text:
Does the Ogre-Faced Spider regenerate part of its eyes daily?
Deinopis Spinosa
A species of the Deinopidae family, characterized by long thin (elegant) legs and the use of them to hold and thrust a net towards their prey.
These spiders are visibly remarkable for their forward-facing twin eyes at the front. Hunting at night, the spider is dependent on their eyes identifying prey in low light levels:

Copyright: Jay A Saftstrom (Alamy stock photo), found Daily Mail 18 May, 2016. Fair usage.
I've found the claim online in more than one place that these spiders react to sunlight in a peculiar way:
https://factrepublic.com/facts/16506/

and a very delicate light-sensitive retina. Their eyes have no irises
and therefore the sunlight destroys their sensitive retina every
single morning only for it to be regrown in the evening.

https://bogleech.com/spiders/spiders10-ogre

the eyes of the ogre-faced faced spider grow a new membrane of similar
function every single night...and as the sun rises, the intensity of
the light dissolves the membrane back to nothing.

There are reference to spiders (some families) being able to regenerate legs during ecdysis (molting), but on searching further, I'm unable to confirm this for eye-parts from any reputable source, not on Google scholar either.
What is the truth behind any such mechanism for regeneration of a part of the spider's eye daily?

Are you looking for evidence of veracity or the physiological/biochemical process? (Both are out there.) Oh, and nice question! TIL.

Ahh, if I only had the correct search terms (or institutional access). The inconsistency bothered me, one source above states "a membrane like the tapetum lucidum", the other stated that it was the retina which regrew. The former strikes me as more likely, but the whole topic has me going now. I'll take any leads, as much as you have. @anongoodnurse

I'm still astounded that this mechanism exists, makes me marvel every time I stumble across this question.

A. D. Blest seems to be the primary researcher responsible for that wild (truly!) information on Ogre-faced Spider eyes, first publishing this finding in 1978, wherein he described this "metabolically extravagant system":

During the day, receptive segments are short, and rhabdomere membrane occupies only a small proportion of their volumes. At nightfall, the segments lengthen, and novel membrane is added in a rapid burst of synthesis almost to fill them. At dawn, the sequence is reversed, and membrane is removed as pinocytotic vesicles which are assembled into multivesicular bodies and lysed in the inter-rhabdomeral cytoplasm and in the swollen receptor axons which underlie the retina. Synthesis and destruction of membrane are shown to be controlled in part by immediate states of retinal illumination, superimposed upon a daily rhythm.

Blest has also done research on the photoreceptors of many other species, reporting frame changing results there as well.
Blest A. D. 1978 The rapid synthesis and destruction of photoreceptor membrane by a dinopid spider: a daily cycle. Proc. R. Soc. Lond. B. 200 463–483 doi.org/10.1098/rspb.1978.0027

Its truly wild - "Dinopis subrufus, are highly specialized for night vision; their
lenses, in particular, have F-numbers of only 0.58." and "f nocturnal vision depends upon filling the receptive segments
with membrane, the schedule of behaviour implies that re-synthesis should be
both extraordinarily rapid and extremely reliable; the bulk of the process would
need to be completed in about 1 h.
Here, it is shown that the postulated cycle does, indeed, take place" It does appear to be under control of the spider, not from light degradation, but rather adaption to different light levels.

@JiminyCricket. see other comments. If you want I'm happy to chuck the article onto a google drive and share. The EM in the article is just beautiful!

No worries, just went to the non-pdf page for the article and copied the citation from there.  It is absolutely amazing; it would never have occurred to me that something like these mechanisms were possible. To quote J.B.S. Haldane the universe is not only queerer than we suppose, but queerer than we can suppose.

Thank you so very much for this. I'm still having trouble entirely wrapping my head around the reality of this. It's truly blown my socks off thinking about this and how it evolved. Very much appreciate the answer and support. The key search term "Blest" yields all sorts of interesting stuff to explore. How particular were the professional interests of this man! Fascinating.

@JiminyCricket. - Agree completely; it's a whole new thing for me too. As bob1's very apt quote states, the universe is queerer than we can even suppose.

@JiminyCricket. His last scientific publication was in 2004 in the Canterbury Museum Bulletin (NZ) it seems - from some time in the 1950's, that's a long career.


text:
Why in acute phorpyria?
I am having confusing about treatment of phorpyria . I read it somewhere that for treating phopyria hemin and glucose is given IV . Please give me an easy explanation of it

Some more background and a link to the source of the "somewhere" is recommended. Until edited, I vote for closure

From book Lippincot review

Hi and welcome! As @AliceD said, this question needs a lot more detail in order for us to help you. This page in our Help Center will show you what she means. We look forward to seeing more of you!

@Sue acute phorpyria is a disease in which there is  accumulation of intermediate compounds in response to defective heme synthesis pathway .what else I can tell u .

@user60180, details like what exactly you are after, what effort you made in finding the answer (if any). You can refer this for a guide: http://biology.stackexchange.com/help/how-to-ask

Since porphyria is not one disease but many, I suppose that with "acute porphyria" you mean acute intermittent porphyria. The reason of the disease is an autosomal dominant mutation on the enzyme porphobilinogen deaminase, an enzyme that converts porphobilinogen to hydroxymethylbilane by a deamination reaction.
Now the heme is produced in many steps, and the enzyme above is important in the early steps of heme synthesis. In persons with porphyria, these heme precursors accumulate, causing toxicity. In acute porphyria the symptoms are mostly from the central nervous system. The figure under shows the steps of the biosynthesis of heme, and as you see at the upper right corner, defect in the enzyme porphobilinogen deaminase (PBG-deaminase) results in accumulation of porphobilinogen.

Glucose and other carbohydrates can help suppress disease activity, are given by vein or by mouth, and are part of initial treatment. Intravenous heme, however, is both more specific and effective than glucose and should be started if the patient’s symptoms fail to improve within 36 hours.http://www.porphyriafoundation.com/about-porphyria/types-of-porphyria/AIP [2015-05-02]
More about carbohydrates and the suppression of symptoms in porphyria http://www.porphyriafoundation.com/about-porphyria/diet-and-nutrition/the-glucose-effect-in-acute-porphyria [2015-05-02].

I like the explanation . But how glucose do this job . Does it help in removing those excessive intermediates?  Or something else

If you see at the figure above you can see at the second step that glucose and hemin (which you mentioned in your question) inhibits the Aminolevulinic acid synthase. Glucose therefore inhibits the formation of the heme precursor 5-aminolevulinic acid and thus downstream formation of porphobilinogen. http://flipper.diff.org/app/pathways/info/6362 [2015-05-02].

source: Stack Exchange

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

sort: votes


text:
Which organs/tissues are defined as "peripheral organs/tissues"
In the following paper [1], I encountered one term "peripheral organs". Literally, based on my understanding, it should be related to the organs/tissues, such as skin, hair and ear in the human, and wing, antenna and leg in the insect. However, in reference [1], fat body, oviduct and hemocytes are listed as peripheral organs. Is there specific definition of "peripheral organ/tissue"?
Thank you!
[1] Verlinden, H., et al. (2010). "The role of octopamine in locusts and other arthropods." J Insect Physiol 56(8): 854-867.

I have the same question.  Saw it used here, referring to humans: , "B cells in peripheral organs and the CNS cannot be reached by intravenous rituximab..."

The most common usage of "central" vs "peripheral" organs/tissues is: central nervous system (brain/spinal cord) vs all other organs/tissues:

"B cells in peripheral organs and the CNS" (from the article linked in the comment)
Nervous system includes central nervous system (brain/spinal cord) and peripheral nerves (spinal and all other nerves) (Central nervous system and peripheral nervous system).
n-3 PUFA and obesity: from peripheral tissues to the central nervous system (PubMed)
Atrial natriuretic factor receptors: distribution and regulation in central and peripheral tissues (PubMed)

However, depending on the context, different organs/tissues can be considered peripheral:

From the liver metabolism viewpoint, liver can be considered central and muscles and fat peripheral (Apoptosis and insulin resistance in liver and peripheral tissues...).
From the intestinal absorption viewpoint, gut can be central and all other organs peripheral (From the gut to the peripheral tissues...).

Peripheral organs and tissues are simply parts of the body that act as a response to a change in the environment, the body's functions, molecule levels, etc. They include the endocrine system organs as well as organs producing hormonal responses such as the pancreas producing insulin. When the skin and therefore the hypothalamus senses a drop in temperature, your body goes through natural responses such as shivering and contracting of the limbs. As for the oviduct, it is an organ that will respond with contractions and movement when an egg moves down it. As for hemocytes, it would make sense for them to be peripheral organisms for the body as they respond to oxygen deprivation in a cell. As a large multi cellular organism, it can be said that peripheral organs/tissues are parts of the body that provide intricate function or a reaction to an endangerment to the body.

references missing.

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

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


text:
natural characteristics of insects used as human disease model
In this paper [1], the author found that the autism-related genes are conserved between honey bee and human. Thus, this paper providing a means to further explore sociobiology theory. In my opinion, the honey bee have the potential to be developed into an model for human autism disease.
My question is: what other examples in insect like this in honey bee that the model species itself has some characteristics, which could be used as model system for some human disease studies?
Thank you!
[1] Shpigler HY, Saul MC, Corona F, Block L, Cash Ahmed A, Zhao SD, Robinson GE: Deep evolutionary conservation of autism-related genes. Proc Natl Acad Sci U S A 2017.

