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possibly unusual spider behavior?
In Cambridge UK there is this spider:

I know not what species but it is common - I think they look good.
But look at this behavior. What are they doing? I thought malting but do spiders do that? Why would they congregate like this?

Those appear to be Daddy Longleg spiders, and they are known for forming spider clusters, which is considered as gregarious behavior. Quoting Wikipedia:

Many species of harvestmen easily tolerate members of their own species, with aggregations of many individuals often found at protected sites near water. These aggregations may number 200 individuals in the Laniatores, and more than 70,000 in certain Eupnoi. Gregarious behavior is likely a strategy against climatic odds, but also against predators, combining the effect of scent secretions, and reducing the probability of any particular individual being eaten.

Thank you, very interesting. After looking it up it appears to be leiobunum rotundum common in the British Isles. It is very hot at the moment in Cambridge and they're under a window maybe some dew forms at night and yes they all appear to move when I came near them to take the photo as suggested in the wikipedia article.


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Larva in cat's water dish
Can anyone help me identify this tiny larva I found in my cat's water dish and tell me how it got there?

It is not likely that identity can be obtained from a larval stage photo only, so you do need to provide more information. Can you provide its size and where you are located? Possibly an insect specialist might have an idea. It is not possible to tell you how it got there.

This is the larva of a moth fly (family Psychodidae: I don't see any legs, there is a well-developed head capsule, and the body segments each have two or three dorsal plates); going further than that requires knowing where you are, and whether or not the Psychodid fauna of that area is well-known as larvae (in practice, this means "forget going deeper" if not located in western Europe).  Larvae of the subfamily Psychodinae (which this is) are aquatic or semiaquatic, which means that a week or so ago an adult laid one or more eggs where you eventually found the larva.

This appears to be the larva of a drain fly (aka moth fly; family Psychodidae).

 Top left is larva; Source: YourWildlife.org; Credit: Matt Bertone
You can use a dichotimous key to help you ID to family. For example, from Bouchard et al. (2004)+:

Body cyclindrical; non-leathery integument...
Head capsule fully visible and completely separated from thorax
Prolegs absent
Thoracic segments not fused or swollen
Abdomen non ending in long respiratory tube
Body segments with 2-3 secondary divisions (annuli); body grey or brown

You can use Arthur Frost's comment to help ID to lower taxonomic levels.
How it got there:
From Orkin:

These pests are particularly likely to be found in bathrooms and kitchens, typically getting into homes through:

Basements
Drains
Windows

 +  Bouchard, R.W., Ferrington, L.C. and Karius, M.L., 2004. Guide to aquatic invertebrates of the Upper Midwest. (Chapoter 13: "Diptera")

source: Stack Exchange

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

sort: votes


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Can you tell me what species of insect this is?
I live in Verona, Italy.
Today I found this black insect and I don't know what species it is. My mom claims it's a kind of mint but I don't think so.

Hello and welcome to Biology.SE! Take the tour to learn about the site and earn your first badge. Also, what do you mean by "mint"? How's that called in Italian?

This looks like a horsefly (family Tabanidae, in Italian "tafani"), maybe Tabanus bromius but I'm not sure. If it's so, be careful: they bite and their bite is painful. Here you can find some quick suggestions about horseflies and their bite.
However, as you live in a city, don't worry too much: as the female horseflies feed on horse and cattle blood, they are normally present in the countryside, so those that you saw are exceptions more than the norm!

The eyes are a bit far apart to be a horsefly; I'm leaning toward Robber Fly (Asilidae) or Stiletto Fly (Therevidae), but can't be sure from the photo (and given how old the question is, I suspect that the model is no longer available for additional photos).

It's obviously not a horsefly

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


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Is this a moth? How do these wings unfold?
I'm having trouble understanding how these wings might work. Are they somehow folded or bent by 90 degrees so that part of the wing is vertical and part is horizontal to be more compact?
If so, how mechanically are they then made quickly more rigid and straight each time it enters flight, which should be fast to avoid being eaten?
Also, I'm guessing this is some kind of moth, but I have no idea. I don't really need an exact species ID, but some classification guidance would be appreciated!
This individual is about 2 cm long, and was seen recently (late July) in Taipei, on a hot, sunny day.

moths don't have 2 wings they have 4 wings, the forewings and hindwings are just being held apart in this image. https://en.wikipedia.org/wiki/External_morphology_of_Lepidoptera

@John oh, that makes quite a bit of sense. Do you think this is in fact a moth? I've just guessed at that.

