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Is there any example of genetic mechanism of delayed onset toxic effects?
We know that exposure to many toxic chemicals during embryonic development may show toxic effects later in life. It is called Developmental Origins of Health and Disease (DOHAD). Most of the mechanisms reported behind these kind of toxic effects are epigenetic. I could not find any genetic mechanism in the literature. Is there any example of genetic mechanisms behind DOHAD?

Are you asking for mutagens that are well known for its long term effects when exposed as a embryo?

I would tend to think that this question is off-topic here as it is a health question more than a biology question. MedicalSciences.SE would be a better fit. See for example their radioactivity tag

Mutagens might work but do you know of any specific mutagen, that can cause onset of toxicity only later in life even when the exposure happened during embryo phase?

Any mutagen would have health consequences later in life. I don't know of study on this question though and I can't really help you any further. You state Mutagens might work which makes me confused as to what other than exposure to mutagens would you be interested in.

@Remi.b this question is asking about a biological mechanism behind a medical condition. It is EXACTLY on topic here per the second of only three bullet points on What topics can I ask about on here.

I posted about this question on meta


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Can a brain process auditory signals at 18 weeks of human development?
According to When a fetus hear , When a baby can hear in the womb and several other similar articles, a baby starts to hear sounds at week 18. And according to How hearing works. Hearing involves

nerves communicate to the brain. The hearing nerve then sends the
  information to the brain with electrical impulses, where they are
  interpreted as sound.

Does this actually mean a brain is actually processing auditory signals at 18 weeks of human development, or is the brain at 18 weeks only processing sounds by a process that doesn't involve the brain? Perhaps the conclusion might seem obvious for some, but not for me considering the supposed inability of the brain to process several others (or any other?) kind of signals at that stage, such as pain At what stage is the nervous system developed enough to interpret neuronal signals as 'pain'? and being the hearing experience directly connected to pain sometimes.

The ear is innervated at 18 weeks, if I recall. There is some evidence of varying quality looking at the response to acoustic stimulation, but good evidence of demonstrating cortical processing puts it much later... i think third trimester. I'd have to do some digging to find this though. A quick search didn't yield anything.

According to a concise review by Graven & Brown (2008) the development of the auditory system (Fig. 1) in the human is as follows:

15 weeks gestational age*: structural parts of the cochlea and the middle ear are well formed;
20 weeks: middle ear and cochlea are anatomically functional;
Around 25 - 29 weeks: auditory system as a whole becomes functional, as the spiral ganglion cells in the cochlea connect inner hair cells to the brain stem
and temporal lobe of the cortex. In other words, only at this point, the peripheral end organ becomes connected to the central nervous system. At 25 to
26 weeks' gestation, a loud noise in utero will produce detectable changes in autonomic function.
28 - 30 weeks: neural connections to the temporal lobe of the cortex are functional. The development of tonotopic columns in the auditory cortex commences. They are needed to receive, recognize, and react to language, music, and meaningful environmental sounds.

* Gestational age is a measure of the age of a pregnancy which is taken from the beginning of the woman's last menstrual period (LMP), or the corresponding age of the gestation as estimated by a more accurate method if available. Gestational age can be obtained by adding 14 days to the point of fertilization.

Fig. 1. The adult auditory system. source: Graven & Brown, 2007
Reference
- Graven & Brown, Newborn Infant Nurs Rev (2007); 8(4): 187-93

source: Stack Exchange

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

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Common english name for tissues which are separated from the blood by blood-tissue barriers
Which general term is used to denote such organs/tissues as: brain, testis, thymus etc., which are separated from the blood by blood-tissue barriers?

I am not aware of any umbrella term: the barriers for each are not identical, the function and reasons for the barriers are not the same.
Often these organs are referred to as "immune privileged" because one of the important consequences of the separation is that immune responses in each of those organs are different than in the rest of the systemic circulation, even though this is of course not the only significance of blood-tissue barriers. The meaning of the term has also shifted a bit, though, and I still see different definitions in different places (for example, the Wikipedia definition is not the one I would use). As a consequence, it is easy to argue that some like the thymus should not be considered immune privileged, so my umbrella suggestion would be to just avoid umbrella terms.

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


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You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time?
A statement I recently read: 'Evolution is debunked and gives no basis for morality. Natural Selection throws away info, it does not add.
You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time. Created.'. Who can shed a light?

Mutual dependence does not imply simultaneous springing into existence.

I think its rather ironic to note that without question, this same "logic" (stupid as it is) could be used to "disprove" the existence of God, since no creator could exist without being created by the creator... Also, evolution has never been claimed to provide morality. Darwin was so repelled by parasitic wasps that he thought that no benevolent creator could have been responsible for such cruelty. That creationists have adopted a business model based on lies (false witness) is also pretty ironic.

What is the source of your quotation? What is your question exactly? What attempt have you made to solve it yourself? Have you searched this site for related questions?

There have been two answers that refer to the RNA World Hypothesis — which I do think is relevant — but both contain aspects I, personally, find unsatisfactory (as I commented originally). As this question has come up again from the Community, let me answer the question in a way that I, at least, find satisfactory.
I am only concerned with the biological part of the question:

“You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time.”

The question deals with something we do not know — the times at which DNA and RNA  came into existence — so all we can deal with is the logic of the argument, i.e. is the conclusion of contemporaneous appearance necessarily true?
To refute that all that is needed is an alternative hypothesis for a sequential appearance that is consistent with biology and chemistry.

Contemporary biological systems exist in which DNA is not need to make RNA — namely RNA viruses. Although these depend on organisms (bacteria or eukaryotes) that have DNA genomes, their replication does not directly/mechanistically involve DNA.
This, by itself, invalidates the first assertion (“you need DNA to make RNA”).
Turning to the origin of cellular life, which currently has exclusively DNA genomes, there is therefore no biochemical/mechanistic problem in envisaging that the ancestor of modern organism had an RNA genome at a time when pathways for synthesizing the precursors of DNA did not exist. Note that this does not require the other aspects of an RNA world (RNA, rather than protein, enzymes). These may be likely, but are not part of this argument.
So all that is required is a biochemically plausible hypothesis for the emergence of pathways for the synthesis of deoxyribose and thymidine, of enzymes to polymerize them, the switch to a (more stable and less error-prone) DNA genome, and the switch to this new genome encoding and transcribing the RNAs that are still necessary for protein synthesis and the like. I maintain that there is no reason in principle that this is not possible.

Whether or not the sequence of events was as in the scenario above, I argue that it demonstrates how RNA and DNA could have arisen at different times but given rise to the inter-dependent situation we see today, and demonstrates the basic flaw in the argument in the question.

According to RNA world hypothesis at some point the organisms had RNA genome only and only later DNA and transcription machinery was built to protect the genome(DNA sits in the nucleus and does not interact much with others).
RNA got both informations storage capability as well as the catalytic activity. Thus it can be concluded that at some point, RNA was the primary genome and RNA alone could let an organism survive due to its catalytic properties.
So to answer your question, it is a probability only but still, RNA appeared before DNA

Please note that the RNA world hypothesis doesn't have anything to do with nuclei - eukaryotes (and therefore the nucleus) for sure evolved much later than the DNA-RNA-protein system itself.

I'm reading your questions as:

Since DNA and RNA co-depend on each other, which one existed first in the course of evolution

The honest answer to this is: we don't really know.
The RNA world hypothesis is a pretty good and also much studied and developed theory, but it's nonetheless a theory still. Even with solid experimental prove that a pure 'RNA world' can over time evolve to make DNA, won't let us know if it actually happened like this in the past or not.
A bit more background on why an intial "RNA world" from which DNA evolves at some point is theoretically possible:
In modern life forms genetic information is stored in DNA, then translated in RNA and a lot of functional elements are the resulting proteins. This is already a pretty complicated system so it was hypothesized that RNA might have one of the first molecules used for all of these steps. RNA can obviously store information (though not quite as long as DNA, since get degraded more quickly) and it can also have catalytic function, which is obvious from e.g. the ribosome, which still uses catalytic RNA units to build up all proteins.

The quotation in the question says nothing about which came first. It asserts both emerged together, presumably as an act of God, given the preamble. The question you want to answer has been asked and answered previously.

@David As far as i understand it the OP does not assert that DNA and RNA emerged together, but saw that statement somewhere and is now asking confirmation or further information on that - presumably from a scientific viewpoint given he is positng on this site (I'm judging from the question title and the 'who can shed light' part in the question). I purposely did not comment on the creation / act of God part since it has nothing to do with science.


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What causes biennial epidemics?
I read the Wikipedia article on acute flaccid myelitis which contains a graph showing confirmed US cases peaking biennially in 2014, 2016 and 2018.
That got me wondering because I found that pattern to seem unusual compared to an annual one tied to seasons or a constant or increasing one. So I did a quick Google search on "biennial patterns in rates of infection" and turned up this paper: Regular biennial cycles in epidemics caused by parametric resonance which discusses, mathematically, the biennial patterns sometimes found in the incidence of measles.
What I'd like to know, in layman's terms, is the causes of biennial patterns such as these in terms of the way these infections spread among victims and develop within them.


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Skin (histology)

Our instructor share this image with us. She didn't specify much. She only said it was a skin sample.
Could you tell me what is the thing that was pointed at with the blue arrow?
I believe that I found a similar image in Ross' Histology (e6) Plate 44.
Thank you

Could you please edit your question and add, what you think this is? And what are the pros and cons of your solution?