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


text:
Expressing bacterial proteins in mammalian cells
Does anyone have experience/knowledge of expressing bacterial (or other microbial) proteins in mammalian cells? I am interested in this for a project where we are trying to introduce a new enzymatic activity in human cells. I have been looking for examples in the literature, but haven't found anything so far.
I can imagine that various problems might arise. Presumably transcription and translation should not be a problem; but I can imagine the protein may not get sorted/localized properly, or might not be properly degraded and so could  accumulate to toxic levels ...  or what not.
Any advice or pointers to literature would be much appreciated!


text:
Contribution of major nutrients to energy in the human body
What is the contribution of the major nutrients -- glucose, fat and protein -- to the human body's energy requirements, in normal conditions?
For some tissues, the fuel preference is known qualitatively -- the brain runs on glucose, the heart preferentially oxidizes fatty acids, etc. I'm looking for quantitative data on the consumption (oxidation) rate of the major nutrients, on the whole-body level. Molar amounts per unit time, or energy per unit time, or relative contributions to the total.
To get a rough idea, I looked at glucose and triglyceride turnover in blood. This article estimates blood glucose turnover at about 8 g / hour, or 190 g / day. If we assume that blood glucose transport equals amount of oxidized glucose, then this corresponds to 3200 kJ / day, or about 1/3 of the daily energy requirement. Similarly, this article estimates blood triglyceride half-life at about 1h; with a blood triglyceride content about 5 g, this yields about 90 g / day, or 3300 kJ / day from fat.
So with this rough estimate, sugar and fat appears about equally important, but about 1/3 of the daily energy requirement is missing. And I would imagine my quick calculation is inaccurate in many ways... Anyone know of better estimates? Some literature on the subject?
(I'm aware of the the dietary reference intake data, but diet composition may not equal the proportions of nutrients oxidized due to all sorts of interconversions.)

Good question... depends on what "normal conditions" is defined as... even during a 'normal day' the transition from prandial to post-prandial changes the fuel utilization for different tissues of the body

@VanceLAlbaugh  Yes, I realize it may differ with feeding.  I would be happy to learn of any quantitative data, in fed and/or fasted conditions.  Haven't found anything besides by own home-cooked estimates ...


text:
Never caught this fish before

After catching a bunch of mangrove snapper using live shrimp, my son caught this fish in about a foot of brackish saltwater water off a dock near a rock wall in  Vero Beach at around 10:00 AM  on July 5th. Fish was about 6 inches long and had a wide mouth with  small pointy teeth and what appeared to be two small horns/bumps that protruded from behind its eyes. Never encountered it before.

Juvenile snakehead?

Looks like a sculpin (Cottoidea, Cottus). Hard to pin down what kind as there are a bunch, but that very wide head is pretty distinctive.

Expanding my comment into an answer as no one else has jumped in-
This fish closely resembles a sculpin of some kind. This is a very large and diverse family, but many of them share distinctive features. The quite wide head and horns that you describe and show are common in this family. Where I am from (Northwest USA), the Red Irish Lord / cabezon is a gamefish sculpin that can grow to be quite large, and closely resembles this picture of yours (a rather small specimen shown in Figure 1).

Figure 1.
Based on where you are in Vero Beach (Florida?), I have looked a little bit and there is a chance that it is a Gulf Toadfish (Figure 2) based on its appearance and where you caught it. Here is another fisherman's account (with pictures) of a similar fish.

Figure 2.
Hope that helps.

My best guess would be that it is a Enophrys bison. Some of the pictures similar to the one you have caught that I found are:

The presence of the horns is one of the indicators similar in both images(mine and yours). Another similar image is:

Also about its habitat I found this:

Might explain why you caught it where you caught it(in a shallow brackish,rocky place). You ought to crosscheck it as I am no expert.

Could be wrong but this species appears to be specific to the Pacific Ocean according to your species range quote? The OP caught the fish in Florida (Atlantic Ocean).

Yes I saw that issue and had deleted this post. But then un-deleted in case there is some connection.


text:
Is "Retinal Glial Cells Enhance Human Vision Acuity" creationist propaganda?
The paper Retinal Glial Cells Enhance Human Vision Acuity is profusely quoted by creationists as "proof" of the "perfect design" of the human eye.
The paper is about biology but published in Physical Review Letters (open access, click PDF). Is it generally accepted as legitimate science, though cited by creationists, or is it thinly veiled creationist propaganda?

I've adjusted the wording of your question to avoid overtly soliciting opinions. In Biology SE we should ask questions that can have fact-based answers. The classic example of the debunking of intelligent design arguments is the flagella motor, looking for a source for that now... Here's one https://youtu.be/jdF-ugdl4mc but just search "flagella motor intelligent design debunked" for more.

@uhoh, thanks. This is my first question here.

apparently these are harder: Determine if a coincident point in a pair of rotated hexagonal lattices is closest to the origin and Can there be an energetically unbounded three-body orbit where escape is impossible due to conservation of angular momentum? which reminds me that I need to post it in MO


text:
Help identifying a mushroom found in Raymond, WA, USA
Hello dear mycology wizards!
Could you help me figure out what's the name of this species.
I found the mushrooms in a forest near to Raymond, WA. The area was quite wet and mossy, but not a swamp. There was a creek ~50-75 feet away. The forest is mostly coniferous trees with a few birches.

Here are the photos of the mushroom of interest:

just as a preface to any responses you get: I have not known this community to be especially knowledgeable about mushrooms (i.e., I don't know of any mycology wizards here), so I would suggest you research further any answer you receive and/or seek additional insight from a known mycologist. (Not that an answer you get isn't correct, but I think fungi are notoriously tricky to ID and easily misidentified by even trained mycologists -- so do more of your own sleuthing with whatever info you glean from this community). Good luck :).

Candy cap is another possibility, which should have brittle stipes, a sweet odor, and a milky latex. However, it can be easily confused with the deadly galerina, so be careful.

To me that looks like Chrysomphalina chrysophylla, which is one of several fungi superficially similar to the chanterelles.
(The chanterelle in contrast has gradual increase in the diameter of the stalk rather than a sharp demarkation between the stalk and cap.)
Chrysomphalina chrysophylla is a species that has been reported in Washington:
 Source: Burke Herbarium Image Collection (for Washington state)

All the mushrooms I saw on the site had straight, not curved stocks. None of them grew on the dead wood/logs. I suspect it's a different fungi, but I really appreciate your attempt to identify it!

I'm pretty sure those are false chanterelles. True chanterelles, like Igor said, have a stalk that gradually widens from the base to where the mushroom cap starts, giving then kind of a fat look, if that makes sense. Chanterelles also aren't so garishly orange, they're more of a creamy orange-yellow, and they have more of a ruffled edge on the cap.
Be really careful because false chanterelles can make you quite sick. Hope you didn't eat any of those before finding out for sure! Good luck in your hunting

No, I did not eat any (in fact I didn't even collect them). I found them a year ago when I was shopping for land in that area... Thank you!

The specimens in OP's photographs don't look like false chanterelles (Hygrophoropsis aurantiaca) at all.


text:
Can someone help to identify this insect?
I found a few of these insects around my house, and I'm curious what insect it is.

Seen mid-August in Singapore
At least several mm but lest than 1 cm long
Seen walking slowly. I can't be sure but don't think it can fly
No sound noticed

For species identification questions it's necessary to include as much information as you can. Can you mention at least roughly your location on Earth? Also, can you estimate the approximate size of this insect? 1mm? 1 cm? What about behavior; was it flying, or walking, moving quickly or slowly? Did it make any noise? Thanks!

Singapore, less than 1cm, walking slowly, dont think it can fly, no noise. Appreciate your help thank you


text:
What kind of insect is this? It looks like a huge spider with one long antenna and six legs

It looks like a huge spider but with six legs and has one very long antenna. It also looks like it has claws. Please I would like to know what sort of insect it is. So I would know measures to take if it is dangerous.
Details:
This picture was taken in Nigeria at night. It's raining season here too.

Similar critter: https://biology.stackexchange.com/questions/93794/what-insect-is-this-looks-like-a-spider-but-with-six-legs-and-long-antennae

While not completely sure, it definitely looks like an Arachnid. Upon further research, I have narrowed it down to either Amblypygi (i.e., whips spiders, tailless whip scorpions), or Solifugae (i.e., camel spiders, wind scorpions, sun spiders). Using whatever perceptional abilities I have, I have made the educated guess that the appearance of the arthropod you posted most closely resembles that of Amblypygi.
The "antenna" is part of the anterior legs (first pair), and not an actual antenna. The other leg of the pair is missing. The appendages in the front that are long and folded are not legs, but pedipalps.

this is a whip scorpion, family Phrynichidae

@JimN So, are we in agreement on what this is? The family of Phrynichidae are in the order of Amblypygi. But, Phrynichidae are not "whip scorpions", unless you meant "tailless whip scorpions" (whip spiders). Whip scorpions are in the order of Uropygi.

I'm sorry, I did mean 'whip spider' ! Let's put the common names aside. I agree with order Amblypygi, Family Phrynichidae. This paper mentions two species of the Damon genus in Nigeria: D. johnstonii and D. medius, and many other species in neighbouring countries, but other genera exist as well

Hm, my previous comment didn't include the paper URL? : https://www.sciencedirect.com/science/article/pii/S1439609205000425


text:
Evolutionarily, why do some animals perceive eye contact as a sign of aggression?
It's said that species like dogs and bears perceive eye contact as a sign of aggression. Primates -- including us humans, in many of the world's cultures -- use eye contact in this way as well, to the point where zoo visitors are advised to avoid their gaze when possible.
Nothing seems intuitively "aggressive" about looking at someone looking at you. So then, why is eye contact commonly perceived as a form of aggression, even across species? Is there an advantage to perceiving eye contact as aggressive?

I am of the belief that this question is better asked with the "Evolutionary" part left off. It is best not to specify how you want someone to answer. This question is better answered with animal neuroscience than with some far-fetched answer about how evolution and eye contact are related.