Yes definitely a moth, although I have no idea what the species is. You could ask for identification as a separate question. just be sure to include the last sentence of the post, where it is found is very helpful.

Okay thanks. I'm still interested in how these wings would OPEN (be deployed) without bumping into each other. There must be some kind of rotation involved; perhaps the ones that are vertical in the photo would rotate forward first?

Not a moth. It is a skipper. Family Hesperiidae. https://davesgarden.com/guides/articles/view/5254

I'd be prepared to guess genus Telicota also known as the Palm Darts.

@bob1 https://www.flickr.com/photos/77600294@N07/17632334189 :-) you're on to something http://dearlep.tw/species.html?namecode=345508, http://butterfliesvietnam.blogspot.com/2015/08/118-telicota-hoara-narrow-branded-palm.html

Uhoh, thanks to @KarlKjer for pointing in the right direction. I just put Hesperiidae into google and found the wikimedia page and browsed through for something similar to your photo, then did a bit more searching based on that.  I think the vietnam link you provided looks like a dead-ringer for your photo. Seems the ID is all around the wing patterns, so very hard to do to species from a couple of photos.

@bob1 well we don't have separate family- or genus-identification tags, so please feel to just write up something; I'm particularly interested in how the wings unfold and I think that part should be similar for many of them.

@uhoh - I'm no entomologist so I don't actually know, but it looks like the vertical wings are the fore-wings and as there are 4 wings (2 fore, 2 hind) each of the 4 is on its own joint (i.e. controlled at least semi-independently). The position is just fore folded up like a moth, hind folded flat

@bob1 I think it's maybe this one? http://dearlep.tw/species.html?namecode=345510 I see what you mean, I was so interested in photographing it that I didn't want to disturb it and make it fly :-)


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Identification of Bug/Insect (with picture)

What is this insect?
I’ve seen a lot of them indoors. The most distinctive characteristic is that single, orange dot in the middle of the back. The picture was taken in Louisiana, USA.

Further information: I’m currently located in Louisiana. I’ve seen a lot of them indoors and they’re quite small if you can see from the comparison to the baking soda box.

What is the approximative size in standard units (not everybody is used to the size of Arm Hammer baking soda box)? Can you get a better picture (a better view of the thorax may help)?

I'll try to get a better picture. They're quite small. This one was by far the largest at probably around a centimeter long. All the others I've seen were a fraction of the size.

It is a cockroach, probably a German cockroach nymph.
Cockroaches are well-known pests. According to the Wikipedia link above, there are about 4600 species of cockroaches, 30 of them are associated with human habitats. Cockroaches are extremely resistant and are able to survive in a wide range of environmental conditions.

@PhysicalFatness pointed out that German cockroach nymphs look very much like your picture and it is likely the species that you've found. Don't be fooled by its name German cockroaches are found all over the world, not only in Germany.

You actually may be right. https://citybugs.tamu.edu/blatella-nymph/ It looks a lot like a German cockroach nymph.


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Why do new atypical antipsychotics like Zyprexa cause TD at lower rates?
When the d2 receptors are blocked for long periods of time they tend to up regulate.  This is what causes tardive dyskinesia.

Why do the newer atypical anti psychotics cause such at a lower rate?  Added tables for clarification of receptors I am referring to.
Zyprexa
D1  35–118  Antagonist
D2  3.00–106    Antagonist
D2L 31–38   Antagonist
D2S 21–52   Antagonist
D3  7.8–91  Antagonist
D4  1.6–50  Antagonist
D4.2    17–102  Antagonist
D4.4    21–60   Antagonist
D5  74–90   Antagonist

Abilify
D1  265–1,170   ND
D2  0.45–3.3    Partial agonist
D2L 0.34–0.74   Partial agonist
D3  0.8–9.7 Partial agonist
D4  44–514  Partial agonist
D5  95–2,590    ND

Haldol(typical antipsychotic)
D1 (silent antagonist) — Unknown efficiency[citation needed]
D5 (silent antagonist) — Unknown efficiency[citation needed]
D2 (inverse agonist) — 1.55 nM
D3 (inverse agonist) — 0.74 nM

If we compare the Haldol to the abilify for example, we see that Haldol is an inverse agonist, which means it turns receptor activity down below baseline. This is more than simply antagonist activity. While abilify is a partial agonist, it can activate the dopamine receptors to some extent, while preventing full activation. Perhaps this is part of the explanation. Haldol really turns down receptor activity, while abilify only partially turns it down. So the cells are less likely to respond to abilify by upregulating dopamine receptor levels. Just a guess, so not an answer.