It is difficult to say based on the limited informations about the sample, but I could assume that this is a Masson's Trichrome staining. Briefly: blue/green - collagen, red/pink - cytoplasm, dark pink/brown - nucleus.
Presence of the adipose tissue (white area on the right) and a lot of collagen (green) suggest that the sample highly likely comes from dermis. The large structure pointed by the arrow looks like an eccrine sweat gland. Here, you can see it in classical haematoxylin and eosin staining:

Alternatively, see: http://medcell.med.yale.edu/histology/skin_lab/eccrine_sweat_glands.php


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What does it mean to use DMSO as a dissolvant in biology experiemnts?
In many biology publications, I saw that dimethyl sulfoxide (DMSO) is used to dissolve drugs. However, the cell-based assays are still performed in water-based medium such as RPMI or PBS.
My question is: If a compound is not soluble in water, what is the purpose of using DMSO? Although the drug can be dissolved in pure DMSO, won't it precipitate after putting the DMSO-dissolved compound into culture medium?

Usually such compounds are dissolved in DMSO to make a concentrated stock solution (e.g. 1000x), which is then diluted into the culture medium. Often, the compound is soluble in water at this lower dilution, but not at the higher concentration required to make a stock. Sometimes the compound has low solubility in water and much of it precipitates. This still lets us test the effect of the fraction that remains soluble.


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Monohybrid Recombinant Frequency? (three point Gene Linkage)
I am curious to know if it is completely impossible calculate recombinant frequency for monohybrids ( three point link, gene map etc.)
Here is an example:
Marker 1

xx= 25
xy=100
yy= 20

Marker 2

xx=30
yx= 89
yy= 20

Marker 3

xx= 100
yx=50
yy= 100

This is what I think it would be like for x:x Marker 1 to 3
grand total = 534
So from Marker 1 to Marker 2 it would be 25+30/534 = 0.1029
Marker 2 to Marker 3 : 30 +100/534= 0.2429
Marker 1 to Marker 3: 125/534= 0.2340
Am I on the right track --- if not can you please show how it would be done for this example?

Can you please clarify what xx, xy and yy are as well as the genotypes of the parents? What are the two loci and the alleles at each locus?

xx and yy are the parents (genotype), the alleles are either x or y

How about the other locus, then? You can only talk about recombinants if you consider at least 2 loci.

This information is from a sample SNP call data indicating the to total calls for those genotypes. That's all the information I have is there no way to calculate RF ?

No, you can't calculate a recombination rate between two loci with only information about a single locus. If your question is a homework question, please use the homework tag

Oh I understand what you are saying ( this is not hw , it a "what if" question) Let give some more hypothetical information--- the information above is for Marker 1 I I will a bit more to my question

Homework questions are off-topic unless you have shown your attempt at an answer. Can you please show your attempt? You can have a look at this Khan Academy article that very nicely explain how to compute genetic distances.

Hi -- My attempt above for x:x


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When does protein folding begin?
I had always assumed that protein folding is an independent activity that occurs after translation is complete. However, recently, I learned that intermolecular forces begin shaping the peptide bonds as they exit the ribosome, while translation is still occuring.
This leads me to ask: when do the "stages" of protein folding take place? What is a general "timeline" for protein folding? For example, when do secondary and tertiary structures begin forming? Or, when do things like chaperones bind and act?

When does protein folding begin?
With reference to time you have asked, it can be after the translation has occurred (called Translational protein folding) or while translation is still occuring (called Co-Translational protein folding). Here is the link to an article for basic understanding of co-translational protein folding.
There is a lot of debate on the true time. Experimentalists have amassed extensive evidence over the past four decades that proteins appear to fold during production by the ribosome. Protein structure prediction methods, however, do not incorporate this property of folding (reference).
If you are looking at particularly some organisms it is advised to refer to the research articles related to them.The primary mechanism is the interplay between several non-covalent interactions such as hydrophobic effect and hydrogen bonding in a cooperative manner (they also follow basic rules of thermodynamics) which leads to a marginally stable tertiary structure.
When do secondary and tertiary structures begin forming?
Ofcourse, after Primary structure forms.The alpha helices/beta sheets then fold in a cooperative manner to form a tertiary structure.
One point to note is that, slight variations in these cooperative act causes misfoldingng of proteins which may cause certain diseases.

@WYSIWYG Thanks for your comment.I didn't understand where is the contradiction. Let me clarify you that Protein cannot go directly to it's tertiary structure without passing through secondary primary and secondary.On the way of attaining it's tertiary structure these two structure will form.During translation the forming polypeptide itself a primary structure.

Okay. I assumed that you meant the full length polypeptide by primary structure. I'll remove my comment.

Folding starts as soon as the protein starts being translated and actually, the ribosome affects the folding of the protein.
You can read more here.


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How would inserting a nonfunctional protein impact fitness of an organism?
Producing proteins costs energy, and producing longer proteins costs more energy than shorter proteins. Producing proteins which have no function, would therefore presumably negatively impact the fitness of a bacteria in culture. So my question is this:
Is there a way of modeling how much a nonfunctional protein would impact fitness relative to the wild-type which doesn't produce this protein? In other words, what is the cost — in terms of fitness — of just producing a protein, if you ignore all the other effects of the protein inside the cell?
How much would the length of the protein effect it? would the impact on fitness vary linearly with the length of the protein?
This would probably depend on many different parameters, I'm just not sure what all of them are and how each of them would factor into the final result. For instance, it would probably depend on the level of expression of the gene (which sigma factor would impact this especially).
I posted a similar question a while ago, but I've reworded it based on feedback from last time. If it helps you to think of a specific organism to answer the question, by all means, do so. Let me know if there is any literature already on a question related to this one!

I expect any empirical investigation would show there would be more to this than the lost energy spent producing the nonfunctional protein. You could transform a bacterial cell so that it produced this "nonfunctional protein", but it's going to take up space, interact with other macromolecules and cellular components, possibly agglomerate... Cells are crowded. Are you more interested in a theoretical model that ignores these possible effects?

Yes, my main question was more how one would even begin to create a theoretical model. But the point you raised is a good one.

Every transgenic cell we ever made to express some fluorescent protein (FP) is doing this. At least we hope that besides fluorescing, the protein is non-functional (which isn't always the case). It's usually the method of insertion that's more harmful than wasting energy on expressing the protein. Reasoning from the fact that my transgenic fruit flies do horribly compared to wild ones (and it's common knowledge that more insertions = sicker flies), but within one tissue, FP-expressing cells don't get displaced by non-FP-expressing cells of the same type.


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difference between animal and plant durring organogenesis
i would like to ask about organogenesis of animals and the relationship with plant as we depends on it. me i do not understand why we are totally different with the plant but all of our body made comes from plant.
please help me to understand

Our development is determined by our genes, encoded in our DNA. This is what makes a human who eats a salad develop differently from a pig, butterfly, or even bacterium eating that same salad.
To understand how all of this works, you can start by studying introductory biology. A nice way to start might be by searching youtube for "introductory high school biology", and selecting a video sponsored by a university. You can also find many free introductory textbooks online.
Then, you will begin to understand the secrets of how life works!


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Hominidae is to hominid as Poaceae is to what?
I considered asking this on English.SE, but decided against it, since it strictly applies to biological nomenclature, which not many of them will know about - particularly that of plants.
So, in animals, all families end in the suffix  -idae - e.g. Hominidae, Apidae, Canidae or Laridae. When referring to members of a family, you can use the suffix -ids - e.g. hominids, apids, canids or larids.
However, plant families are usually named with the ending "aceae" - such as Poaceae, the grass family. If I want to refer to members of Poaceae (without just saying the common name), what do I say?

Is this a question for an assignment or are you asking out of more general interest?

@BryanKrause Out of general interest, for the most part. Plus, it may come in handy in the future.

Since Poaceae is the plural of Poacea in Latin - like aquae is the plural of aqua - I would say a Poacea, but I'm not a native English speaker so I don't know if this form would be acceptable in English. My guess is that you will have to use the long form a member of Poaceae. In languages like Italian and French it's easier because the Latin nomenclature and grammar are translated. So in Italian you will say una Liliacea for the singular and due Liliacee for the plural, while in French it would be une Liliacée and deux Liliacées respectively.

Seems like most people just call them grasses (or they use the actual family name). I wouldn't suggest using Poacea.

+1 for "a member of Poaceae." Don't use "a Poacea". Definitely don't try the -id ending since that is used for several larger plant clades (e.g. "Rosid" is a much larger category of plants that includes Rosaceae).


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How can I measure the population growth of yeast?
I will soon have to carry out an experiment. I want to estimate the rate of growth of a population of yeast, although I don't know if it is possible to at least estimate the number of yeast bacteria in a set yeast population. Does someone know of a way this can be carried out? Thanks.

Otherwise, is there any other fast growing organisim that someone can recommend me to use in my experiment? I am looking for an organsim whose population increases rapidly (such as yeast) and that the population growth can be effectively measured.

The standard way to measure growth in a liquid culture is to measure the optical density (OD) of the solution – basically, how cloudy it is. Bacteria or yeast in a solution will absorb light that passes through it, making it more cloudy (or turbid). Within a certain range of turbidity, the OD of the solution is directly proportional to the concentration of organisms in the solution, and you can use it to accurately estimate the population in your sample. Outside of this range, you'll need to accurately dilute your sample to get it into this linear range.
Generally, we use a spectrophotometer to measure absorbance of red-orange light (this is called OD 600, for optical density for light with a wavelength of 600nm). A google search turns up a number of plans to make cheap, homemade spectrophotometers that could let you take these measurements without having access to a lab, though I can't speak to how accurate they may be. You might also look at home-brewing supplies, as brewers are also interested in measuring yeast growth and tend to have lower budgets than molecular biologists.
You only need a spectrophotometer that uses visible light to measure bacterial/yeast growth. Many specs also work in the UV spectrum which allows them to measure DNA concentration, but you won't need that.