Perhaps that would be an alternative approach, but I believe that the evolutionary approach offers a relevant and valid approach when considered in conjunction with the neuroscience - we don't want to exclude things from our toolkit do we? @Arrow Edited to add: Also worth taking into account; the condition the animals are kept in, their health, their conditioning and developmental stage. Oh, and their gender and if they've young....

Eye contact being perceived as aggressive across species, including in humans, stems from evolutionary and behavioural factors. In primates and humans, direct eye contact can signal dominance, threat, or territoriality. This is rooted in survival instincts where maintaining a safe distance and avoiding confrontation are advantageous. In social species, interpreting eye contact as aggressive helps in navigating hierarchical structures and minimising conflict. This perception likely evolved as a way to establish boundaries and maintain order within groups. So, even though eye contact itself isn't inherently aggressive, seeing it that way helps animals and us humans promote social cohesion and keep things in line.
For a popular science publication discussion see here.
Also, keep in mind that the "aggressive" interpretation is not solely due to a gaze/stare. There are still tiny facial expressions and changes in facial muscles that provide cues.

different but related: Term for a prey animal's recognition that something potentially threatening is looking at it?

Savalli et al 2016 argues this isn't applicable to dogs: when dogs go into threat displays there's eye contact, but its the other gestures that are conveying the threat. Specifically, Eye Contact Is Crucial for Referential Communication in Pet Dogs by Carine Savalli et al in PLoS One 2016 argues dogs extensively use eye contact to communicate to their owners (but they are not threatening their owners), whilst primates use vocalisation for communication for equivalent communication of needs or requests. Thus, when primates use threat displays eye contact is key because its not used in request behaviour, whilst Savalli et al 2016 is arguing in dogs eye contact ain't for threats, but critical non-verbal communication to convey their needs to owners. In summary, you don't bite the hand that feeds you, you don't use threat displays for requests.  The dogs system of non-verbal communication isn't trivial, but intricate involving obtaining eye-contact as the initiation of communication (see the diagram below). The study sample size was not huge "Twelve male and ten female" but it is a convincing behavioural study.

My personal view is that it is very clear from Russian breeding program for fox domestication - and their owners reports - that dogs have been through extensive layers of evolutionary selection far beyond simply "tolerating humans", which is what domesticated foxes display after considerable directed selection.


text:
What kind of snakes are in this photo?
What is the name of these snakes? I saw them in the street and I don't know if they are dangerous for people? Photo is taken near to Tbilisi, Georgia.

Welcome to Biology.SE! Identifications questions should include: 1) the species-identification tag; 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this information as it can be essential for a proper identification. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
Can twins that develop in separate sacs but share the same placenta be identical?
I have two younger non identical twin sisters. When my mum was pregnant she was told they were both in different sacs when developing but shared the same placenta.
We have done hours of research on the topic, as we have reason to believe they could after all actually be identical.
After all this research we’ve just found a load of fancy names for twins and no information on non identical twins that share the same placenta and are in different sacs.
Another thing that may help is that they are mirror twins.

Welcome to Biology Stack Exchange! I modified the wording of question a little bit to bring out the actual question about biology.

they were both in different sacs when developing but shared the same
placenta

This suggests that they were monochorionic diamniotic twins, which would mean they are monozygotic, i.e. identical.


text:
Black flying bug infestation

What is this black bug in my house. There is literally an infestation. They are everywhere. The size of a small tick. They fly and just keep coming. Im from pakistan, lahore.
I've never seen these before in my life and have lived in this house for over 10 years.

Have you noticed anything about their behavior? Are they attracted to anything in particular? Light, water, food, windows, each other?  Do they stay airborne a lot, for long periods of time, or just "buzz" a short distance before landing and walking around again?


text:
Is Eastern diamondback rattlesnake swimming an example of adaptation?
I have read that Eastern diamondback rattlesnakes are capable swimmers. Can we consider that as an adaptation?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

I think a better question is." Are there any snakes that can't swim?"

All snakes can swim. The ability likely was derived from their lizard-like ancestors.
In his book, "How Snakes Work", Harvey Lillywhite (2014) mentions that "all snakes can swim, some better than others" (p 80). Harvey is a renowned herpetologist.

Even if all snakes can swim, perhaps OP would like to know if the ability of snakes to swim, was an adaptation of some kind.

That question was answered by stating that the ability to swim was inherited from ancestors, not an adaptation in snakes.


text:
What kind of spider is this? First time I have ever seen one

This was taken 07/06/19 in Cape Breton, NS, Canada.
I would say that it is about an inch (2.5 cm) in length and seemed to be pretty uniformly grey. The belly was the same colour as the legs, it had a few small brown spots but I couldn't tell if that was an actual marking or maybe just environmental.
It was just hanging out right beside the handle of the door exactly where you don't want a spider to be.
In usual spider fashion it has dipped and is now...somewhere :(

It appears that you have a leafcurling sac spider:

They are observed all over east and west north america:

Here is the eye arrangement from bugguide:

I labeled with arrows the two thin dots at the top, which are eyes that point upward, which are easily visible in your picture. Would need a front-facing photo to see the rest of the eyes.
The spinneretes out the back of the abdomen are also diagnostic of clubionids.
The colours can span dark yellow to light brown, and the jaws are dark and sometimes the entire front face is dark as well.
A gallery of clubionids filtered on only Canadian observations is here:
https://inaturalist.ca/taxa/121774-Clubiona/browse_photos?quality_grade=any&place_id=6712


text:
What is this nighttime creature?
I almost stepped on this little critter. It blended into my garage floor. It is about about the size of my hand, with huge bulbous eyes that immediately caught my attention. There was a distinct white bump below\between the eyes.  It froze when I turned on the light and did not move at all until I turned the light off. Then it moved faster than my eyes could follow in the direction of my garden.
I am on an island in the San Francisco Bay, California. The current temperature is ranging from 50 (night) to 65 degrees and rainy season has just started (late this year). It blended so well with the garage floor that my camera had problems focusing on it.

Likely some type of gecko, they are active at night.

Welcome to Biology.SE! Any noise when startled (e.g. "barking")? Please also [edit] your post to include the location. Location can be an essential clue for identifications and should not be hidden in comments, which are ephemeral and often overlooked. ——— If possible clearer, closeup photos of the creature from multiple angles would also be helpful since this could be one of several salamanders native to your area. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

Something like this perhaps? Found here while searching for "gecko" in California Lizards It may not be an exact match due to geography, but perhaps it's a start. It at least sometimes has a white spot between the eyes, though not as pronounced as this one.

I believe this is an Arboreal Salamander (Aneides lugubris).
http://www.californiaherps.com/identification/bayareaherps.html#Lizards
http://www.californiaherps.com/salamanders/images/alugubrisbr1108.jpg


text:
What is the name of this flower (on a tree)?
Here is a photo of a big red flower-like structure on a tree on Lama Island, close to Hong Kong. Does anyone know the name of the tree and what the black "berries" are attached to the "flower"?

I think this may be an aril or arilode rather than a flower, but I cannot be sure (see here).  If you have or can get more pictures from different angles, also some shots of the leave and bark that would be helpful.

Welcome to Biology.SE!  In addition to what @BryanHanson suggests, it could be helpful to edit your question to include size estimates for both the red flower-like and the black egg-like structures.  Thanks!


text:
Which mold species are these?
A friend of mine in Los Angeles recently put a petri dish with some mold-friendly substrate under a vent for two days, and a whole rainbow of mold species grew on it.

What are the different mold species present on this dish? Are any of them dangerous to human health?

you need to give a lot more information and if possible take pictures with 50x magnification of each type in your sample.

I'm not sure the OP can give "a lot more information" except maybe what the "mold-friendly substrate" was, but I think an answer linking to a resource for common household mold species would be a wonderful and helpful answer. +1 for home experiments!

@trondhansen - I am happy to give any other information that I have and that might be relevant, if you tell me what you are looking for. I did not take the picture, and my friend does not have a microscope, so I cannot easily get you 50-times-higher-resolution pictures. I imagine some "best-guess" answer might have to do if there are various mold species with similar phenotypes.

The wet pink ones are likely to be either a yeast or something like Serratia marcescens. We would need microscope pictures of stained samples from the others to attempt ID. Filamentous fungus is about as close as you can get otherwise. Huge range to choose from...


text:
Cloning problem. Digestion test at the end of the cloning is always negative
I have a problem with my cloning, I'm trying to clone a 483 pb in a pSecTag vector with restriction sites HindIII and BamHI. Here are the procedures I'm doing:
•   I introduce the restriction sites BamHI and HindIII into my insert by PCR with Pfu (blunt end polymerase) and gel purified it.
•   I clone my insert in a pJET1.2/blunt vector. I get enough colonies and I tested few of them with an internal insert primer and a vector prime via PCR. The results are positive.
The problem came when I digest my insert from pJET and try to clone it in a pSecTag vector.
•   I digest my insert and the vector with HindIII and BamHI in Buffer Red during 1.5h at 37ºC (fermentas). I purify the insert and the vector from the gel and checked that all fragments run at the correct size on a gel. All correct.
•   I do the ligation (T4 DNA ligase) using a 5:1 Insert:vector and less tham 100ng of total DNA. The ligation (20ul) is performance at 22ºC for 30 minutes.
I get few or not transformant colonies. When I get colonies, I tested them by PCR:
**
•   With internal primers, the result are positive

With a primer for the vector the result is negative.
The strangest thing is that when I use pJET primers that do not anneal in the pSecTag I get positive results.**

For transformation i'm using chemocompetent DH5-alpha, with a heat-shock of 42°C at 45 seconds. I tested the bacteria with a plasmid before using them.
I change condition several times but always obtain the same result. I follow all the protocols but I don’t get my construction.
Anybody knows where the problem is? Thank you.