@user137 that was my guess as well, but then I would assume abilify would have lower TD rates then the other drugs which no literature seems to suggest

So I'm leaving this as comment for now because it isn't well the perfect source.  According to Dr. Peter Breggins book he says they are using lower doses in comparison to the older typical anti psychotics.


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What kind of species is this?
Does anyone know what this is? It is seen in France. It looks like it has eight legs and is about 8-10 cm long.

It is a longhorn beetle, family Cerambycidae. Two of the "eight legs" are antennae. It looks a lot like the one pictured here: https://hiveminer.com/Tags/cerambycidae%2Cfrance


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How do we perceive weight?
How do we perceive weight of our own body or something we are holding?
It might turn out that we don't perceive weight so is it subjective? Is it similar to pain, or something different?

Do you mean the weight of our body? Or the weight if something we hold or carry?

@Marzipanherz hi! Both...

@santimirandarp We sense tension in our muscles and tendons which are affected by the force that is opposing the movement (hence by the weight of the object we are trying to move; here "object" can also refer to one's own body). Would this answer your question?

There are specific nerve cells that sense this tension in the tendon and send the signal up to the brain. Without considering a formal definition of "sense" (I don't think there is a commonly agreed upon definition) but just to my intuitive notion of a "sense", I would most definitely consider this a sense, yes.

@santimirandarp People are voting to close your question as unclear; I thought it was fairly clear to me, but if people want to close a question that I don't think needs to be closed, I feel like the best way to prevent that is to do whatever possible to remove the reason for closure.

This would most likely come under the category of Proprioception - the sense of how our bodies are arranged in the world, and how much effort each part of our body is expending.
From Wikipedia, 'In humans, it is provided by proprioceptors in skeletal striated muscles (muscle spindles) and tendons (Golgi tendon organ) and the fibrous membrane in joint capsules. '.
So our brain receives signals from muscles, tendons and joints, and integrates these into an internal sense of how we are arranged and what our bodies are busy doing.


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What kind of NW USA insect Is this?

What kind of insect is this? I saw it outdoors.

Looks like a nymph of some sort, the wings aren't developed yet.

This is a leafhopper nymph (order Hemiptera, family Cicadellidae); going deeper than that will depend on whether or not the species seen here has been reared.


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About The Selfish Gene Book - How Replicators Molecules forms duplicates?
I was reading The Selfish Gene. In the 2nd chapter - "Replicators" I read:

Think of the replicator as a mold or template. Imagine it as a large molecule consisting of a complex chain of various sorts of building block molecules.
The small building blocks were abundantly available in the soup
  surrounding the replicator. Now suppose that each building block has
  an affinity for its own kind. Then whenever a building block from out
  in the soup lands up next to a part of the replicator for which it has
  an affinity, it will tend to stick there. The building blocks that
attach themselves in this way will be automatically arranged in a
sequence that mimics that of the replicator itself.  It is easy then to
think of them joining up to stable chain just as in the
formation of the original replicator. This process could continue as a
  progressive stacking up, layer upon layer.
This is how crystals are formed. On the other hand, the two chains
  might split apart, in which case we have two replicators, each of
  which can go on to make further copies.

I don't get the part in bold.

If these molecules joins the replicator then the replicator wouldn't change?
To what refers with "The building blocks that attach themselves in this way will be automatically arranged in a sequence mimics that of the replicator itself"? A new sequence? The same sequence?
In the part "It is easy then to think of them joining up to stable chain just as in the formation of the original replicator", what is it joined? replicator with this building block? these building blocks with other building blocks in the soup to form a copy of replicator?
Why you can infer that is how the crystals are formed?

Take into account that I don't have a solid biology background, so it would be great if you can answer it in detail. I really appreciate your help!.

If you have a crystal of table salt, sodium chloride (NaCl), and place it in a saturated solution of NaCl in water, the salt crystal will start grow as the individual Na+ and Cl- ions in solution, settle on the face of the crystal, and enter the solid phase.  In the example, the Cl- building blocks align to the Na+ ions in the crystal (so it is not “like with like”).

So, Ci- ions joins the Na+? And what about the others Na+?