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Why do soap molecules not break down your skin cells when you wash your hands?
Soap molecules are similar in structure to phospholipids and interact with the cell membrane.  They can clearly cause damage to the cell membrane.
If this is the case, why then, does soap not break down your skin every time you use it?  The skin cells, keratinocytes still have a membrane, so wouldn't soap attack our skin in the same way it does to plant cells and cause deterioration?

You know skin has really complicated structure. It really depents on what do you mean by break down skin. Did you mean by this something like tear it a part ??

@L.Diago I think this is an interesting question. Soap destroys lipid bilayers. What structures/mechanisms exist in the skin that prevents the destruction of our own cells?

@James i just want to know what did he mean by break down your skin. If he want to know why does his skin is not damaged after he used soap i rather recommened to study some basic anorganic and organic chemistry.

Still it is not biological problem rather chemistry problem. By chemical point of view its just a combination on neutralization of pH from NaOH, and saturation of fatty acid by NaOH.

@James wouldn't that just be the top layer of your skin, the epidermis, which has keratinocytes that cover your skin with keratin protein so that things like soap don't reach the cell's membrane.

@LDiago it's exactly a biological problem (how does soap interact with mammalian skin). If you want to be reductive, you could say any biological problem is either a physics problem, a math problem, or both.

The outer most layer of the mammalian epidermis (cornified layer or stratum corneum) is composed of 15-20 layers of dead cells called corneocytes, which are basically dead keratinocytes filled with keratin intermediate filament cross-linked other proteins as well as some lipids. As keratinocytes differentiate into corneocytes (a process called cornification), the plasma membrane is replaced by what is called a conified envelope which is composed of cross-linked structural proteins and some lipids (more details in here).
Surfactants in soap do interact with components of the cornfield layer such as keratin but not in the same way they would with the lipid bilayer of a typical plasma membrane. Outcome of such interaction depends on the kind of soap as well as amount and duration of application among other factors, but even a normal soap, upon normal use on a normal skin, may cause some keratin denaturation. But the cornified layer is actually continually shed (process called desquamation) and replaced by keratinocytes that proliferate in the inner most layer of the epidermis.
You can find more details on effect of detergents on skin here and here. You can also find useful info on skin structure here and here.

So is the answer that soap does break down your skin, but just a little bit and it gets replaced quickly?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674689/
"The SC [stratum corneum] consists of corneocytes, keratinocytes that have undergone terminal differentiation, surrounded by a neutral lipid-enriched, extracellular matrix composed primarily of ceramides, cholesterol, and free fatty acids. The hydrophobic extracellular lipid matrix provides the principal barrier to the transcutaneous movement of water and electrolytes."
The keratinocytes have an extracellular ground substance that basically bar things like soap and water from diffusing/otherwise entering the body; this is even a part of our innate immune system.
The answer then is the keratinized stratified squamous epithelial extracellular matrix.


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Where to find fossil databases
Looking for sites with fossil data in the following categories.

Fossil cells
Fossil invertibrates
Fossil fish
Fossil amphibians
Fossil reptiles
Fossil dinosaurs
Fossil birds
Fossil mammals
Fossil insects
Fossil plants
Fossil mushrooms
Fossil humans

I would like for the sites to be copyleft (i.e. free, public domain, or creative commons type license) if possible, not necessary though. However, some museums such as the British museum are copyleft. Also, many other sites that google brings up are not working.
The sites I have found are mostly not copyleft:

American Museum of Natural History - Paleontology (4.75 million specimens) (very restrictive, only personal/educational use)
Paleoportal (aggregated stuff from the University of California Museum of Paleontology, the Paleontological Society, the Society of Vertebrate Paleontology, and the United States Geological Survey). This may touch on all of the fossil categories above.
Paleobiodb. (top categories: Mollusca, Brachiopoda, Arthropoda, Mammalia, Cnidaria, Radiolaria)
Fossil works
Florida Museum - Natural History Collections (botany, plus others)
Bryophyportal. Unfortunately, the images are only for personal/educational use. Looking for sites that allow free use of the content (such as copyleft licences like creative commons, or as public domain).
UCMP (not copyleft, personal/educational use only)

Wondering if these are good enough, or if there is anything else that should be added to this list to cover the categories above.

No such database exists, you have already found the best that is available. there is a current effort to build one, but these are disconnected, poorly funded and in some cases dead( poor dinosauricon). Sadly wikipedia is currently one of the better websites for finding such things. Part of the issue is for many of those categories there are only a handful of scientists even studying it.


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How does the brain fake itself into hearing our own sounds even when we are not speaking?
Typically When we are talking to our own selves at any time in the day,the Brain thinks that it's me who's speaking , how does it create illusion of speaking ?

Two points.  First, does it really create the illusion of speech, or is it just processing language?  E.g. my mental "voice" doesn't sound at all like my actual speaking voice, even if it could be said to have a sound.  Second, why limit it to speech?  I can internally "listen" to music, either works I'm familiar with, or things I make up.  (Indeed, sometimes it's hard to get the music out of my head - see "earworm" :-))

That's true :) it isn't just limited to my own voice you're right !

Our brains treat 'talking to ourselves' very similarly to talking to others. There's a small amount of evidence in studies to suggest that when we talk to ourselves, it's like verbalising the speech out loud.
Before you speak out loud, the part of your brain responsible for creating speech copies that information, and moves it the appropriate verbalising areas of the brain. However, at the same time in a process called efference-copy, it also copies it to the area of the brain responsible for listening to sounds. This process overall means that our brains can distinguish sounds that come from ourselves, and sounds that come from other people.
This also partially goes to explain why people with schizophrenia have difficulty recognising their own internal voices as 'own'. It's likely that this process has gone awry in these people, meaning they're not able to recognise their internal voice as themselves.
Here's a link to some research done in Sydney on this matter.


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Is there a record of species kept in zoos worldwide and number of individuals? If yes, can one have access to it?
Looking for the number and species of wild cats kept in zoos to assess the potential pool of individuals available for reintroduction programmes.

A potential data source could the data base that stores zoo animal data, where the most comprehensive (to my knowledge) is Species360 ZIMS (Zoological Information Management System). It contains animal records and current breeding programmes, but also information on how to care for animals (best-practices and studbooks).
In your case, the ZIMS for Studbooks module should be relevant, which contains:

ZIMS for Studbooks improves Studbook Keeper efficiency and record accuracy with suggested animals, notification of records updates, and extensive data quality tools. [...] enabling users to conduct intensive population analysis, improving species and conservation management

However, I do not have access to the data base myself, so I cannot say how accessible the data is. If you are connected to a zoo, teaching institution or research facility you can however apply for access and a membership, but I don't know the specifics of this process (or possible costs). It might be worth checking out either way.


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Can I simulate a previous and next sequence of my fasta files?
I have fasta sequences of a virus protein that had suffered a mutation in 2008 and this mutant had increase it fitness when compared to wild strain (according to literature).I want to simulate if my sequences were submitted in 2009(I have sequences from 2009 and 2010) or before to mutation and simulate next sequences to verify if the population of mutants really turns majority.
How can I do that?My virus is a RNA -ss. Any tool to use that i can represent it graphically?
Or simplifying..I want to simulate the past and the future sequences of my dataset.

From the description of the model you are interested in, you probably don't need numerical simulations. A simple analytical expectation might be enough. But anyway, if you want to perform numerical simulations (maybe you don't want to assume panmixia), then there are a number of choices to you.
The simulator that you will need needs to be able to implement selection. It hence need to be a forward-in-time simulator and not a coalescent simulator. I personally have experienced with 4 different forward-in-time simulators; SimBit, SLiM, SFS_code and Nemo.
If I am not mistaken, SFS_code won't be able to simulate haploid individuals and will probably be slower than SimBit and SLiM. In SimBit, SLiM and Nemo you cannot do haploid either, however, you can set the cloning rate to 100%, which will essentially be the same as simulating haploids.
To my experience and generally speaking, SLiM and SimBit are faster than Nemo. Because your mutation rate is high and because your recombination rate will be very low (will probably be zero), SimBit should be very very fast and SLiM relatively slow. Also, SimBit will offer much nicer outputs for the statistic you are interested in than SLiM does.
Please note that I am the author of SimBit and I therefore might have a conflict of interest here. Here is the link to SimBit.


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Data for giraffe subspecies population change over the time.
Is there a historical data for the number of animals in the wild for every subspecies of the giraffe and where it could be found?