It sounds like the insert is still in pJET doesn't it? Is there any chance you mixed the two vectors somewhere in your purification step after the digest? Instead of PCR you could try doing a restriction map.

Thanks for your answers Yes, the insert is still in the pJET. One of the times that this happened to me, I digested it and the bands corresponded with my insert and the pJET. I sent it in sequence and the result was the same. There is no possibility of having mixed the vectors, given the problems I have had I have been doing the steps on different days to avoid any kind of misunderstanding in the manipulation.

Why are you blunt cloning it in to pJET first?

I can't digest my PCR insert directly, the RE can't cut.

Even minute amounts of undigested vector will contaminate your transformation. You could PCR amplify your insert from the pJet cloning plasmid and then digest the PCR product with BamHI and HindIII. In order to get rid of the pJet template either gel purify the digested insert, digest pJet with some times which cuts it multiple times (less preferable) or put everything on a column and hope that pJet is diluted enough (less time consuming but a bit risky).
The other thing you could exploit is that pJet is ampicillin resistant while your target vector is also Zeocin resistant. If you add Zeocin to your E. Coli it will kill a pJet positive clones while sparing the pSecTag positive clones.
Your insert is fairly small so using a bit more DNA than usual won't hurt.
If you can post some pictures of your gels this might be helpful as well.

Thank you very much. I was thinking of doing that, amplifying by PCR, digesting and purifying it from gel. Or also try sequential digestion. I must have some contamination but it is difficult to know where.
I would upload some photo of the gels but I do not know how.


text:
Building a PDB file from amino acid sequence of non-folded structure
I am interested in experimenting with folding simulations and algorithms for arbitrary sequences. I'm wondering if there is an easy way to convert an amino acid sequence into a PDB file for further simulation. To be clear I only want the primary protein structure.
If possible, I'd like to be able to characterize the bonds as well so that I can treat the molecule as a rigid body with rotational joints. Does anyone know something that can do this?

You may be confused about the terms. If you only want the primary structure you don't need a PDB file. There is no easy way to "convert" sequence into 3d model (PDB file), but the opposite is true - you can get sequence from a PDB file.

@marcin - I believe he does need a PDB file (or cif, or xyz, or whatever) as it would be an unfolded 3D model, with coordinates for all the atoms, but without a realistic geometry. As in fold.it, basically

yes, exactly @gilleain -- I want the 3D geometry of the unfolded model. It seems to me this is a relatively easy task since the geometry of the amino acids is known ... you just need to stack them together and preserve the peptide bond length. I'm just wondering if there is a library for this or do I need to write one.

So to be clear, it sounds like you want the 'coil' or unfolded structure of a protein based on the sequence?
There are plenty of programs out there to do homology modelling, which is taking a sequence of unknown structure and modelling it onto one with a known structure. On the other hand, there are many libraries for analyzing existing structures. What you want is somehow in between these two.
I'll add some links here as I find them:

There is a Lua library that might be useful : https://github.com/rob-miller/rFold
Modeller has functions for this: https://salilab.org/modeller especially this page
The Structural Bioinformatics Library : http://sbl.inria.fr/doc/index.html
The Rosetta library (as used in fold.it): https://www.rosettacommons.org/

I'm sure there are more, but it really depends on what programming language you want to use, or if you are implementing stuff yourself versus running some standalone software.

Thanks. Yes, I explicitly do not want the folded structure or to predict the folded structure via analysis or analogies to existing structures. I just want to convert the amino acid sequence into an unfolded 3D configuration of the protein where bond lengths are close to their average lengths. I want to then explore the conformation space solely based on perturbations to torsion angles (sample the energy for various configurations of the protein backbone) starting from the unfolded state.

rFold seems to be exactly what I am looking for, though I think I need to specify the relationships, native bond lengths and dihedral angles for each amino-acid manually

I wanted to do the same thing, and ended up writing my own very-hacky script for this. It can be found here: https://github.com/pb1729/seq2pdbchain


text:
Meaning of red blood cell volume expansion
In the scientific papers about EPO I read RBC volume (mL) expansion. What is it? The volume of a single cell or the volume expansion (=that is the increase of the number of cells) caused by the EPO?
Thank you in advance.
EDIT: see fig.1 page 3 please http://s000.tinyupload.com/index.php?file_id=08669957844938542361

Please provide context in the form of a citation from one of the papers together with a link. Otherwise your question is likely to be voted as off-topic because it is unclear.

Hi @David. See fig.1 page 3 please http://s000.tinyupload.com/index.php?file_id=08669957844938542361

Fine, by the place for this in your question. Please edit it accordingly.

Red blood cell volume is the percent of blood taken up by red blood cells (also known as the hematocrit), and is expressed as a percentage (so, normally, RBCs should comprise x% of blood by volume.) It says nothing of the size of the red blood cells.
That needs to be done by measuring the mean corpustular volume either by special machine or by looking at a slide of cells. So if the MCV is not mentioned, you can assume that expansion is referring to increased number of RBCs.
Smaller than normal RBC's are called microcytes, larger than normal are called macrocytes.
Recombinant EPO just increases the production of RBCs (and, unfortunately, it has some other effects as well.) It should not affect the size of the final erythrocyte.

Hi @anongoodnurse. If possible, can you link me some references about the sentence "It should not affect the size of the final erythrocyte." please? My unreliable professor said that EPO causes the increase of the size of RBCs. Thank you for your answer.

@GennaroArguzzi - I appreciate that you would like sources. I actually read a couple of papers about recombinant human EPO and in all the papers, it just discusses RBC volume, which is already defined. In none of the papers does it list RBC indices (that is, cell size, hemoglobin, the number of reticulocytes, etc.) If there's no problem (EPO has been used in dialysis patients for decades now) with the end result for erythrocytes (there are other problems: too many plateletts are produced as well, and a few other things), then it boils down to accepted terminology, as above.


text:
Can anyone tell me what type of worm this is?

I sure hope you can see this picture. Need to know what type of worm this is. Found one in July and one just now inching its way across my tiled floor. I live in Florida. It is one color all the way around, dark red.

I can't see the head clearly but based on
1: it is a big worm cruising around on land
and
2: you have never seen one before
I bet on this

From linked article.

The flatworm (Platydemus manokwari) has few natural predators outside
  of New Guinea, and it likely will have no predators in the United
  States, Justine says. It gobbles up soil-dwelling invertebrates like
  snails, which could have a big impact on the environment.

I checked wiki for this worm and it says it has a lighter colored underside. This worm is the same color all-around

Does your worm have a semicircular head?  Or a pointy head like an earthworm?

I'm not sure. I don't know anything about worms but I think it has a pointy head?


text:
Mathematical representation of "gene signatures"
According to Wikipedia's definition, "a gene signature is a group of genes in a cell whose combined expression pattern is uniquely characteristic of a biological phenotype or medical condition."
While the above definition is very useful to understand the concept, I am looking for a "more practical" definition or, rather, a mathematical representation (e.g., a vector) of gene signatures. Hence my question.

Possible duplicate of Is there a formal definition of signature of natural selection?

I think the WGCNA package in R is an interesting and relevant take, the related paper is here.

Let's say you have a list of genes that you derived from a RNA-Seq and made a differential expression analysis. You can rank genes by p-values or fold-change values, or convert to membership values between 0 and 1. This ranked list and any its subsets are gene signatures.

@MaximKuleshov thanks for your reply. Could you, please, provide a full answer listing the three methods you just highlighted (attaching a short discussion of applications would be great)

@mrb If you could comment on whether or not you think your post is a duplicate of the one I marked as possible duplicate. If it is not a duplicate, could you please highlight why? That would help to know what you're after.

Hi @Remi.b, the other post provides a definition of the concept, which is very useful, but my question is about a common mathematical representation (eg, the comment above by @MaximKuleshov).

@mrb You edited your post from genetic signature to gene signature after the question had been answered. You should rather roll this edit back, accept or comment on the given answer and open a new post for your new question. Also, it will bring more attention to your new question to open a new post than to change a previous one.

No, i haven’t. I am sorry about the confusion but i edited the post immediately after the first comment a few days ago. Dunno way you could not  see the edited version until now.

There are mathematical definitions of "gene signature". Please have a look at the supplemental material of Subramanian et al. PNAS 2005, one of the first papers on "gene signatures", and a method and tool which is still commonly used in basic research.
Note that Subramanian et al. have multiple definitions and that copying them here would exceed the scope of this page.

There is no mathematical definition of genetic signature. Please first have a look at Is there a formal definition of signature of natural selection?. As explain the term genetic signature is used in a very broad sense.
There are a number of processes for which one might be looking for a signature of this process. Such signature can take the form of various statistics. For example, a historically important statistics is Tajima's D defined as
$$D = \frac{\Pi - S/a}{SE}$$
, where $\Pi$ is the average number of pairwise differences between two randomly sampled haplotypes, $S$ is the number of segregating sites, $a=\sum_i^{k-1}1/i$, where $k$ is the number of sampled haplotypes. $SE$ is the standard error for the numerator which takes a complicated formulation (have a look at Tajima 1989 for more information).

Why would anyone use pi as a variable?!

@canadianer What do you mean? $\pi$ is very commonly used to represent the expected heterozygosity. Note that to avoid confusion, I used $\pi$ to $\Pi$ in my answer.


text:
What gene targets associated with the new coronavirus (SARS-CoV-2) have been identified so far?
One hypothesis for which we have some supporting evidence is that the new virus (SARS-CoV-2) "enters human cells through an interaction with angiotensin-converting enzyme 2" see here. Although it is still unclear what genes to target in order to prevent the infection (entry or reproduction).
Is there empirical evidence suggesting what genes can be modulated to fight the infection?