Check out this page: https://en.m.wikipedia.org/wiki/Sodium_chloride. Na+ attracts Cl- AND that means Cl- attracts Na+.

This is how I think about it.  Here is the original large molecule, with each of its 'parts' represented by a letter.  There are a few different kinds of part:
C-A-A-C-T-A-T-A-C-G-A-C

As it drifts around in a 'soup' of parts, new parts stick to it one by one, like for like.  Here it is after two parts stick to it:
C-A-A-C-T-A-T-A-C-G-A-C
  A         T

Here it is after a few more:
C-A-A-C-T-A-T-A-C-G-A-C
C-A   C   A-T   C   A

Eventually, all the parts have got a similar part stuck to them:
C-A-A-C-T-A-T-A-C-G-A-C
C-A-A-C-T-A-T-A-C-G-A-C

Now, if the two halves split, the molecule has replicated itself.

So,

The replicator, in fact, changes, but it can only contains copy of itself?.
The string just mimics the original sequence of replicator?
These building blocks are joining with others to form a copy of the original string?
When the replicator repeats his string multiple times, it converts in a crystal?

Finally, just to confirm, duplicates of the replicator occurs when the replicator halves?

Yes to 1, 2, 3.  For 4 I don't think he meant exactly that the molecule forms a crystal, but it was an analogy - the idea of one layer being built from another layer by joining like to like is similar to a salt crystal being built up.  Finally, yes, when the replicator halves there are now two identical copies when there was only one before.


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Why does protein have 4 calories per gram?
As I understand it, protien that isn't used for building and repairing the body is inefficiently converted into glucose in the liver (at a rate of roughly 3 grams of protein per gram of glucose produced). Glucose has 4 calories per gram. So does that mean that protien would provide 12 calories of energy if the body could convert it at a 1:1 ratio? If not, Where does the 4 calories per gram number come from?

Did you check, if the conversion ratio is indeed 1:1?

It's not 1:1 it's closer to 3:1

Ultimately, the 4 kcal/g numbers come from calorimetry. That is, scientists take a small amount of glucose or protein, put it in a device which burns the material and figures out how much energy is released. Now, this doesn't account for certain factors which complicate matters, such as the fact that humans excrete waste nitrogen as urea and not fully oxidized nitrogen (as is produced in a bomb calorimeter). As such there's some corrections which are applied to account for those differences. When you do the math, you find that carbohydrates and proteins both have about 4 kcal/g energy. As such, most people these days don't actually bother to do the calorimetry to find the energy content, but instead take the content of carbohydrate/protein/fat/etc. and do the calories-per-gram calculation from there.
Now, you're correct that those numbers (from combustion calorimetry) don't match the number you got from the mass balance in gluconeogenesis. Part of the reason for this is that, like most processes, gluconeogenesis isn't 100% efficient. You get some loss as heat due to steps not being 100% reversible. The nutritional content is intended to be more of an estimate of the once-through energy content. (That is, the amount of energy you'll extract if you go directly from the input into a totally metabolized state.)
But perhaps a more important difference is that the mass/energy balance equations for gluconeogenesis from protein can be more complicated than your simple 3:1 analysis suggests -- there's various offshoots of ATP, NADH, etc. generated going from the raw amino acids to glucose. Each of these carries away some energy, and to get a true energy balance. You also need to account for these alternative offshoots of energy.
Which amino acids you're talking about also makes a difference. Alanine is probably the simplest amino acid to feed into gluconeogenesis. It's transformed at a 2:1 molar ratio, which works out to an approximately 1:1 mass ratio (as expected from the calorimetric ratios). Other amino acids like leucine are ketogenic, meaning that they cannot be converted in gluconeogenesis at all (at least in humans). The differences in how different amino acids metabolize can account for the discrepancy. The 3:1 ratio may refer to a "typical" amino acid distribution, which includes a mix of some 1:1 converted amino acids, some which are only partially converted, and some which aren't converted at all.

Super informative. Just to make sure I understood, you're saying that the calories from the expenditure of the product of gluconeogenesis on one gram of  protien is something less than calories from the expenditure of one gram of carbohydrate, and that that number depends on the amino acids in the protien?

@Hal No, what I'm saying is that the "4 kcal/g" figure is for turning protein into energy, not for turning protein into carbohydrate. When you try to turn protein into carbohydrate, there's a number of other considerations to figure in (inefficiency, side products, different behavior of different amino acids). That's why the two values don't match up.