OK. It seems that I found something in IUCN website: http://oldredlist.iucnredlist.org/details/9194/0

In a recent paper in Current Biology, Fennessy and colleagues conclude that there are four species of giraffe and that their numbers are declining in Africa. Giraffes (Giraffa camelopardalis) are presently classified as one species, with nine subspecies, which are considered ‘Vulnerable’ on the IUCN Red List. The present consensus of one species divided into nine subspecies has previously been questioned (Supplemental information), and Fennessy and colleagues provide another viewpoint on giraffe taxonomy. The fundamental reason for different taxonomic interpretations is that they are based upon different datasets that adopt different statistical techniques and follow different criteria for nomenclature.
Its basically a form of evolutionary process.
Living giraffes were originally classified as one species by Carl Linnaeus in 1758. He gave it the binomial name Cervus camelopardalis. Morten Thrane Brünnich classified the genus Giraffa in 1772. The species name camelopardalis is from Latin.
The giraffe is one of only two living genera of the family Giraffidae in the order Artiodactyla, the other being the okapi. The family was once much more extensive, with over 10 fossil genera described. Their closest known relatives are the extinct deer-like climacocerids. They, together with the family Antilocapridae (whose only extant species is the pronghorn), belong to the superfamily Giraffoidea. These animals may have evolved from the extinct family Palaeomerycidae which might also have been the ancestor of deer.
The elongation of the neck appears to have started early in the giraffe lineage. Comparisons between giraffes and their ancient relatives suggest that vertebrae close to the skull lengthened earlier, followed by lengthening of vertebrae further down.One early giraffid ancestor was Canthumeryx which has been dated variously to have lived 25–20 million years ago (mya), 17–15 mya or 18–14.3 mya and whose deposits have been found in Libya. This animal was medium-sized, slender and antelope-like. Giraffokeryx appeared 15 mya in the Indian subcontinent and resembled an okapi or a small giraffe, and had a longer neck and similar ossicones. Giraffokeryx may have shared a clade with more massively built giraffids like Sivatherium and Bramatherium.
Further on researches are also being made till now!

It would be helpful to at least name the paper mentioned, or better to link to it since it is open access and available on the web.

Dear@mgkrebbs 9 its brief description you can find on wikipedia.

OK, with your answer you addressed the subspecies/species classification problem that I haven’t addressed in my question, but at this case I am looking for the historical data of animal numbers in the wild.
9 subspecies option would be best fit as I could adopt it to other variations, but I think I am talking more about perfect world solution for me.  Any source would work at this stage, for any species/subspecies interpretation.

Sure most of the sites have data related to it but depends on u that which specific data u want to choose...

@ME. To reiterate mgkrebbs comment. Please do cite the paper as "Fennessy et al. (year)" and add the link to where we can find this paper.

The table is a rework of the information that I found
on giraffe and okapi specialist group website with additional taxonomy perspective from Wikipedia page.


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Complete metabolic map of humans
Do we have the complete metabolic map for humans? Do we know from the genome what enzimes are expressed and what each enzime does?

Simple rule of thumb: If your question is about biology and contains the word "complete", the answer is "no".

As Armatus notes, we don't know ALL human metabolites and the enzymes + metabolic reactions that produce them. Identifying small molecules is hard and metabolism is dynamic, it depends on what is being fed into the system.
The virtual metabolic human (VMH) is an attempt at compiling the information that we do know. You can read their paper here. The human build currently includes (and links together);

13 543 metabolic reactions
4138 metabolites
3695 genes (enzymes)

It also attempts to compile all known metabolic reactions that result from the gut microbiome, nutritional metabolic pathways and genetic diseases that alter metabolism. Everything is linked via stable identifiers which is a real challenge.
The human metabolic database (HMDB) is also very good. It contains more metabolites than the VMH as it includes many partially or poorly characterised metabolites. The HMDB is really useful if you are working to identify metabolites while the VMH focuses on how they connect to one another.

Roche has a pretty amazing map of metabolic pathways in the cell. You can find it here. During my Bachelor degree I contacted Roche and the mailed one to me for free (in a large poster format).

Amazing — Yes. Useful, other than wall decoration? The problem with such composite maps is that they don't distinguish between species — never mind tissues. And they mislead students into thinking that there is a mythical "cell" in which all the pathways are present.

The answer is not yet.  The sequencing of the human genome, considering its size (@ 3.2 bbp), and contrary to what's been hyped in media, is not the end of the quest for understanding the human body.  On the contrary, it is only the first and the simplest step in the elucidation of the intricate workings of the human body.  Even though a lot has been accomplished already, all of those tons of accomplishments still barely scratches the surface.
I can safely estimate that human genome sequencing represents less than 1% of the work that lies ahead, enormous work required to make sense of the whole base pair sequence.  Each succeeding step multiplies the complexity exponentially, and so, even considering the exponential advancement in technology, it is again safe to say that at the rate things are going, the complete elucidation of the human metabolome and metabolic pathways cannot be accomplished within the next 50 years.
To get an idea of the complexities involved, one only has to consider the next step after genome sequencing; the next step is to identify all the human genes making up the coding sections of the genome, which account for less than about 2% of the human genome.  Most genes do not transcribe into RNA in a straightforward manner; introns (which separate the exons that hold the coding sections), have to be spliced out; then the exons making up the code for the protein must be joined together.  All of that accountws for less than 2 % of the human genome.  The rest is non-coding DNA, the function of most of which hasn't yet been figured out.

You don't appear to mention metabolism in your answer. I thought that was what the question was about.

I did mention it, albeit indirectly; i used the words 'metabolome' and 'metabolic pathways' instead, because that was the post was asking for, to wit: "Do we have the complete metabolic map for humans?".
Oftentimes, an entire metabolic pathway has to be determined before the function of a  single enzyme can be known with reasonable certainty.


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Do ring species exist?
In trying to understand evolution better, I have been looking at examples of speciation, and have thus come across the topic of ring species.  I have tried to find concrete examples of how these work, but have been unable to.  This paper deals with one of the frequently quoted examples of ring species, but concludes:

In conclusion, although ring speciation is theoretically
  possible, the few well-studied examples suggest that it
  occurs infrequently, because the dynamics of species’
  ranges are more likely to result in fragmentation, i.e. periods of allopatry, before the slow process of isolation by
  distance leads to sufficient divergence to allow for circular overlap.

The paper does, however, cite an article on a bird that appears to be a strong example of a ring species, but buying access to it is more expensive than a year´s supply of toilet paper.
Is there hard evidence that ring species exist?  And if so, what is the evidence and what does it teach us about the nature of speciation?

Good question +1. I don't think there is very obvious examples of ring species. There are however, examples that are quite promising such as the greenish warblers (Irwin et al., 2005) and the polytypic salamander (Moritz et al., 1995).

I'm not sure if I +1'd just for the toilet paper.

Please confine your remarks about access to scientific works to whether or not you have this. If you do not have access, someone here may help you or you may try to help yourself by emailing the author and requesting a PDF. I personally do not have funds to pay for others to read my papers but I am happy to respond to individual requests for reprints, whether or not this is in technical contravention of the agreement with my publisher.

You can get a free download of the paper from here: [https://www.researchgate.net/publication/12128943_Speciation_in_a_ring].  Or email the author(s) and ask for a reprint.

yes ring species do exist like the herring and lesser black-backed gulls in Northern Europe.

Have you read the Examples section on the Wikipedia page you link?

I looked at the sources for the examples.  For most of them I had to go through more than once source to find the primary article with the evidence, and I was unable to access several.  The few where I found the primary article with the evidence seemed more speculative than definitive.

Ensatina eschscholtzii is a classic example it is a salamander species. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1558-5646.2009.00722.x

While no perfect example exists, there are various different 'ring species' in nature where you have which species are able to interbreed with closely related populations, but there are least two "end" populations in the series. Examples include:

Alauda arvensis, A. japonica and A. gulgula: Species of Skylark birds that coexist around Central Asia

In central Asia, a northern form,, arvensis, a southern form,gulgula, and Oriental,japonica , coexist without interbreeding.These forms are separated
by a gap in distribution in northern China, but a morphologically intermediate
form, japonica, occurs in Japan. Northern japonica are similar to arvensis and
southern japonica resemble gulgula. -Ring species as bridges between microevolution and speciation

Lalage leucopygialis, L. nigra, and L. sueurii: Species of triller birds that coexist on Sulawesi Island.

The existence of ring species like this can, as biologist Ernst Mayr puts it, illustrate "how new species can arise through 'circular overlap', without interruption of gene flow through intervening populations…" and offers proof of speciation through a method other than allopatric speciation: speciation that happens when two populations of the same species become isolated from each other due to geographic changes.


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Would boiling water kill microorganisms in clothing that had feces spilled on it?
Lets say there is a piece of clothing that had a small amount of human feces that spilled on it.
Would placing that clothing in boiling water destroy the microorganisms on that clothing?

I'm voting to close this question as off-topic because it is about health or domestic science rather than biology.

It has nothing to do with health or domestic science.  It is about biological concepts and biological mechanisms.

The question you quote is just a question from one person expressing his opinion in the same way as I was. His opinion is not SE policy, and mine is not unless four other list members with sufficient privilege vote to close your question.  2. I do not think disinfecting clothing is to do with either biological concepts or mechanisms. 3. If your comments are addressed to a particular poster you should include an @ followed by his name. That way he will be notified of your posting.

Whether boiling water is hot enough to kill skatole, stercobilin, haem, bilirubin and biliverdin are biological concepts.

...kill skatole, stercobilin, haem, bilirubin and biliverdin... -- these are names of chemicals, but your question asks about microorganisms. Are you interested in the denaturing / removal of chemicals or the killing of microbes?

Using boiling water alone will not destroy all the toxic compounds found within faeces. One example is skatole, this is found in faeces and is partially responsible for the foul smell faeces gives off. By laundry I assume you mean laundry detergent? If so, it would depend on the detergent being used.
I hope this answered your question :)


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Why we can't feel the different parts of ear during hearing which is mentioned in all biology books?
We can't feel our outer ear, middle ear and inner ear during hearing something. Why is that such a complex phenomenon is happening all the time but still we don't have any clue regarding that in our practical life?  We just get the sensation of hearing something and get no sensation/feeling how  different parts of our ear work all together .why all these happening within our ear and we never conscious about them ? In fact , we can know them only after studying biology.