The linked article does not suggest "targeting the gene that modulates ACE2"...I think you've misunderstood.

Hi thanks for your comment. Could you please expand

"The researchers concluded that their research could contribute to structure-based designs of decoy ligands or antibodies able to specifically target ACE2 or coronavirus spike proteins to prevent viral infection." - They're talking about making decoys that look like ACE2 (virus binds these rather than real ACE2), or antibodies that bind ACE2 or the coronavirus spike protein. Antibodies that bind ACE2 sounds like a horrible idea to me and one they probably didn't think through too much.

This is an interesting question. A recent study published on bioRxiv by researchers from Xi'an, China (pre-print) argues that CD147 can also be an entry receptor for the virus. They showed virus entry can be blocked by an antibody to human CD147.


text:
Non-coding DNA correlation with rate of evolution
Non-coding DNA can be helpful in generating useful mutations that can go on to become new features/functionality of an organism.
Non-coding DNA also indirectly reduces chances of mutation of useful/functional genes.
So if an organism has a larger proportion of non coding DNA it'll be safer from mutation. Humans have 80%-90% non-coding DNA. But this number is far lesser in many other species especially plants. Some plants have as few as only 3% non-coding DNA.
My question is, do these species with less non-coding DNA undergo evolution faster? Because their functional genes are more susceptible to mutations (which would be disadvantageous on average I guess). Would it be fair to say that evolution tries to keep expanding this proportion of buffer DNA? Lastly, is my question related to C-value paradox?

My assumption that non-coding DNA indirectly offers adaptive advantage (evolutionarily speaking) seems to be questioned. Let's consider the following case:
Let A and B be two genomes of equal size. Let A have 80 % non-coding DNA and 20% coding DNA. And let B have the opposite i.e., 20% non-coding DNA and 80% coding DNA. Let both A and B be exposed to the same amount of UV radiation for the same amount of time. All conditions being the same, let's assume that this causes the same amount of mutation in both A and B, say 10%. Now what is the probability that this mutation happened in non-coding DNA (which means it doesn't harm the organism) in each of A and B? Evidently, the probability is higher in A meaning it's safer from mutation caused due to UV radiation. So A has an advantage of surviving over B.

Humans have 80%-90% non-coding DNA Wasn't it 98% as per as my limited knowledge is concerned?

@FailedScientist 98% was the popular understanding which is now changing due to broadening of the definition of what is 'functional' part of DNA sequence.

“Non-coding DNA also indirectly reduces chances of mutation of useful/functional genes”  — It does?! How? The rate of mutation doesn’t change because of the size of the genome.

@yathish “functional” ≠ “coding”. Regardless of the definition of “functional”, the percentage of coding (= protein-coding) DNA has barely changed.

@KonradRudolph Let's assume mutation is bad and it can happen anywhere on the genome with equal probability. If non-coding DNA is 95% of the genome then the probability of mutation happening over coding DNA is only 5%. I understand functional!=coding.. it's a broader definition.

@yathish Again, the rate of mutation is independent of its size. Yes, if you add 95% non-coding DNA (= 20-fold increase in genome size) then only 5% of mutations happen on the coding fraction, but the absolute number of mutations also increased 20-fold, so the number of mutations on coding genes remains identical! In sum, non-coding DNA does not “indirectly [reduce] chances of mutation of useful/functional genes”. And to your other comment, it’s still wrong to speak of “80%–90% non-coding DNA”, the actual number is roughly 98%.

Thanks for adding the explanatory paragraph to your question. Unfortunately, as my previous comment and David’s answer explain, your calculation is wrong. You need to think more carefully about what “10% mutation amount” means. In fact the term “mutation amount” is vague and problematic. That’s why we instead speak of “mutation rate”, and this rate refers to a per-base probability.

@KonradRudolph I'm assuming that the genome size is same. We merely vary the proportion of coding and non-coding DNA within the given genome. Is it wrong to assume that the genome size could be same? Regarding 98% please refer to latest sources (ENCODE project) or Wiki. This 98% figure was revised over time as it was discovered that certain non-coding DNA is also 'functional'.

@yathish “Is it wrong to assume that the genome size could be same?” — No, but it is still wrong to assume that the mutation rate depends on that size (or, conversely, on the fraction of noncoding DNA — both assumptions are equivalent; reread my previous comment and think about what 10% mutation rate actually means). And, again, you do not distinguish correctly between “coding” and “functional”. The “98% coding” figure has not been substantially revised in the last 15 years, and ENCODE had nothing to say on this figure.

Let us continue this discussion in chat.

Whether or not species with less non-coding DNA evolve faster, the assumption that this could be explained by their genomes being more susceptible to mutation would seem to me to be based on a false premise.
Let us examine the logic of the assumption by making an analogy to drawing of tickets from an urn in a lottery. If you buy one ticket (coding region), and only one ticket is drawn (there is a single mutation) from the urn (the whole genome), the probability of winning (your gene suffering a mutation) decreases as the number of tickets (the size of the genome) increases.
So the question is “does mutation follow this model?”, i.e. are the number of mutations in a genome independent of its size? To answer this, let us look at two examples of known mechanism of mutation.

Misreading during DNA replication: Here (and in other types of misreading) the error frequency is, quite logically, related to the number of bases replicated i.e. it has a specific (if very low) value of n per 1,000,000 bases — not n per genome.
UV radiation: Here the source of the radiation is external and its flux will be proportional to the area it strikes — hence the larger the target area the more interactions with thymine causing dimerization. Although our linear-centric view of DNA tends to ignore its area, the larger the genome, the larger the target. The only way I can see the non-coding DNA buffering the coding DNA from radiation is if it somehow formed a protective shell around the latter. I know of no evidence that this is so.

It seems my question is unclear. May I request you to read a portion I added in the question as an edit? Assuming mutation is harmful on an average, my argument is that having more non-coding DNA in a way shields the coding DNA from mutation. There doesn't need to be physical protection - I'm only talking in terms of probabilities (averages). Note that I've also assumed the size of genomes under comparison to be same.

@yathish — Again, I question your assumptions. I do not think it valid to compare two genomes of equal size, or if you do you are asking a different question. You clearly talk about increasing the amount of non-coding DNA, not the coding DNA. For this you have to compare two sets of coding genes of equal size, but associated with different amount of non-coding DNA — something like Drosophila, with a genome with a similar number of genes (ca. 18,000) but more non-coding DNA. And for that my argument holds.

I was definitely assuming the size of genome to be immaterial. I wanted to highlight the PROPORTION of non-functional DNA and not the amount of it. Would my argument hold for species of comparable genome sizes but with widely varying proportions of coding to non-coding DNA?


text:
Rationale behind Most Recent Common Ancestor (MRCA)?
My main question is this -
I heard Richard Dawkins say in a video that after 1000s of years, any given individual alive today will be either an ancestor to ALL of the humans (in that future time) or none of them. What is the rationale behind this?
I'm unable to find the link to that video. I'll keep searching and add it once I find it.
But my fundamental question is perhaps this - is it necessary that a given species must have at least one common ancestor? I understand that there are multiple common ancestors to humans, the most recent one being MCRA. But could it have been otherwise? I think there's some underlying logic that I'm missing.
I'd appreciate it if someone could answer in a non-technical manner since I know very little about genetics and how all this works.
Update:
Consider the following example. Here's there's heavy inbreeding and as you can see no matter how many generations pass, the population are never going to share a common ancestor from current generation or later. (They could still have a common ancestor from before). But this case violates Dawkins' statement.

But this is an unrealistic example with no mixing and cross breeding. Let's consider another example as shown below. I want to see how the individual A from current generation can be related to all the population in future. As shown in the diagram, although A is related to everyone in some future generation, he is not a common ancestor to all of them. The actual common ancestor belongs to some earlier generation.

For any given no. of generations, theoretically, I could conceive similar lineages by which someone from current generation need not necessarily be a common ancestor to all of the future population (or none). So I don't understand how Dawkins' statement is inevitable.

Your examples don't have sexual reproduction: everyone has just 1 parent. Why?

@BryanKrause first example does show two parents each. Avoided that in second example because the diagram was getting cluttered. The point of my examples is still conveyed correctly, I hope.

It isn't at all, because you are missing that for each prior generation, the number of ancestors approximately doubles. This is only not true in your extreme example of inbreeding.

@BryanKrause that's a good point. So the exponential increase in number of ancestors makes it extremely likely for the case of having a common ancestor. But it still doesn't prove that there has to be a common ancestor.

Actually it does. Try drawing it out.

@BryanKrause I feel like the argument is turning silly. You agree that it fails in my extreme example of inbreeding. All I have to do is retain some of the columns and cross-breed the rest. That will be another example where it fails. If the claim is that everyone after n generations MUST be related, then it must be provable. The burden of proof lies with you even if I'm unable to produce counter examples (which in this case I'm anyway able to provide). What am I missing?

The obvious assumption is that there is no complete isolation. You are missing from Dawkins claim the very very long time scale. If you go back 100 generations, you have 2^100 = 1.3 x 10^30 ancestors. Of course many will be repeats (they have to be) but the chance of anyone both a) having living ancestors, and b) not being your ancestor goes down dramatically with each subsequent generation. If you aren't willing to draw it out to test your thinking then it's not worth my time to convince you. The existing answer from Pelinore already explains this.

Let us continue this discussion in chat.

is it necessary that a given species must have at least one common ancestor?

