop fermentation assuming a closed system. Or maybe the question is about the balanced pH in a chemostat when one or the other pathway is imposed?


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Would gargling with salt water every day increase blood sodium levels?
Would gargling and rinsing with salt water every day for a few minutes increase your blood sodium levels? Considering the fact that sublingual medication is a very effective way for introducing substances straight into your bloodstream very quickly.
Below's a link to a study on Pubmed about this issue. Does anyone here have access?
https://www.ncbi.nlm.nih.gov/m/pubmed/3474267/

Do you think this question would be more suited for the medical science stack exchange?

Personal medical questions and health advice are off-topic on Biology.

@David it's a general question about sodium levels with regards to gargling salt water


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How can we digest lactose even though it has Beta glycosidic linkages?
I have Read that we cannot digest cellulose because we do not have enzymes to digest Beta glycosidic linkages in Cellulose
Then how is it that we have an enzyme called Lactase to digest the Beta glycosidic linkages in lactose?
Also If we have evolutionarily developed Lactase ,Why didnt we develop "Cellulase " too ?

Humans have β-galactosidase (lactase) which allows them to break down the β-glycosidic linkages in lactose. This enzyme is inactive against cellulose. We also haven't evolved a cellulase, probably because we didn't need to. It's quite simple. Are you asking any further questions beyond these?

Please quote or provide a reference to what you have "read" when asking questions on this site. It is quite likely that you are misquoting or misunderstanding, and by checking the original we can put you right. Enzymes recognize their substrates — in this case not just a chemical bond, but the two sugars that it joins. These are different for cellulose (glucose only) and lactose (glucose, galactose). Also, please restrict yourself to one question at a time. The second question about why few animals have cellulases is quite separate. (It should be obvious why we evolved lactase.)

@SPr — I'm not sure it's quite so obvious why very few animals have not evolved cellulases. Ruminants and most insects that do "need to" use symbiotic bacteria. I think this might be an interesting question in itself. Is it something to do with the waxy coat on leaves, perhaps? I don't know.

Few animals have evolved cellulases, but they are a very tiny minority and they tend to be aquatic invertebrates or small insects with little gut tracts like termites; always different to large mammals. I must admit I don't understand "why didn't we develop X" questions though. I think the onus is on the person to reason that it would have been beneficial in the first place, at least to a more competitive degree than the absence of a trait. Consider free glucose in the anaerobic gut, in the presence of a diverse microbiome... Consider a lifelong lack or reduction of fiber... No thanks.

What I meant by the Second Question was that ,When we have developed β-galactosidase ,just based on the nature of the bond making the cellulose  must also be possible....that too Given the high advantage an animal with cellulase will have ,So, What property of cellulose has made the evolution of cellulase so rare? Or does the answer have nothing to do with the nature of cellulose but some  factors at the organism or ecosystem level?Or is it just pure luck?

One simple  reason is physical interaction.
lactose is only composed of two sugars, while cellulose is giant network of interlocked sugars. Cellulose keeps the sugars tightly packed in three dimensions. even getting to the bonding site is difficult.
human and many other lactases are a huge molecules that would never be able to fit on to a cellulose chain, while cellulase of often a tiny molecule as enzymes go and the active site is not buried in the center. Compare the two enzymes.

lactase

two different cellulase enzymes
Note the big difference in size. Also look at cellulase in action.

Notice it has to peel up the cellulose strip by strip, while lactose is just floating free in solution. This even limits the speed of cellulose breakdown. which means organisms that breakdown cellulose have to spend a log time doing it, while humans have a relatively short and fast digestive timeframe, so even if we could we would not get much from it.
These functional limits also makes a cellulase enzyme harder to evolve, since it can't be too large or in organisms with fast digestive processes.  We often forget the physical necessities of enzyme function. there are plenty of other reasons enzymes do not function on multiple substrates, but this is why is basically impossible to for evolution to change lactase into a cellulose cleaving enzyme.


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Can two proteins activate/inhibit the same gene at the same time?
Suppose there are two proteins inhibiting a particular gene. Its not necessary that both will inhibit the gene at the same time instance right?
So if one protein has already inhibited that gene before the other protein, what is left for the other protein to inhibit this gene? It has already been inhibited right? What more does the other protein inhibit?