Can you think of a benefit we would gain? I can see only drawbacks, like "investment" in additional sensors and extra processing.

Going to be productive instead of posting unhelpful snarky comments and downvoting.
You can only perceive what you have nerves for. Considering humans are unaware of all the rattling going on between the eardrum and inner ear, the only logical explanation is that there are no nerves in the region made to perceive said rattling.

That's not quite true actually, the brain is really good at filtering out / ignoring unnecessary (mostly constant) sensory input. For example there are blood vessels above the retina, which you normally can't see (I think with a quickly moving light source or something like that you can make the shadows visible)

Your comment isn't quite true actually, tell that to the many people living with chronic pain. I'm sure their brain is doing an excellent job at filtering out or ignoring it. /sarcasm

I didn't want to say that the brain filters out all constant (sensory) input (pain is different than normal sensory input anyway), just that it can do it - therefore the 'logical conclusion' that any area we don't actively notice doesn't have nerves is wrong.


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How do plants take in only carbon dioxide?
There are only 400 molecules of CO2 in 1 million molecules of air.
How do plants only take in CO2 but not the other gases?
My teacher told me that's because there is less concentration of CO2 in the leaves than the air and the CO2 rushes in the leaves.But, then how does the leaf maintain the concentration of CO2 and other gases?

Plants don't take in only CO2, they take in whatever the atmospheric concentration of gases is: gases travel freely across membranes, so it is difficult to select for certain gases.
What your teacher is explaining is based simply on the laws of diffusion in that diffusion results in a net flow from areas of high concentration to areas of low concentration. If CO2 is being used up in chemical reactions in the leaves of a plant through photosynthesis, that means that concentration of CO2 is low there, so the net diffusion of CO2 will be from outside the plant to inside.
Calling it a rush might be a bit misleading, but in general gases mix fairly rapidly (compared to, say, liquids). The plant doesn't really have to do anything to facilitate this except to have surface area available for gas exchange.

where do the other gases go?

@Dhruva They don't really go anywhere, you will find gases of all types in the atmosphere dissolved in plant tissue, they freely come and go.

@ Bryan Krause         If other gases are also found in the plant tissue why don't they combine with hydrogen or oxygen?

@Dhruva Why some reactions happen and others don't is what chemistry is all about. Hydrogen is not present as a gas in any appreciable quantity, it's in other compounds like water, so you are really asking "Why doesn't water react with nitrogen gas?" for example.


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Why doesn't it feel suffocating when taking a shower?
When one walks into a bathroom where someone is (or just finished) taking a shower it is hard to breathe, because it's filled with steam, yet the person taking a shower can breathe just fine despite being in the area with even more steam.
Why is that?

Can you support that this is a general perception? I've never felt suffocated when entering a steam-filled shower.

@fileunderwater: Nor have I, in an actual steam room.  Seems like an individual idiosyncrasy.

Most likely a matter of relative perception.
For example, if you start with empty hands and pick up a 20 pound weight, you will perceive it as heavier than if you start with a 10 pound weight and then pick up a 20 pound weight.
Likewise, whoever's in the shower had plenty of time to get accustomed to gradually increasing steam, while you walked in and got the full blast immediately.


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How "unique" human vagina is?
Regading penis Dixson showed that it is not really unique and complex. This argument (and there were some others) was used against the idea of human polygynandry.
But what about vaginal shape? I know it is wider as deeper it goes and cervix is convex shaped, which could  give an advantage for storing semen. However, I am actually wondering if other primates have similar vaginal shapes (because it can shed light on the question of mating system). Are there any studies on the topic?

Check the wiki page for clitoris and some mammalian orgasm research... ostriches have a clitoris and other species such as spider monkeys and spotted hyenas have clitorises as long as their male counterparts, so we are different form spider monkeys.

@com.prehensible Well, I know, say, that bonobos have 3x larger clitores (given they are smaller). But I am asking about unique features of human vaginas, not primates'. I am pretty sure there are primates with clitores comparable in relative size with human ones.

This page talks about labia http://aquatic-human-ancestor.org/anatomy/sexual-features.html


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Where can I find hemagglutination inhibition (HI) assay data?
I am looking for hemagglutination inhibition assay data for type A influenza virus. I've checked in databases such as fludb.com, however it seems to only have genetic data. A lot of the time, scientific papers don't include the HI assay data they used, so I was wondering if anyone knows where to find such data. I specifically need influenza type A HI assays, not influenza type B.
HI data comes in the form of titers (the reciprocal of the last well plate concentration of antibody that was able to inhibit the virus from binding to the blood sample and forming a shield on the well plate.)
Could someone please give me a link to a database with this information?
Thanks.

You can search in the NIAID Data Discovery Portal: https://data.niaid.nih.gov/

I don't think there's any universal database containing ongoing, widely representative HI assay output. The Antigenic Cartography group has made available some historical datasets that were used in published articles, such as

Influenza A/H3N2 data published in Smith et al. 2004. Science 305:371-376
Data from H1N1pdm09 assays in 2009/2010 (click on the links for html/Excel/OpenDocument tables)
Data published in Koel et al. 2013. Science 342:976-979

Trevor Bedford et al. make their large set of historical HI data described in Integrating influenza antigenic dynamics with molecular evolution available in DataDryad.


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Does the deletion of Chromosome 20 cause immunity against prion disease?
I was reading recently about prion disease and it caught my attention that a normal prion protein is coded n chromosome 20, therefore, in order for an infectious prion protein to attack, there must be already normal unsedimented prion proteins, does that mean the deletion of chromosome 20 in meiosis lead to immunity against prion disease, since the protein is not coded, that is if the human survives without chromosome 20

"That is if the human survives without chromosome 20". I suggest you consider the likelihood of that being true or do some investigation to discover how many other genes are encoded on chromosome 20. You may then wish to delete your question.

I read an article that says chromosome 20 deletion occurs so I am quite unsure, I mean why would I ask in the first place

It seems very unlikely to me that a person can survice without chromosome 20. Please cite the article that leads you to think it possible.

Welcome to SE Biology phenolicdeath. Including a link to the article will help other users to answer your question. It sounds interesting.

I see one report of a viable autosomal monosomy,
(https://www.nejm.org/doi/full/10.1056/NEJM196710122771502)
but in general, they are not survivable.
https://www.ncbi.nlm.nih.gov/pubmed/4086989
https://www.biology.iupui.edu/biocourses/N100/2k2humancsomaldisorders.html
https://www.ncbi.nlm.nih.gov/pubmed/29164644
A better question would be if person with a deletion or natural knockout of that gene are susceptible to that prion disease.  Those subjects likely exist in larger numbers, though it's likely that few have been exposed to any particular prion disease.


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(Aquatic gastropod) Physae identification
I need help to identify a physa.
What are the identification keys to make the difference between:
 physa fontinalis,

physa marmorata
, physa acuta (syn. Physella acuta)
The difference that can been seen with the eyes, no microscope, and except their biotope? (As they are in my house, not in their biotope)
differences or identification criteriae? What are the right organs to check of the difference in eggs, etc.
There is a variability of color in snails, and a variability of sizes. One specimen in some conditions can be much bigger or smaller than the average, so it's very difficult to identify them.
Some aquatic naturalist here?
Important remark: I don't guarantee the pictures are accurate, the site posting the picture may have confused physae!
I got physae from a vendor, some have a pale body and a more yellowish or partially yellowish shell, some have the tip ot the antennae dark, and have a dark shell and a dark body. The vendor had them together, and it seems they interbreed, but I'm not sure if it's only one ssp or 2. I see nowhere color mutation of physae on the internet.


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What creature is this?

Found on a beach in Brisbane, Australia. Only a few cms of it was visible but I dug the rest of it out, it was about 20cm in length.

That is a Priapulid worm, also known as a "penis worm". In its own phylum, Priapulida. https://en.wikipedia.org/wiki/Priapulida

Thanks, I would never have worked it out as it is quite different looking from the other photos of Priapulid worms available through google search (i.e. I couldn't find an example of a similar looking specimen). Thanks for helping.


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Garden plant in south of France
When visiting the south of France (around St Tropez) I had a plant in the garden which I initially mistook for mint but the aroma of the leaves (when rubbed) was distinctly different (I cannot put a name on it, it is sweet and remotely reminds of orange).
The plant has bare branches (it is a bush), and beside the leaves there are some round things which I took a picture of (sorry for my abysmal lacks in correct botanical words - these are the last two photos).
The photos are as of end of October.
The leaves are not smooth, they have some kind of tiny barbs which I can feel when rubbing the leave upwards (towards the petiole). The other way round (from the petiole) is smooth.
I cannot tell about the taste yet as my wife suggested that I wait for more information (just kidding).


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Why does photosynthesis occur even in blue light when the photocentres are activated in red light
From Engelmann's experiment

Engelmann used this device to illuminate a strand of Cladophora (not Spirogyra) with light from the visible spectrum, exposing different sections to different wavelengths (or colors of light). He added the oxygen seeking bacteria B. termo to this setup and noted where they accumulated (Note: Four years later, Hauser concluded that B. termo had been mislabeled and was not one, but three species of bacteria of the genus Proteus [2]). Their clumping allowed him to see which regions had the highest concentration of oxygen. He concluded that the most photosynthetically active regions will have the highest concentrations of bacteria. The bacteria accumulated in the regions of red and violet light, showing that these wavelengths of light generated the most photosynthetic activity.