I remember reading somewhere that only 2 out of the ~20 aminoacids were “glucogenic”; that would make the conversion even more inefficient than your answer suggests. In any case, counting calories for weight loss is only meaningful if you keep the macronutrient ratios constant, I guess. Otherwise it’s Apples to Oranges…?


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What are these bugs ?

There are a lot of these little bugs in my backyard. The floor, walls, the bbq island.
Are they hurtful to my dogs ?
What are these ?

Could you please edit your question and add the size of the insects as well as your geographical location and the season(s) when you see those them? That could help to identify them.


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

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

Obesity is an important confounder here as well.

Adding another question.

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

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


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Cultivate snails and maintaining them alive
I found snails in my garden, I want to create a good house for them. I don't really know how to do. Sorry if this is not the good site to ask that but I don't want them to die so I'm trying to be quick.
This is a temporary terrarium for them, is it good ? What do I need to keep them in good health ? What do I need to put in the box ? Is it too small ? I will inquire all about later, I want them first in a safe place.
Thank you :)

I think you might need to put some large leaves and some water.


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What if the luminosity of Sunlight increased by 10%
If the luminosity of sunlight increased by 10%, would people be able to survive outside? Would such brightness of light be very harmful to them, for exemple as much as the Mercury Vapour Lamp deprived of its protection from UV light? I omit the temperature issue, I mean radiation itself, because I'm curious whether man (or bacteria) could survive if he went outside completely naked?

We don't typically like these sorts of speculative questions here, you might be better off at Worldbuilding.SE. That said, there's quite a bit of additional critical thinking you could do here, such as thinking about how the intensity of sunlight changes seasonally and with latitude. Also omitting the "temperature issue" is a pretty big step, but I think I understand that you mean to just talk about UV. Maybe ask on worldbuilding about a planet that got more UV radiation from its star.

I'm voting to close this question as off-topic because it isn't really on topic for Biology; I'd suggest another stack like Worldbuilding.

People from PhysicStackExchange said it would be better to ask this question here. This is the proof that the users in here complain only about the questions etc. No more questions here, promise! Bye bye.

Well it didn't belong on Physics either - they aren't responsible for determining what is on topic at Biology, they were just trying to help you out.

If not Worldbuilding, then Earth Science.  But since Earth orbits close to the inner edge of the "Goldilocks Zone", I would guess that a 10% increase in solar radiation might be enough to kick the planet into a Venus-like runaway greenhouse.  If that doesn't happen, then sure, humans could survive outside on most of the planet, just as they do in tropical areas today.

From the total luminocity at ground level ~$1000\space W/m^2$ only $3-5\%$ consititute of UV-rays, so UV part is $30-50 W/m^2$. Hence increase of luminocity for $10\%$ means that UV part will increase to $3 - 5\space W/m^2$ so it is quite miniscule increase if we are talking about going naked outdoors. E.g.  tanning beds however have different spectra have stronger UV components than current Sun radiation.


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Why there is no vaccine against Human Immunodeficiency Virus (HIV)?
I was informed by my teacher that this retrovirus changes its RNA, so there is not a drug which can recognize the RNA and somehow inactivates it. Are there any other reasons explaining why there isn't a vaccine for the HIV?

That's a good answer, and I'd say it's a duplicate.

On review, I see this question is asking for other reasons, as well as the antigenic variability. I'll undelete my answer.

One of the reasons we don't have an HIV vaccine yet is we've only been trying to make one for a little over 30 years. It can take a long time to develop a vaccine. Beyond that, there are a number of specific challenges.
One of them is that, yes as your teacher said, the virus is highly variable. Specifically, the parts of the viral proteins involved in binding and infecting a host cell are highly variable. There are a number of other challenges. One important and related challenge is that, unlike with many vaccine preventable diseases (e.g., measles), an successful HIV vaccine will have to entirely prevent infection  rather than just control and clear infection without developing disease. Once a reservoir of infected cells is established, the opportunity for clearance is gone. This makes the production and maintenance of high titers of neutralizing antibodies that much more important.
There is a very good review of the challenges and current directions of HIV vaccine development here

"Once a reservoir of infected cells is established, the opportunity for clearance is gone." So with current advances crispr to cut out the established DNA is a good idea? (and not just me being spontanous (as I don't remember if I remember, sorry...):):-) Thank you.