You could imagine a species divided into groups, each group having a single common ancestor.  In that case, you might ask, do the common ancestors themselves have a common ancestor, somewhere further back? Our current hypothesis is that, if you go back far enough you can find a creature that was the common ancestor of any arbitrary group of individuals.
The alternative hypothesis is that life evolved independently several times, and there were originally more than one 'tree of life', and that these independent instances of life somehow evolved in parallel, maintaining compatibility with each other, enough so that there could be cross-breeding between the two trees at a later date.  In that way it might be possible that some species may not have a single common ancestor.  This seems so unlikely to be true though that it it not generally even considered, for current species.
The common ancestor of all humans might not necessarily look exactly like a human (Homo sapiens) though, it may have existed at a time before Homo sapiens evolved, because it is possible that branches on the tree of life can diverge a little and then cross again, as human and neanderthal branches did.
The wikipedia page on the human MRCA (https://en.wikipedia.org/wiki/Most_recent_common_ancestor) says the time since the MRCA is unknown, but has been estimated between 100,000 to 200,000 years ago.
 This is around the same time Homo sapiens first appeared in the fossil record, that we have found so far.

any giving individual alive today will be either an ancestor to ALL of the humans (in that future time) or none of them. What is the rationale behind this?

It's a simple mathematical observation nothing more than that.
One that doesn't actually require doing any math to understand.
Take a few billion people, let them mix & breed freely within the confines of a limited environment (the world) & eventually (after enough generations) every single one of the current population will be be related & therefore descended from every single one of the original population that have any surviving descendants.

Those whose line doesn't die out will inevitably be an ancestor of every living person at a future generation, eventually.
Those who die with no offspring or have last-descendants do it for them, have no descendants.

It's just a simple statement of something that's obvious when you think on it.

Why is it necessary that after enough generations everyone will be related? Is it an assumption based on enough cross breeding?

@yathish It's not "necessary", it is inevitable.

but why is it inevitable? For example, if two populations of humans are separated in two different islands, it won't hold true. I feel like I'm missing something very obvious.

@yathish: But the populations on those islands must have come from some common source (if you look back far enough), e.g. the populations of say Hawai'i, Tahiti, and New Zealand prior to European contact.  Or the population of North America, effectively isolated from other humans for ~10,000 years.

@yathish Your not thinking in big enough numbers when it comes to generations & years, if people got there once they can get there again so in the time scale of hundreds of thousands of years & more your islands aren't isolated, at all ~ besides that, where did these two populations come from & how are they the same specie if they didn't ever share a common ancestor?

@Pelinore: The islands could possibly remain isolated for the population to diverge enough that the inhabitants could be called a different species.  For example, Homo Floresiensis: https://en.wikipedia.org/wiki/Homo_floresiensis  But they still have common ancestors who were humans or pre-humans.

@jamesqf "besides that, where did these two populations come from?" think about it.. also (from OP) "is it necessary that a given species" so, if they're not the same species you've then gone & wandered outside the parameters of the question haven't you.

I don't mean to be pedantic, but distinguishing near certainty and absolute certainty is an important part of my question. I'm trying to think of this visually and it's still not obvious to me. I've added a couple of diagrams to elucidate my confusion in the question. Kindly check it once. The usage of terms like enough cross breeding and eventually by you suggests to me that it's extremely highly likely but need not necessarily be true with absolute certainty. I feel like my thought process is misdirected.. I appreciate your help.

@yathish That is very much the point, statistically speaking it is absolutely certain, that you can't see it is problematic for me when it comes to answering your question because to me it seems almost like being asked why 2+2=4 in at least the sense that I'm having difficulty formulating an explanation of why beyond "because it is" now, not that I'm trying to be derogatory the inability to explain may be a fault on my side.

^ Perhaps because I can (as you say) "visualize it", so to me it seems obvious.

Oh blimey! But what about the counter examples I provided in the question? I can scale them up to howsoever many generations as you like and disprove the statement.. Also, I'm not sure statistically speaking and absolute certainty go together.

Statistical certainty may have been a poor (pedantically speaking) choice of words then :) I'll come back to this & give it another go later, I'll need to set my eyes on it when I'm fresh & see if I can't come at it from a different angle, maybe not today though, bit groggy right now (fell asleep in the chair & didn't get enough sleep last night) o7


text:
Hoverfly Identification Wing Resting Position
I've found an interesting insect which I believe to be a hoverfly:

length: approximately 1/2 inch.
However when compared to the Wikipedia poster on Syrphidae or the InsectIdentification.org Hoverfly entry (as well as the flower fly entries) the resting state of the wings differ. In my photographs the wings are resting above the back while hoverflies appear to keep their wings extended.
I know wing position is important in identification, i.e. dragonfly vs damselfly, moth vs butterfly. Does it matter with true flies?

Your geographic location would help in going deeper (if it's any consolation, you do have the family right).  A better size indicator (say, a distance shot) would also help.  If you're in North America, the site bugguide.net should be your next stop; if in Europe, diptera.info is a good place to start (either way, given how many species of hoverflies exist, you will be spoiled for choice).

You're right, that family is large. Though I'm not interested in tracking down the exact species. I want to know if the wing resting position can be a species indicator, or just a matter of the insect's personal preference and time of day of particular photograph. Most of the Syrphidae samples from bugguide.net are shown with open wings, with some exception.

This is indeed a hoverfly. Most if not all hoverflies fold their wings in this position when not flying.

@RHA: that's exactly the answer I'm looking for. If you could write a brief summary detailing certain unimportant aspects of insect identification for two or three common families of insects - i.e. wing resting position, antenna resting position - I think it would be a very useful acceptable answer.


text:
ID please SE Brazil

Noted higher in the hills of the Atlantic rainforest in SE Brazil during October 2016

Looks to me like a Lonomia obliqua, from South America, particularly southern Brazil.

(Coursety of inaturalist.org)

(Courtesy of televisionsworld.com)
The same hairy green projections, the same red bottomed legs, pointed at the front of the caterpillar.  You also notice on the second photo that it has those two black projections on the back.
The one thing that makes me just a hair uncertain is the colouration of the skin in your photo - it looks whiter.  But then again, your photo is much more saturated than any others I found, so it make be an illusion, or even just a genetic variance.

The similarity is definitly there - maybe a different moth of the same family ? The bright yellow head and orange dots on the flank were very obvious


text:
Low migration rate in Papadopoulou et al. (2008)
In the paper "Speciation and DNA barcodes: testing the effects of dispersal on the formation of discrete sequence clusters" by Papadopoulou et al. (2008), is there an explanation as to why the authors simulated very low migration rates ($m$ between $10^{-8}-5\times 10^{-5}$)? The population size was 160,000, which produces $Nm$ between 0.0001-0.5. This is much less that a single migrant per generation.
Any insight would be most appreciated.

After a quick look-up, they don't seem to comment much on this choice of parameter unfortunately. Here are my quick thoughts.
They are dealing with quasi isolated species. They explored a range of values and I would like to assume that made sure that more extreme values won't yield to drastically different results.
These simulations can be pretty computationally intensive, it is possible that they considered $Nm$ to be the important statistic but they would assume that the results could scale up and down for different $N$ and $m$ values. In fact, they almost systematically refer to their migration rate as $Nm$.


text:
Simulating DNA sequences in R with a given value of $\theta = 4N_{e}\mu$
This might not be the most appropriate site to be asking such a question, but perhaps someone has a solution.
My question is: is there an R package or function for simulation of DNA sequences of a given basepair length generated according to a prespecified value of the population mutation rate $\theta = 4N_{e}\mu$, where $N_{e}$ is the effective population size and $\mu$ is the per-generation mutation rate
I have real sequence data from GenBank, but I would also like to simulate some random DNA sequences according to a coalescent process.
Essentially the function would output the generated aligned DNA sequences as a FASTA file.
I have been rather unsuccessful in tracking down a suitable package, as most only output generated phylogenies.

@Remi.b Thanks. I'll do some sleuthing. If I don't come across anything, I will code it myself, or use SimBit..

There are a number of tools but I don't know any that comes with an R library. They are usually all called from the command line. I don't either of any that produce FASTA file. SimBit (my own software) can produce vcf files which can easily be converted into FASTA with PGDspider.
However, if your simulations are so easy, you might not need these individual-based softwares. Just write the code yourself. It might only be take a few tens of lines. Here is a simple example
freq = 0.1 # initial frequency
N = 1000   # Constant population size
mu = 1e-7  # mutation rate

for (generation in 1:nbGenerations)
{
   # Drift
   freq = rbinom(1,N,freq) / N

   # Mutations
   oneWayMutations   = rbinom(1,N*freq,mu) / N
   otherWayMutations = rbinom(1,N*(1-freq),mu) / N
   freq = freq - oneWayMutations + otherWayMutations
}

If you need something more complex (such as several loci), then you should probably use one of the existing individual-based software. See the post Sequence evolution simulation tool

What is the 'freq' variable in your example?

'freq' is the frequency of a one allele at a single bi-allelic locus. If you want several linked loci, then you'll have to use some individual based software, such as SimBit, Nemo or SFS_code for examples. See edit in the post.

Thanks! I just came across @EliKorvigo 's post, as it was recently commented on.


text:
Why can't nucleotides when mixed together form an RNA on their own?
Why nucleotides when mixed together in the absence of a template
RNA molecule do not readily link up into a chain? We know that the bond between nucleotides side by side is stronger than the hydrogen bond between the two RNA strands, a negative and a positive one. Shouldn't then the nucleotides form chains of RNA more readily by just attaching to each other than making a dimeric RNA through a lock and key type latching?
The book that caused this question is "What Is Life?" by A. Pross (p.68), who unfortunately doesn't provide an answer.

Before asking questions about the chemistry of biological reactions you should learn some basic chemistry. This online resource may help. The role of enzymes in relation to the thermodynamics of reactions is also key.

RNA nucleotides will form chains spontaneously, having a catalyst however makes it happen faster.