It can be concluded that the photosynthetically active regions of light are present at the blue-violet region and the red region
What I am unable to understand is , if photosystems I and II are activated at light wavelengths of 680nm and 700nm (primarily at the red region of the spectrum) then what type of photosynthesis is happening at the blue region due to which there is oxygen evolution?
My attempt:
The antenna molecules (light harvesting complex) which absorb majorly at this wavelength are transferring energy to the photocentre due to which there is excitation of the photocentre and thus OEC gets activated.
Even if this were true, then should'nt blue light be as effective as red light in helping in generating the quantum yield?

See the following related questions: Why are so few foods blue?  and  Why do plants have green leaves and not red?.

While it is true that strongest activity of Photosystem I and II happens with 700nm and 680nm light, these are not the only wavelengths that can be used for photosynthesis.
The green color of plants comes from chlorophyll, which is the main light absorbing component in the photo systems. If chlorophyll had only a single absorption peak at 680-700nm, it would have a blue(-ish) color instead of a green one.
Looking at the absorption spectrum of chlorophyll (which wavelengths it can absorb how well), you can see that there is a a second peak around 400nm:

This both explains the results of Engelmann's experiment and the green color of chlorophyll (with both red and blue colors removed only green remains)
Picture taken from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html

but this still doesn't explain why oxygen is evolved under blue light.The PSII is activated by red light and OEC coupled to this, splits water to reduce the photocentre... However, I am unable understand that even though blue light does not directly excite the PSII photocentre, how it is capable of causing oxygen production. As you can see there are oxygenic bacteria in the blue region indicating that there is oxygen evolution.

You didn't quite understand my answer. the 400nm absorption peak of chlorophyll means that blue light does directly excite chlorophyll and thereby PSI / PSII. Also the bacteria cause oxygen production, not evolution.

blue light does directly excite chlorophyll and thereby PSI / PSII. Do you have any references to back this up?

Thanks to @theforestecologist for giving me the lead in this answer
Just to clear up, in short:

The photocentres, as it goes by their names $P_{680}$ and $P_{700}$ cannot be said to be activated by the blue violet light directly because they can directly absorb light only at the wavelengths 680nm and 700nm for PSII and PSI respectively.
The antenna molecules are the only pigments absorbing directly at this low wavelength (also called Soret's band) which makes these molecules important in protection against photooxidation.
However the chlorophyll a as pointed out in @Nicolai's answer still show absorption at the 400nm range.
This could be explained by the transfer of energy from the antenna molecules (carotenoids) to the photocentre.
The entire  mechanism has been summarised in this paper

Thus it may account for the oxygen evolution in the presence of blue light
To the last part of my question on the effectiveness of red light over the blue light it can be said that:

Of the total blue light incident on the antenna molecules only a part of it's energy is transferred to the photocentre. Whereas in case of the total red light incident , almost all of it gets absorbed by the photocentre to be used in light reaction.

For further reference see  theforestecologist's answer on the photosynthesis

The answer you are looking for is most certainly here:
https://en.wikipedia.org/wiki/Cryptochrome

thanks for the link. But how does the cryptochrome pigments couple to the OEC? The link basically states about photosensitivity but I cannot understand why there there is oxygen evolution in the presence of blue light.


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Papers where protein oligomerization has been engineered away
I have a protein that acts as a monomer, but appears to have a relatively high self-affinity in vivo (measured using transient transfection of a plasmid coding for the protein), which is annoying because I'm trying to engineer conditional self-association like with FRB-FKBP w/ rapamycin. Have there been any papers where self-clumping of a protein has been engineered away?
My current approach is to use threading to identify a protein structure and a docking program to identify sites of self-interaction and mutate those sites away.

“Clumping” to mean means aggregation, but it sounds like you wish to change the oligomeric state. One approach I recall used in streptavidin was to introduce charged residues at the subunit interface to create a repulsive effect. I’ll find the paper when I have a moment.

Engineering Soluble Monomeric Streptavidin with Reversible Biotin Binding Capability

Stable, high-affinity streptavidin monomer for protein labeling and monovalent biotin detection

You should define your question properly. Does "self-clumping" means oligomerization or aggregation? You should also give more details about your preparation. How do you prepare your protein, is it recombinant, it is a known protein?

I have updated the question

The authors of the dronpa protein, mention that the initial WT protein they identified oligomerised and they introduced mutations to stop this. However, the explanation of how/why they chose the particular mutations (only shown in the supplements) is lacking.

You have not provided enough information to support your statements.  In what types of experiments does it behave as a monomer (and how can one determine whether it is acting as a monomer or a higher oligomer?)? What evidence do you base your assertion that in transient transfection assays it is clumping, or aggregating, or oligomerizing?  If the pure protein is soluble, you might be able to crosslink it to a matrix and construct a affinity column.  In a mixture of cellular proteins does this protein bind specifically to such a column?


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Why do autumn leaves on the eastern sides of trees change and fall before the western leaves?
I've noticed that for the autumn leaves in my area (Great Lakes region of United States), if a tree's leaves are changing or falling asymmetrically, they almost always change first on the East-facing side of the tree.
I can't find any explanation for this phenomenon online; but in the spirit of "showing my work", I'll give some hypotheses from this non-biologist. :)

If there is a temperature at which direct sunlight destroys chlorophyll or reduces its effectiveness, there might be pronounced coloring effect on eastern leaves. The air temperature at dawn is usually 5-10 degrees Celsius less than at sunset.
If direct sunlight instead prolongs color change or leaf detachment, it could be that this asymmetry is caused by an increase in cloud cover in the mornings relative to the afternoons.

Any thoughts? I've noticed this in past years, but this year seems really extreme: many trees in the region have lost all of their eastern leaves but have a western side covered in bright orange leaves; they also had orange eastern leaves while the western sides were green, so wind gusts aren't the culprit.

Nice question. Do you have a photo to illustrate this?


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What is this trilobite-like creature?
This was found under a rock in a freshwater creek in Maryland. Stayed like this for while, then stretched out long, then contracted, and then JUMPED off the rock back into the water. Looks like a trilobite. Rock-colored.

well I don't know of any freshwater chitons, so I'm going with a leech. In fact, if by "stretched out long" you mean it literally became long like a ribbon, then this is almost certainly a leech.

Yes, a leech. I don't know the species, or even family.

Very nice image of a leech (probably of family Glossiphoniidae). Please consider sharing a cropped version somewhere like iNaturalist.org

Thanks, everyone. Never seen a leech before. I always assumed they were more squishy-looking!


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Gene expression: which allele is considered?
For human beings, we have two copies of each gene inherited from the parents. The question is, when referring to gene expression, which copy (or allele) is considered?

Could you explain what you mean by "when referring to gene expression". Do you mean in general conversation, in anlysing the results of an RNAseq experiment, or are you asking whether expression occurs on both alleles? At the moment this is quite unclear. You need to edit your question to make it more precise what you are after.

Genome assemblies usually feature a haploid set of genes, unless particular effort is applied to assemble separately the homeologs. With that said, the gene copy you have in the assembly is usually one of the two, and usually the one you had more genomic reads for.
In terms of gene expression, if you measure it by RNASeq you will get reads from both and both of the read pools will map on the same gene. The ones that come directly from it will map with no mismatches (ideally) and the ones that come from the homeolog chromosome will map with a few mismatches (probably).
The expression of the "gene" will therefore be the expression of both genes, summed together. If we consider it as the same gene, though, it doesn't really make a difference if you sum them up or count them twice separately; unless we are talking about specific homeolog silencing like the Xist mechanism, in which it is important to remember that one copy of the two is off.


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What don't we know about cancer?
I was wondering, after decades of research what we do not know about Cancer yet as in what unanswered questions are still puzzling biologists about cancer?
I have read that cancer research, in its modern form, is a quest for biological immortality. Does this hold any truth?

I think this thread will become a jungle very fast and very soon, so I suggest you to have a look at the cancer research reviews of the last 2 years to get a grasp. Have a look at cancer hallmarks and at other important key concepts, you will most certainly answer your question yourself :) I am not a cancer researcher so I cannot comment on the topic in a detailed fashion (I work on plants), but that's what's going to happen.
In general, I'd say that what we don't know about cancer is a "common ancestor" of all types of it that will enable us to tailor a one-sized cure.


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Why is erythropoietin produced in the kidney?
Erythropoietin is a hormone produced in the kidney to stimulate the generation of more red blood cell. It is triggered by low oxygen via HIF transcription factors. Makes sense. Oops, oxygen is low, let's make more erythrocytes to carry more oxygen from the lung to consuming cells.
What doesn't make sense is why evolution would locate the production of EPO in the kidneys. These are organs tasked with excretion via the urine - pump and retrieve. They have very little to do with red blood cell gas exchange (lungs), generation (bone marrow), or removal (spleen).
Can somebody think of a good reason why you would locate the synthesis and release of the primary hormone to trigger red blood cell generation in a seemingly unrelated organ like the kidneys?

There's no reason that an endocrine tissue should be related to the target tissue of the hormone it produces. Think of other examples, e.g. liver glucagon, islets insulin, adrenals epinephrine. The only requirement is that it should be able to detect conditions in which it is appropriate to release the hormone. Your question would be better if you removed the false premise and just asked how the kidney detects a change in oxygen tension.