Also, it'd be interesting to hear about a general principle of antibody vaccinaton not being fast enough - with aids, it's the establishment in the genome that has advantage, in case of Covid the equivalent would be infectivity, i.e. if antibodies are too late the person might not get sick ut it will spread the virus for a while, before antibodies get to grips and stop the replication. That's correct?


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Is sweat salty because we eat too much salt?
The Yanomamo Indians eat about 100 times less salt than we do. It has been argued that their salt intake is the natural salt intake for all humans. Obviously, if the salt intake is this low, then there is no room for there to be much salt in the sweat. However, most guidelines will say that if you sweat a lot, you should replenish the salt lost via sweating. But if the natural salt intake is much lower, then we're only losing excess salt via sweat.
So, is our sweat salty only because we eat way too much salt, or are we really losing essential salt via our sweat that we must replenish?

I feel like the sentence "Obviously, if the salt intake is this low, then there is no room for there to be much salt in the sweat." isn't necessarily true. Is there data on Yanomamo sweat saltiness?

@kmm Yanomamo sweat saltiness cannot possibly be high, given their extremely low salt intake and the fact that in the tropic rainforest where they do very strenuous work, they are bound to sweat a lot.

I think the question is Yanomamo sweat saltiness relative to western diet sweat saltiness. Your certainty that Yanomamo differ from western diet needs some justification, I think.

The article you reference is only referring to supplemental use of salt; many foods are naturally salty, and I don't see any evidence there that Yanomamo are actually low on salt, merely that they have adapted to a lower sodium diet. The authors are simply making a case that the contemporary diet is very high in salt.
When animals move water around their bodies, such as by excreting water to sweat, they do it by creating an osmotic gradient by pumping some ions: this is why sweat is salty.

Consolazio, C. F., Matoush, L. O., Nelson, R. A., Harding, R. S., & Canham, J. E. (1963). Excretion of sodium, potassium, magnesium and iron in human sweat and the relation of each to balance and requirements. The Journal of nutrition, 79(4), 407-415.
Schwartz, I. L., & Thaysen, J. H. (1956). Excretion of sodium and potassium in human sweat. The Journal of clinical investigation, 35(1), 114-120.

Human sweat is hypotonic and body fluid sodium content and osmolarity are regulated by the kidney, not the skin. I think these are two key misunderstandings in the OP (and the marketing of sports drinks ).


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Where do I get an annotation file for yeast genome with ENSEMBL ids?
Even the annotation files hosted on  the Ensembl site have systematic names (starting with Y..) instead of ENSEMBL ids (starting with EN..).
I bet there would be a place where I can get an annotation file (GFF3 preferably). Please let me know if you know such.

With a further search for the answer, I realised that unconventionally, ENSEMBL ids for yeast start with Y. That is strange. I guess this is because the yeast annotations are primarily maintained by SGD (yeast genome database) and ENSEMBL just hosts a copy of that.
Also these ids are called Stable Gene IDs.


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Could we back-breed birds into dinosaurs?
Do some species of birds have dinosaur DNA? Seeing as how birds evolved from dinosaurs. I presume this isn't possible as I haven't seen anything else about it on the internet but it's interesting to think about!
If we discovered that some bird species had traces of dinosaur DNA in it, could we selectively breed individuals with dino genes together repeatedly, over thousands of generations perhaps, until we eventually create a baby dinosaur? (Sort of like what the Tauros project is currently doing.)

Welcome to Biology Stack Exchange. You seem to have some misunderstandings  about what a dinosaur is: all birds are dinosaurs. To clarify things, you may be interested in reading:
https://biology.stackexchange.com/questions/35370/if-dinosaurs-could-have-feathers-would-they-still-be-reptiles
or

As I see it, you are thinking that birds (and probably all organisms) have a history log of mutations in their DNA that tell how their DNA looked 100 million years ago. AFAIK this is not so ;)

Do birds descend from dinosaurs?
First, it is confusing to say things like

Birds descend from dinosaurs
Humans descend from monkeys
Mammals descend from vertebrates
Snakes descend from animals

It is much more correct to say

Birds are dinosaurs
Humans are monkeys
Mammals are vertebrates
Snakes are animals

You should definitely have a look at the post If dinosaurs could have feathers, would they still be reptiles?.
Can we resurrect an ancestor from a modern day individual?
By looking at your genome, we can't know the entire genome of your mother. By looking at any modern day genome, you cannot fully know the genome of an ancestor. That being said, we can find DNA in pretty good conditions in fossils (ancient DNA aka. aDNA), so that there are ways to get to a pretty good aproximation of an ancient dinosaur genome without having to even consider the modern day descendents (or rather modern day most closely related lineages).
Can we resurrect an ancestor aDNA?
Bringing an extinct species back to life is called de-exctinction (or resurrection) and, if I am not mistaken, it has never been done. Candidate species for de-exctinction are species that are closely related with extant modern species so that we can use our knowledge of their biology and use the zygote of this extant species and just replace its genome. It is hard to imagine doing so with a species that disappeared in the Jurassic as it is already an important challenge with, more recently extinct species such as the wolly mammoth or the passenger pigeon.