The dNTPs don't just come together. They require a polymerase to break off 2 phosphates and bond the hydroxyl group to the remaining phosphate. To take a nucleotide triphosphate and add it to a growing chain of nucleic acid, the polymerase checks the fidelity of the hydrogen bonds that precede the new bond. dNTPs provide the energy for this reaction, but the enzymes require a double stranded molecule to copy. In other words, they can copy double stranded nucleic acid, but not form it from scratch.

Thanks for your answer! I only would like to clarify if the same laws apply to the self-replicating RNA (autocatalytic), with no enzymes, since the book is talking about prebiotic time.


text:
If wolves (or foxes) are fitter than rabbits, why rabbits have not become extinct?
I do not pretend to "demolish" the Darwinian theory of biological evolution and the "survival of the fittest", that's far from my intention.
I have this doubt because of the fact that humanity, as Homo sapiens sapiens, extinguished the Homo sapiens neanderthalensis because we were fitter to survive.
Please consider this question as if the humanity hadn't appeared yet (because we have domesticated rabbits).
Thanks in advance.
Edit: I have assumed that wolves and rabbits (or hares, maybe) live in the same ecosystem.

It doesn't make much sense to talk about 'the fitness of foxes' as an absolute thing, because 'fitness' is not a fixed quantity - it changes depending on environmental conditions. So the crux of the answer is 'because ecology': an environment with fewer rabbits is an environment where it is harder to make a living as a fox.

Do you agree with me in saying that no one can talk about survival without talking about a catastrophe? Like a war, or maybe an ice age.

Er. No. I talk about survival all the time, as part of day-to-day biology. Like: "the rangers have started putting out supplementary food, so the chick survival rate for [species] at [site] has increased by 15%". No catastrophe is necessary.

Neanderthals were already on the verge of extinction when they met sapiens in Europe.

Simple: wolves and foxes are not fitter than rabbits. If they were, rabbits would be extinct.
This question is like asking "If Gary Kasparov is better than Michael Jordan, why hasn't he won a chess championship against him?"
And the answers are the same:
- "what do you mean, 'better'? Better how? At what?"
- "either way, they've never played in a chess championship against each other, so..."
"Fitter" in evolutionary theory means "better at something"; in general it will be "better at surviving", but better at surviving under what circumstances? There isn't a single "fit" or "fitter". Maybe you thought that wolves are better at surviving than rabbits because wolves kill rabbits and not vice-versa, but I could as easily argue that rabbits are better at surviving than wolves because rabbits would survive fine without wolves, but wolves would go extinct without rabbits (not completely true because they have other prey, but you get the idea). The truth is, as far as we can tell wolves and rabbits are equally good at surviving because both have survived.
So you can only talk about fitness if you focus on one specific circumstance to be fit in. But then there is the other implied idea in your question, which is that fitter species drive less-fit ones to extinction. This is true only if the species are in competition. Two species (or individuals, or anything) are in competition when if one species does badly, the other will do well as a result, and vice-versa. For example, maybe they eat the same food, and there is only so much to go around, so every additional bit of food A gets is less food for B, and vice-versa. In that case it is clear that one species being better at surviving than another is bad for the other species, and can (and, according to theory, will) drive it to extinction. Like fitness however two species can be in competition in some ways but not others. For example, two species might compete for food, but have a mutually-beneficial relationship with respect  to predators, where if there is more of A the predators will go for them which is good for B, and vice-versa.
Wolves and rabbits are clearly not competitors: things that lead to more wolves will indeed lead to fewer rabbits, but things that lead to more rabbits will also lead to more wolves. As such, even if one were measurably fitter than the other by some metric, it would not necessarily lead the other to extinction. For example rabbits being better against the cold than wolves could promote the existence of wolves in cold places, because a lot of them might freeze but the abundance of food might make it worth it.
This does involve an interesting ecological paradox, which is that according to theoretical models, if you have X species in perfect competition, all but one will eventually go extinct. There is a lot of research in how and why our world's massive biodiversity exists despite this. A big factor is that as I have pointed out, perfect competition is extremely rare in nature. Most species aren't competitors at all, and those that do compete usually don't compete on everything, everywhere and at all times. But when they do or close enough, yes, one should drive the other to extinction. Whether this is why the Neanderthals went extinct is another question

It's also relevant to look at predator-prey cycles, like the Canadian lynx-rabbit cycle.  If your predator species is so "fit" that it eats all its single prey species, it starves.  So without predators, the prey species increases its numbers until it consumes all its food supply, whereupon it starves, too.  So neither species is fit in an evolutionary sense.


text:
What is this thing found in my saliva?
Found in my saliva
(Optical microscope 40x)

Just to make sure, since you have a lot of external objects in the field of view: are you sure that it's part of the sample and not some dirt on the microscope?

I don't think so, we cleaned everything before, and it seems to have a nucleus


text:
Are the bacteria doing the same photosynthesis as plants do?
I mean Plants during photosynthesis produce  oxygen but Do bacteria also produce oxygen during photosynthesis or produce  other gases?
If yes , how do these bacteria process photosynthesis by producing other gases?

There are bacteria that do anoxygenic photosynthesis but, afaik, cyanobacteria (which produce oxygen) are the most important phototrophic bacteria on modern Earth. I suggest you do a bit of reading on Wikipedia.

Photosynthesis is always about using solar energy to oxidize a mineral molecule and reduce an organic molecule, which becomes an energy source for the photosynthetic cell.
Bacteria and plants have different types of photoreceptors. It is not always the same chlorophyll, maybe even no chlorophyll at all ! The different colours in algae come from the different pigments they are using to do photosynthesis.
Plant cells carry out photosynthesis in chloroplasts, which are organites, whereas bacteria carry it out in their plasmic membranes.
Plants do aerobic photosynthesis, which means they reduce dioxygen into water. Some bacteria do anoxic photosynthesis, which means they can reduce hydrogen sulfide into sulfur.


text:
Can the theory of natural selection distinguish between two correlated phenotypic traits?
Consider the following two situations:

A species X has trait $T_1$ that is gradually selected for by some characteristic $E_1$ in some ecological niche but it turns out that the genes for $T_1$ also "turn on" genes for trait $T_2$ so that eventually species X with trait $T_1$ also have $T_2$. Then it turns out that $T_2$ is evolutionarily advantageous i.e it does help in increasing fitness because of some characteristic $E_2$ in that same ecological niche.
A species X has $T_1$ that is selected for by some characteristic $E_1$ in some ecological niche, this ecological niche also has characteristic $E_2$ that separately selects for $T_2$.

Both of these cases have as the end product $T_1$ and $T_2$ being advantageous for survival but in one case $T_2$ was selected for and in the other it's usefulness was accidental. What in the theory of natural selection distinguishes these two cases? To put things more bluntly, you are an evolutionary biologist and you are telling the standard story that corresponds to situation 2, how do you know (from the theory of natural selection) that we can discount situation 1?
I did a research project for my undergraduate research where I simulated mutations of cells in a petri dish and I know that mathematically these two cases can be disentangled because they lead to two different cluster size distributions with different scaling laws. As a physicist I know what to do but does a evolutionary biologist using theory of natural selection know what to do.
Update: The point is that in case 1 $E_1$ and $E_2$ could act at different times so that only $T_1$ is responsible for survival and $E_2$ while acting $T_2$ was completely useless for it's survival i.e other species disappeared not because they didn't have $T_2$ but because they didn't have $T_1$. Then a naive biologist could tell separate evolutionary stories assuming that $T_1$ and $T_2$ were selected for separately because when the biologist is observing the situation both $E_1$ and $E_2$ are present and $T_1$ and $T_2$ are present.  In other words, he or she would assume case 2 occured. In this case, random mutations and natural selection as told in science classes is completely useless because of $\textit{dynamics}$ in the environment and $\textit{correlations}$ that prevent mutations from being just random.
Why does this bother me? Well, because I hear evolutionary accounts that span hundreds of millions of years and it would seem simply applying the Darwinian story naively could make wrong predictions all over the place. I haven't seen people worry about this as they give evolutionary accounts for everything. From sexual behaviors to marketing.

I am not sure I understand the question. How is your question different from a classical correlation vs causation question in statistics?

Note by the way that you seem to confound the concepts of "environment" with the concept of "ecological niche". You might want to have a look at their definitions.

@Remi.b that may well be true that in my question I confound the two, but looking at the definition of "ecological niche" I think my question still runs through.

@Remi.b I can rephrase the question in terms of correlation vs causation. The simple story is that traits that correlate with survival or fitness are responsible for survival i.e they are selected for. But in case $1$ $T_2$ is correlated with survival or fitness a posteriori but is in fact not selected for.

So is your question "Are biologists aware of the causation vs correlation problem or are they noobs in statistics?" :)

@Remi.b they could be aware of it but ignore it. But I am really interested in people who apply evolutionary reasoning like evolutionary psychologists.

I am not sure why you talk about your interest in evolutionary psychologist. Note that evolutionary psychology is for the moment an extremely theoretical field with very little empirical testing.

mutations are not truly random nothing in the real world is, they are statistically random enough.

Are biologists aware of the causation vs correlation problem or are they noobs in statistics?

Evolutionary biologists tend to be pretty good statisticians. For historical consideration, Pearson is the father of the concept of correlation and was a biostatistician and Fisher is (one of) the father of evolutionary genetics and is also a famous statistician (invented the Fisher's exact test, t.test and Anova). Many of the modern developments in modern statistics were brought about by geneticists (incl. developments in HMM, ABC, FDR, etc...).
So, yes we are aware of the causation vs correlation problem.

In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years[?]