Evolution adds randomness but function is still selected for. The hunger hormone ghrelin is produced in the stomach when it's not stretched by food and the satiety hormone leptin is produced in adipocytes when fat stores are filled. Insulin and glucagon both come from the pancreatic islets, strategically positioned in the blood stream right after nutrient uptake in the gut and before the liver, the main storage organ.
The question remains is EPO the exception without a good reason?

As I pointed out, it isn't an exeption any more than insulin, glucagon or epinephrine. However, if I were a developmental biologist I might think about the role or developmental stage of tissues in early foetal (and even embryonic) development to consider why the bone marrow might be inappropriate. I'm a more molecular biologist, so I can't, but I suspect the more physiological biologists should be able to discuss this. Seems there aren't any on this list that want to dip their toes in the water. ( Is your 'surprise' partly psychological because of the association of kidneys with urination?)


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Why do I feel nauseous at the sight of blood, despite not being afraid of it?
Every time I ask google this question, all it spits at me is info on blood phobias ^-^; basically, I've always been hugely interested in morbid stuff, but I noticed that I always feel sick when interacting with any sort of gore IRL - when I volunteered at a hospital to keep patients company, I had trouble staying calm around patients who had been in accidents when they were getting their bandages changes, or around patients who've had surgery when they drained their tubes. Yesterday in Anatomy we dissected a pig's heart, and I was super excited until we finally got them & I felt sick seeing it! I'm just confused because mentally I'm fine & don't mind being around that stuff, but physically I feel ill & its pretty annoying tbh :/
If it helps explain it at all, I do have issues with vasovagal syncope & tend to faint when getting blood drawn & being in a very warm, humid place, & I kinda have the same feeling with it? I'm not afraid of needles or heat, but I feel sick in those situations & end up fainting

Your last paragraph is helpful. A vasovagal response is not fear. Anecdotally, one of my medical school classmates struggled with this but was able to overcome the problem over time (by continuing to expose himself to the stimulus). Dissecting a human cadaver helped.  Posting this as a comment as it is anecdotal and I have no references at hand to back it up.

I usually experienced this as well in biology classes. I'm not particularly afraid of needles or anything. But in classes where we were talking about the internal body or blood (or similar topics), I would often get very dizzy--despite me finding it interesting!


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Crispr complex in human cells?
Is the crispr (where the parts of Virus DNA is saved) section of the DNA existing in human cells aswell or is it just in bacteria cells?

No analogues of the CRISPR-Cas system have been found in any eukaryotic species, including humans. So far, it appears to have evolved only in prokaryotes and archaea.
Reference: Evolution of RNA- and DNA-guided antivirus defense systems in prokaryotes and eukaryotes: common ancestry vs convergence


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Why is this spider wound in such a dense web?
I saw this thing yesterday on my window curtain, and I've been wondering what this is.
It looks like a dense network of spider web, and the spider inside it is visible. I thought the spider was dead, but I saw the spider making very small movements inside it. So, that made me more curious to know what it is.

This is probably made to protect eggs and young spiders, a sort of nest.

From the look of the spider outline, it looks to have short legs and is dark. A yellow sac spider is quite light-coloured and has long legs. Yellow sacs and clubionids will sometimes make themselves a sac for resting or eating or molting or laying eggs. Yours is probably a jumping spider, and here is a youtube timelapse video of a jumping spider laying eggs while inside its own protective sac:
https://www.youtube.com/watch?v=yoqMNX0RWuc


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Firefly mating displays
I live in the northeast US, and really enjoy firefly displays at dusk in the summer. However, when paying attention this summer, I noticed that the fireflies were not displaying every night, but somewhat irregularly, and only over a short period (both within an evening and across the season). I could not figure out what combination of environmental conditions were associated with their display behavior. What are the environmental conditions in which fireflies are most likely to engage in light displays in the temperate eastern US?

Welcome to Biology.SE, thank you for asking a specific question and for taking the tour :)


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speciation in a single population
Most examples of speciation describe a population splitting (via various mechanisms) into two or more populations that eventually become separate species from one another.  However, what if the population never splits? In other words, at some point in the evolution of a single species, an individual member would become (theoretically) unable to reproduce with its own ancestors--thereby becoming a distinct new species.  How can we say that this has happened, given the impossibility of the example?

Allopatric speciation

Allopatric speciation [..], also referred to as geographic speciation, vicariant speciation, or its earlier name, the dumbbell model, is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with gene flow.

Sympatric speciation

Sympatric speciation is the process through which new species evolve from a single ancestral species while inhabiting the same geographic region. In evolutionary biology and biogeography, sympatric and sympatry are terms referring to organisms whose ranges overlap or are even identical, so that they occur together at least in some places.

Yes, sympatric speciation appears to be a thing but estimates of how common that is avery hard to come by.
Now, what you describe is not so much sympatric speciation as you refer to a case of reproductive isolation between extant individuals and their ancestors. I am not sure that was really what you had in mind because otherwise you would have not put it in opposition to allopatric speciation but it is what you seem to phrase. Of course, such type of "temporal reproductive isolation" is obviously a thing.

Thanks for adding the sympatric clarification... yes, this is what I'm referring to.  Obviously there is reproductive isolation...isolated by time, not geography.  So at what point do we say that speciation has occurred; how do we know that a given individual has become the next iteration of speciation?

@charlie-k3 now you are simply asking questions about definitions, not biological facts or theories. You're focusing on one definition of "species", of the many that exist, and you're choosing one that is explicitly not designed to address the question you're asking. Wikipedia introduces the question and there are many other discussions. Remi.b might want to update his answer with other pointers.

@charlieK3 Your follow-up question is an entirely other question and should be asked on a separate post. If the current question has been answered, please check it and consider opening a new post for your new question. That being said, before you open a new post, please have a look at How could humans have interbred with Neanderthals if we're a different species? that might already help you a lot.

actually I'm not asking for the definition of a species, and I know there are many. 2) my first and second questions are variations on the same concept.  3) I'm specifically NOT asking the "Neandertals" question, as stated in my first post, because that is an example two separate species descended from a  common ancestor.  It's OK to answer "I don't know."

I don't understand your follow-up question. To me your follow-up question seems to be How can you tell whether two populations are of the same or of different species in the special case where one population is ancestral to the other one? The answer is it depends upon the definition of species you are willing to considerate, whether or not the two populations of consideration exist in the same time or not. If I misunderstood your follow-up question, can you please clarify it?

Btw, It's OK to answer "I don't know." can be considered a bit rude. It suggests that I am being too pretentious (or dishonest for some other reason) to admit that I don't know what I don't know. Please believe, my goals are to help, to improve my knowledge in biology, to improve my communications skills and not to impress.

Allow me to try this again.  I am specifically NOT describing a situation with or comparison between two (or more) extant species.  I am referring to ONE extant species (say a hermit crab, E.gilli).  At some point in the evolutionary past, E. gilli did not exist--because its ancestor had not yet evolved into E. gilli.   Agreed?  If so, how can we show when speciation has occurred, i.e. when the ancestor evolved into E. gilli ?   For the purposes of this question, let's assume the definition of a species is that in which reproduction is possible and produces fertile offspring.

@charlieK3 Yes, I understood that you are talking about question of species distinction among two populations where one is the ancestor of the other (and hence only one is extant). You have now suggested a definition of species to work with which is good. The definition is not sufficient as explain in the post How could humans have interbred with Neanderthals if we're a different species? but let's work with that anyway....

Reproduction is not possible as they don't exist at the same time but of course, I expect it is not what you want to hear. Maybe you want to hear there is no absolute solution to test whether two individuals would be fertile without actually trying to mate them. Of course, some cases are obvious (such as reproduction between an oak tree and a snow leopard) but there is no general solution for knowing whether two individuals can reproduce without actually trying to make them mate.


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Structure separating the left atrium from the ascending aorta?
With reference to the (adult) anatomy of the human heart:
The left atrium (LA) and the proximal part of the ascending aorta (Ao) abut one another, as shown nicely in this image [1].  Is there a name for the wall(s) separating the LA and Ao?  And is this a single structure (i.e. septum), or is there a sinus?
[1] http://www.radiologyassistant.nl/data/bin/w440/a5097978b829cd_3-chamber.jpg

There isn't any particular structure there: you have the wall of the aorta/adventitia, and if you have an explanted heart there is a space and then the auricle of the left atrium on one side and the right atrium on the other. These would all be contained within the pericardium.
Where the aorta is most "touching" the left atrium is where the pulmonary veins come in: I think this picture from Gray is most helpful.

Figure 494. Henry Gray (1825–1861).  Anatomy of the Human Body.  1918.
There really isn't much to distinguish these veins from the non-auricle part of the atrium, similar to the vena cava on the right side. If you were to cut along the veins eventually you would just open up into the atrium.
The Visible Heart Lab is another good reference http://www.vhlab.umn.edu/atlas/aorta for cardiac anatomy.


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Why are fungi and algae microbes?
Both fungi and algae have very small cells but so do most animals. Yet both of them are visible to naked eye just like other organisms.
Why do we call them as microorganisms then ?

Not all fungi and algae are considered microbes, just the unicellular ones.

Because both of those produce single-cells able to viably survive and grow on your own. For example, take a fungal spore and it can grow into a full fungus given enough food. I assume algae cells are the same way. In a single-cell form, fungi and algae qualify as self-sufficient microbes.
Animal cells are typically specialized and dependent on a support framework. Usually, a single animal cell left out on its own is largely doomed.