Probably the proteins are competing (like a % downregulation) to bind at the gene or they bind at different parts of the gene? it depends, do you refer to a specific example?

Inhibition does not necessarily need to be competitive, i.e. in the same place, i.e. the inhibitors work on different targets at the same time. Inhibition also need not be 'total', it can be partial. The inhibitors can be partial, additive or even synergistic (joint inhibition is greater than the sum inhibition of its parts). Single inhibitors can also sometimes inhibit multiple targets, so any 'extra leftover' inhibitors can work on other targets. Or work at different times in development; i.e. an inhibitor can have different targets in the embryo vs. the adult, or in tissue A vs. tissue B.

Can you give me a link to study more about inhibitors? These information that you gave me,  would these be available from any source?

This is general information available in any biochemistry or molecular biology textbook. I think you could start with Wikipedia, it has pages upon pages on molecular inhibition. A good starting point would be enzyme inhibition. Though many targets or processes can be inhibited - not only singular enzymes - such as the transcription of genes, or the progression of the cell into the next phase of its cell cycle, or the polarization of cells, and so on and so forth.

the inhibitors work on different targets at the same time.- does this mean multiple molecule of the inhibitor is in action at this time?

Are you referring to protein inhibition at transcription/ replication level or in general?     As you are mentioning the effect of protein on gene?

@Twinkle in general

Then its already explained in comment section. If you are particularly concerned at DNA level, then there are different proteins like transcription factors which bind to upstream elements located on DNA and regulate the DNA transcription.


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Calculating the ripeness rate in fruits
I need a way to calculate avocado ripeness rate in my experiment so I need a quantitative way, I'm not sure if calculating the cellular respiration for the avocado will result in ripeness rate for the fruit, if that's true I need references if you got.
And if you got another better quantitative ways to get the "rate" of the fruit ripeness.

Generally, ethylene production is used to gauge fruit ripeness.  This paper (PDF download) outlines an experiment measuring ethylene production from Hass avocados at different temperatures over several days.  It appears they used gas chromatography to measure both ethylene and CO2 concentrations.


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Why do chromosomes uncoil back to chromatin after cell divisions?
At the telophase of meiotic and mitotic cell divisions, the chromosomes of daughter cells uncoil back to chromatin, but after interphase, it coils up again to form visible chromosomes. Why do this happen? Isn't it simpler and more convenient for the chromosomes of the cells coil up in 1 cell cycle?

Isn't it simpler and more convenient for the chromosomes of the cells coil up in 1 cell cycle? -- please clarify.  Are you asking why chromosomes uncoil at all, considering they just need to condense again before the next cell division?

@Dirigible Yes, I don't know why this happens since it sounds redundant. Thank you

The condensed form of DNA that exists during cell division is tightly wound and therefore unavailable to the enzymes and transcription factors that interact with and read DNA.  So, if chromosomes are constitutively condensed, the cell will not be able to transcribe RNA, and thus will not be able to make new proteins, and thus will not be able to grow and divide.  The process of selectively condensing certain regions of DNA to prevent binding of transcription factors and RNA polymerase is actually a conserved method of epigenetic transcriptional regulation in eukaryotes.
You may be thinking Then why condense DNA at all?
Uncondensed chromosomes are difficult to separate, and failure to properly segregate homologous chromosomes during mitosis (a phenomenon called nondisjunction) can lead to aneuploidy.  Aneuploidy in germ cells is often lethal, and aneuploidy in somatic cells is a characteristic of cancer.

It’s happening because genetic information from DNA can be read only if it’s in the chromatin form, it can’t be read from chromosomes and so the cell can’t fulfill its functions. But if it’s need to take apart cell’s genetic material, the form of chromosomes makes it easier

Would you please edit your post and add a reference to back-up your statement?


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How to calculate grams of fat used during hibernation?
In Humphries et al. 2002. Nature, the authors report number of grams of fat bats use during hibernation. However, their equations results in values in mlO2/g.
How can one convert the energy requirements to amount of burnt fat resources?
I found an equation $f = \frac{20.1 \times E}{3930}$, whre $f$ is fat in grams and $E$ is energy in mlO2/g (Hayman et al. 2016. Sci. Adv.). But the paper is without any explanation as to what the numbers mean, and why they are used. Does anyone know, how to convert oxygen consumption to volume of burnt fat?