Just like in any other causation vs correlation problem, no it is not easy to disentangle the two. If the specific hypothesis put under testing is subject to experimental manipulation, then yes, it is often feasible to disentangle the two. Otherwise, in a purely observational study, one can logically reason and argue for one rather than another causality relationship but in essence, you cannot know in a purely observational study whether a correlation is representing a direct causation.
The follow-up question might then be

Is experimental manipulation feasible in evolutionary biology?

The answer is yes. Not for all questions though.
First there are evolution experiments. An evolution experiment is just like what is sounds like. You put a population in a controlled environment and let it evolve. Repeat the process many time to have a decent sample size. There are also many question of interest to evolutionary biology that can be studied through experimental manipulation (and not only observatory studies) that do not require an evolution experiment.
You seem to be particularly interested in the reconstruction of past evolutionary history of a lineage (evolution biology is much more than a 'historic' reconstruction of life on earth), I would like to highlight that in purely observation studies and in experimental studies not involving evolution experiments, there are plenty of methods to reconstruct past events. Consider for example the loss of genetic diversity at linked variants (selective sweep) caused by positive selection. If two traits are correlated through time (which is very hard to figure out in absence of good fossil records) or correlated over several species (consider having a look at phylogenetic contrasts methods and more modern version of inference of selection over phylogenies), then if selection occurred in a single of the two traits, you should expect to see a differential loss of heterozygosity among the genetic markers explaining ariance for one trait and for the other.

I am sure biologists are aware of the generic problem of causation vs correlation problem any one in the sciences is. You have merely diluted the force of my question to simply being about whether biologists have opened up books on statistics, I know they have. But that is not my question. In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years. How would one do that generically in the theory of natural selection.

First selection does not occur at the species level. Scientist don't talk about a species going extinct due to the lack of a gene.
Second you seem to be confusing what evolution can "tell" with what scientists can tell. The spread of a gene is a statistical correlation occurrence, evolution cannot tell what gene causes a phenotype, genomes are selected for whole hog so to speak, (there are some rare exceptions). It is only through recombination that gene can be segregated, in your example it could be determined that T2 is only active when combined with T1 such situations are well known. indeed this is one of the hypothesis as to why various forms of sex/transfer evolved in the first place, to allow the decoupling and loss of disadvantageous genes.
Third entangled linkage and selective pressures are quite common many traits have multiple effects including counter effects and effects contingent on other genes. What you are describing is a regulatory or linked genes vs  independent genes. This is the norm for genetics and is extensively studied and is the reason genetics is not as easy as laymen think it is.Very few genes have only a single selective effect and control genes are quite common.
There is even investigation in the fact that un/successful genes are physically linked by and can effect the survival of other genes in the population just by being physically close to anther gene on the genome and thus likely to be passed on together even with recombination. Entire branches of genetics exist to study linkage.
In your own example there is no accidental usefulness, one is simply a linked or regulatory trait while in the other both are independent.  So to answer your question yes evolutionary biologist are quite aware of the issue.
What is told in a classroom, especially a basic classroom is a simplified more abstract version of what is known,  in your own field nobody is going to start teaching physics with quantum dynamics, or the relativistic effects on a normal trains mass, you start with simpler and somewhat outdated/incomplete equations until the students can grasp the basic concepts. You are not going to talk about Neutron diffraction with students before they understand what friction and mass are. In a description of the evolution of the avian respiratory system or the function of the human facial recognition system, linkage of individual genes is irrelevant, what is being discussed the dis/advantage or function of the phenotype NOT the genotype that brings them about.

I am not confusing what biologists can tell with what evolution can tell. In fact this is precisely why I asked the question, the point is when a biologists decides between the two cases does he or she use the theory of natural selection i.e random mutations and survival of the fittest or do they claim to use theory of natural selection but what is really doing the explanation is something else. From the answers it seems what is really doing the explanation is not theory of natural selection per se .

As to your physics analogy, no physics teacher would claim frictionless incline planes and massless pulleys describe the real world; they are presented as highly idealized simple models. On the other hand, the theory of natural selection is not described in school as a simplified abstract model and it seems to me there are professions that do not treat it as an simplified abstract model i.e evolutionary psychology, hence my confusion. Anyways I think I am getting the idea

no but they use them in class problems all the time, I'm just trying to explain why your teacher or a paper may not have described in the detail you want. Or to put it another way if I am describing a pulley system used to lift trains the gravitational pull the pulley exerts on the train is not worth worrying about. Everything you are taught in school is simplified.

As for what biologists do without an example I can't comment on what you think is happening, It is far too generalized and unclear. If you want to make another question and give an example and ask what is being talked about that's a great use for this site. any number of things could be going on everything from a bad source to  confusing phenotype with genotype to mistranslation, ect.

For examples Gad Saad a youtube personality and evolutionary biologist claims to study consumerism from an evolutionary perspective or people who speculate about the evolutionary origin of language. It seems to me that in these two examples the back bone of explanation is the simplified abstract model.

Unless the selective pressure applied by $E_1$ and $E_2$ are applied at different times, it seems like the two scenarios you described are equivalent. In other words, if in both ecological niches, $E_1$ and $E_2$ were present from the start, and both $T_1$ and $T_2$ were present from the start, then absent other factors, the process and result are the same.
However, if you are saying that in the first scenario, $E_2$ was applied only after $E_1$ was selected for, then it is likely that $T_2$ was a genetic hitchhiker, i.e. it didn't provide any advantage before, but the niche has changed and now it provides an advantage. If this is what you're talking about, then you want to look into the concept of genetic drift. Basically, genetic drift is the random mutation of alleles. Genetic drift can lead to speciation if groups of the same species are separated by some sort of barrier to reproduction.
One way to determine if a gene is being actively selected for is to calculate the $K_a/K_s$ ratio which compares the rates of non-synonymous and synonymous substitutions, respectively.

In case 1, $T_2$ only appeared because a mutation caused $T_1$ so that $T_2$ is a hitchhicker and was not selected  for and so $E_2$ was applied after $E_1$. A naive post hoc evolutionary story would simply observe that $T_2$ is advantageous and so was selected for but this would be wrong. I know these can be disentangled mathematically but these sorts of stories are told about evolutionary processes that happened over billion of years where we might not have access to data that could disentangle these two situations. This is my worry. Has this been thought about?

"A naive post hoc evolutionary story would simply observe that T2 is advantageous and so was selected for but this would be wrong."
This wouldn't necessarily be wrong. T2 was in fact selected for, just at a later time than T1. So it sounds almost like you're after the relative time of emergence/selection of 2 traits? In that case, you could maybe build separate phylogenies for each gene/set of genes, and then compare branch times, but other than that, I'm not sure.

Yes relative time of emergence is everything!  Because in the first case it is possible for species $X$ to survive only because of $T_1$ while other species disappear. $T_2$ would emerge later on but it would serve no purpose in the competition because $E_2$ emerged in the environment and acted on $X$ much later on. A naive biologist would simply conclude that $T_2$ was selected for because of $E_2$ but that would be wrong. It would seem random mutations and natural selection is too simplistic. There can be correlations in mutations and dynamics in the environment

Ok, I understand now! It seems to me that there are some methods that exist to determine the relative age of certain segments of a genome based on how many/what type of mutations have been accumulated, but I am not familiar with these methods. Additionally, you may be able to tease out relative emergence by looking for other organisms that have $T_1$ but not $T_2$ (or vis versa), indicating that certain subsets of the population were exposed to $E_2$ while others were not. But this is getting beyond my expertise.
At least I finally figured out the proper mathematics formatting!


text:
Immune System - B-cell receptors
How do the B-cells, which are a part of our body, develop antibodies against antigens of the outside world (outside of our body), which they don't even know about? Is it just a random match?

This is an excellent question. You are on the right track with the random match idea. B-cells (as a group) develop receptors that bind every possible antigen and then get rid of the receptors that match antigens in our body. Some textbooks are a little more careful in their language, though, and say almost every possible antigen.
See Alberts

The preimmune repertoire is apparently large enough to ensure that there will be an antigen-binding site to fit almost any potential antigenic determinant

I'd note, though, that we've yet to identify an antigen that can't be bound by an antibody.
The process by which an individual's set of B-cells is able to generate all these different B-cell receptors was discovered by Susumu Tonegawa. He was given a Nobel prize in physiology or medicine for the discovery in 1987. You can read about it at nobelprize.org.
In broad strokes, each B cell has multiple copies of different types of gene segments that make up the B cell receptor. When the B-cell develops, it selects one of each kind of segment at random and pastes them together. At the level of the human organism, this generates an awful lot of diversity, but not quite enough to produce receptors that bind every possible antigen. The additional diversity is produced by adding or deleting additional DNA bases at random.
This produces a new problem, though, because with B-cells that have receptors that would bind every possible antigen, we would end up attacking ourself. The details here are the answer to a new question, but the basic answer is that B-cells that would recognize self are selected against, leaving us with a complement of B-cells that have receptors that bind literally every possible antigen that is not self.
Lauren Sompayrac has an excellent introductory book on the immune system that makes these very difficult concepts much more approachable. It's called How the Immune System Works, and I highly recommend it.
Here's a diagram from that book, showing the random selection and pasting together involved in one of the parts of an antibody (the heavy chain):

So, can there be B-cells that are identical to each other during the development of B-cells ? What can be the number of a particular B-cell before we get attacked with pathogens ?

@ShawnDypx Sompayrac estimates that, with 3 billion circulating B-cells, in the pre-immune state you have about 30 B-cells with the same antibody (at that point, a B-cell receptor, or BCR). The way the B-cell finds its antigen, and the clone, or set of B-cells with the same BCR, expands and produces a response is fascinating. It takes about 7 days. Again, I highly recommend Sompayrac's book.

Oh I didn't know that. I'm new here. Thanks for letting me know. I will do it.