And egg is an animal cell and usually left out in case of reptiles and mammals

*avians ..not mammals /sorry

Most eggs need to be tended to regularly, watched over, kept warm, or placed in a specific environment, which arguably serves as a "support framework"


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Do biologists believe in the existence of an intelligent creator who designed the architecture of life ?
I am referring to the biologists who does not support the theory of evolution or Darwinism .

Are you asking for the specific biologist or a general statement about biologist? because there are about as many biologists  who don't agree with evolution as there is medical doctors who don't agree with germ theory. which is to say a statistically insignificant number who are unable to scientifically defend their position. Basically there are ones who disagree because they are deeply religious but none that are religious becasue they disagree.

I'm voting to close this question as off-topic because this is not a question about biology but about the religious beliefs of biologists.

As the question is phrased, there are almost none.
A 2009 Pew survey concluded that

95% of Americans believe in some form of deity or higher power ... just over half of scientists (51%) believe in some form of deity or higher power; specifically, 33% of scientists say they believe in God, while 18% believe in a universal spirit or higher power.

That's American scientists in general; "biologists and medical" more specifically are in the same range. Americans in general tend to be far more religious than many other nationalities (95% of Americans vs. less than 50% of British, 60% of Germans, 65% of Canadians) and it's likely that scientists from other countries are proportionately less likely to believe in a God. I don't have numbers for those but let's say 60% of the American number, or roughly 20%.
So there is a significant minority of scientists who are religious, but probably 70-80% of biologists worldwide do not believe in God.
Does that mean that 20-30% of biologists reject evolution based on their religious beliefs? Not at all. The idea that evolution conflicts with religious beliefs is a very niche view, mainly held by small (but very noisy) American religious groups. For example, the Pope has stated that there is no conflict between Catholicism and evolution. Francis Collins, the director of the NIH, is famously religious and also argues that there is no conflict between religion and evolution.
So there's no reason to believe that religious scientists should reject evolution, and in fact they don't. Surveys show that around 97% of scientists understand that evolution is real. That survey says that "87% say evolution is due to natural processes, such as natural selection", which leaves 13% as open to the idea that it's guided. That survey doesn't break down different fields, but other surveys and general experience says that few of the 13% are biologists.
The number of biologists who reject evolution based on their religion is tiny.
As a side note, please be aware that "Darwinism" is not a real thing; it's made-up phrase used by people who know little or nothing about biology, who are unaware that Darwin's arguments have been irrelevant to our understand of of modern evolution for close to 100 years, and that modern evolutionary theory has many branches that supplant and extend classical natural selection.

But the question is so clearly off-topic that you are doing a disservice to the list by feeding this troll.

@user1136 IMO, the question is completely and obviously off-topic. Asking about the sociology of religious believes has nothing to do with biology even when the population of interest is "biologists". This question is as off-topic as it gets!


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Why is beta thalassemia major not lethal while alpha thalassemia with loss of all 4 genes lethal?
So why is beta thalassemia major with two B0 alleles not fatal in utero (despite the hemoglobin not having any B chains), while alpha thalassemia with deletion of all 4 genes encoding for the alpha chain fatal? Is the alpha chain more important than the beta chain?

This has to do with the fact that fetal hemoglobin (HbF) isn't made of the same chains as adult hemoglobin. The latter comes with 2 alpha chains and 2 beta chains while the main fetal hemoglobin is made of 2 alpha chains and 2 gamma chains. Hence any disease affecting the quality or quantity of beta chains won't have nearly as much impact on a fetus as it does on an adult.
Reference: https://www.uptodate.com/contents/fetal-hemoglobin-hemoglobin-f-in-health-and-disease

In essence, yes, the alpha chain is more important than the beta chain, because there are alternative forms of hemoglobin that can deliver oxygen without beta chains, but the hemoglobin forms without alpha chains cannot.
Hemoglobin has a bunch of different forms, depending on which four globin chains make up the protein. While there are even more, here's an overview of the most important forms:

Hemoglobin A is α2β2, this is the normal form, and in adults this makes up 95% of our hemoglobin.
Hemoglobin A2 is α2δ2, with 2 delta chains instead of beta chains. It normally makes up about 2-3% of hemoglobin, and its properties are nearly identical to HbA.
Hemoglobin F is α2γ2, with 2 gamma chains instead of beta chains. This is the primary form in utero, because it has a higher affinity for oxygen, and thus can extract oxygen from the maternal circulation. It normally decreases after birth, and makes up <1% of adult hemoglobin.
Hemoglobin H (β4) and Hemoglobin Bart's (γ4) are defective forms of hemoglobin that occur without alpha chains. Both of these are unstable molecules, and are poor at delivering oxygen because their affinity for oxygen is too high (not allowing it to be released in the tissues).

What you'll notice from the above is that there are functional hemoglobin variants that don't have beta chains, but no functional variants without alpha chains.
If someone has beta thalassemia major, with loss of both β alleles, the body compensates by ramping up production of HbA2 (with delta chains) and HbF (with gamma chains), which compensate for not having HbA. That's not to say that everything is okay... it's still a very serious condition, and usually progresses to death before age 20 if untreated. But, the hemoglobin variants are sufficient enough to allow people to live.
If someone loses all 4 alpha alleles, the only hemoglobin they produce is Hb Bart's, which isn't functional. There are no alternatives to the alpha chain like there are with beta thalassemia, so there's no mechanism to compensate for this loss. Because forming HbF isn't possible without alpha alleles, this condition is fatal in utero.


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Is a fatty acid a polymer?
From my understanding, polymers are long chain molecules containing repeating units of monomers.
For example, proteins are polymers called polypeptides with repeating units of (different) amino acids. Therefore, a fatty acid, saturated or unsaturated, would classify as a polymer as they are long chain molecules with repeating units of alkyl monomers?

You are wasting your energy on a semantic question of no biological importance or interest . This is not unusual for people with chemical backgrounds. For the record you will seldom read the word polymer in biochemistry books. But if you know the structure of these molecules that is sufficient — focus on what the functions of these molecules are and how it relates to structure.

From a chemistry perspective they would be considered oligomers rather than polymers, since they generally have quite a short and specific length. (P.S. don't let anyone tell you that chemistry is not important in biology, nor that nomenclature is not important in chemistry!)

In the IUPAC Gold Book, IUPAC defines a polymer as follows:

A molecule of high relative molecular mass, the structure of which essentially comprises the multiple repetition of units derived, actually or conceptually, from molecules of low relative molecular mass

Fatty acids are relatively high in molecular mass compared to the monomer (which is essentially a carbon atom), although they're quite low in mass compared to all other biological polymers. Since we consider proteins polypeptides, as you rightly note, the monomers clearly don't have to be chemically identical, so the variations around a simple carbon that are present in various fatty acids should be fine.
The definition states nothing regarding typical numbers of repetitions or minimal numbers of repetition.
The IUPAC definition also mentions that for most (but not all) polymers, the specific number of repetition has little impact on the molecular properties of the polymer. Fatty acids do generally work more or less the same regardless of their specific length.
Sounds like fatty acids are carbon polymers to me, even if indeed we don't usually think of them like that.

The monomer for fatty acids is ethane, not methane.  Most of the biochemical reactions that handle fatty acids work on pairs of carbon atoms.

It is interesting that polyketides have a similar biosythetic pathway (and the enzyme complexes too) as fatty acids but the former are still labelled if not considered as polymers but not the latter.

Fatty acids are usually not considered polymers.
From a biological viewpoint this is simply because there is only a very limited set of chain lengths that exists in nature (~2-20 or so) and also even numbered chains are much more common than uneven numbered ones. In contrast to this 'true' polymers can have an arbitrary length of chain length (of course there is still a limit in biology, but not a super strict one) and no specific lengths are favoured.
From a chemical viewpoint fatty acids are also not really a polymer: you can't just take a bunch of alkyl monomers and fuse them to one long fatty acid  chain, because simple alkyl monomers don't have chemical groups that allow this reaction to take place (making C-C bonds is chemically not the easiest thing to do).

I'm not sure about your last paragraph; after all, the same could be said of polyethylene, which is certainly a polymer. (The name "polyethylene" is a hint to how it's made, but its actual structure is just a long chain of single-bonded carbon atoms with hydrogen atoms attached where appropriate.)

@ruakh : That reaction takes places at high pressure and temperature.

I've never heard of anyone consider fatty acid to be a polymer.
I'm not a biologist, but all of my research is on polymers-specifically paints and coatings.  Fatty acids are often used in the coatings industry as one of the building blocks to make an alkyd coating.  In my eyes, fatty acids would be seen more as a monomer or oligomer.  Like you've observed, fatty acids do have repeat units; but many would opt to use other words to describe the molecule


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Are unsaturated fats antioxidants?
Unsaturated fats contain double bonds like carotenoids (which is an antioxidant), and from my understanding, what makes carotenoid an antioxidant is that its double bonds allow it to undergo oxidation, hence they can donate electrons to free radicals. Therefore, would this suggest unsaturated fats (especially those with more double bonds) are also antioxidants?


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What is the name of this tiny spider?
Found this spider on the flower bud in my garden. It measures about 5mm. I am from Kuching, Sarawak, Malaysia.

it's a jumping spider, there's some south east asian jumping spiders here: https://image.shutterstock.com/display_pic_with_logo/3499364/481322845/stock-photo-jumping-spider-in-southeast-asia-481322845.jpg

It looks like some kind of jumping spider, possibly an iridescent jumping spider based on your location (Family: Salticidae, Genus: Cosmophasis). Here is some information on it! https://en.wikipedia.org/wiki/Cosmophasis

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