The Pyrenean ibex was briefly resurrected, except it only survived for ten minutes. But thanks for your help!


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Can anyone identify this grey spotted insect -- is it a tree bug species?

This insect was found in Pune, India near a Bauhinia variegata (orchid tree). I think it's a bug. What species is it?

It may  be a nymph of a bigger local bug.

Id say press it, see what it pees, if it isnt deadly and its a bit hot and bitter, then its probably a "CAFARD" NYMPH. cafard is french.dunno eng word sry.

This is one of the last instars of a bug nymph from the genus Erthesina (Family : Pentatomidae). There are two common species, but according to David Rider, the only species in India is  Erthesina acuminata (Source here, also for the image).

You can recognize it from other bug nymphs by its grayish colour and the distinctive orange patterns on its back. Also, the base of the last antennal segment (where it turns from grey to black) should be orange, but we cannot see it on the picture.
These bugs are phytophagous, and quite generalist. They are phloem-feeding insects that feed from leaves, stems and fruits of various species of trees.

Fore more proper classification and identification of Indian bugs, you can look at:

Ahmad, I., Memon, N., & Kamaluddin, S. (2004). A Revision of Hayline Stink Bug Genus Erthesina Spinola (Hemiptera: Pentatomidae: Pentatominae) and Their Clasdistics. Pak. J. Zool, 36, 285Ğ293.
Salini, S., & Viraktamath, C. A. (2015). Genera of Pentatomidae (Hemiptera: Pentatomoidea) from south India—an illustrated key to genera and checklist of species. Zootaxa, 3924(1), 1-76.

This is exactly the caliber answer that we want to see on this site -- great explanation, informative, reputable sources, easy-to-read formatting, clear picture, etc. Great job! Please keep up the good work! :)

Thank you for this very encouraging comment! I'll do my best ;-)


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Grape ivy tendrils
I have a peculiar question. I keep a grape ivy, Cissus alata as a houseplant and I cannot but wonder what exactly makes it decide to grow tendrils? most offshoots have none, only one leaf growing from a node, no matter how many nodes there are and it seems the direction of the growth - vertical, horizontal - is also of no significance. Yet, from time to time, it is like the plant randomly chooses an offshoot that starts to grow quite quickly and grow tendrils. Do you know what processes in the plant cause that?


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What would the RBCs of someone heterozygous for sickle cell anemia look like?
Would half of the RBCs look normal, and the other half sickled?
Or would all of the RBCs have slight deformation/sickling?
Thanks!

The peripheral smear in a patient with sickle cell trait typically appears normal (see Cecil Medicine Ch. 166). Each cell has only 30-40% HbS, and so the polymer that causes the sickling doesn't usually occur.  You can find some examples online of smears with target cells and maybe one sickled cell, but these are the exceptions to the rule. This is one of the reasons a smear is not a good screening tool for sickle cell trait.
To clarify, RBCs in the blood of a patient with sickle cell disease aren't all abnormal either. See this smear from this case published on the NEJM blog:

Again, this is sickle cell disease, not trait, and you see many normal RBCs, even from this patient (honestly, it's not clear whether this is that patient's smear, but this would be typical). In sickle cell trait, the smear would likely be normal (image from webpath tutorial at the university of utah):


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Biological validation of computationally determined gene-gene interaction
How can a computationally determined three-way gene interaction be biologically validated? What kind of assays or tests must be performed using cell/tissue-based and/or mouse models to prove that the three genes may indeed have a joint effect?
Let's say, it is easier to identify and validate gene interactions that involve transcription factors like FOXM1. Consider a three-way gene interaction in Breast cancer - FOXM1-BUB1-CHEK1 - that can be tested for direct interactions via western blot and reporter assays. But such interactions may or may not be interesting - given the fact that transcription factors may be affecting expression levels of other genes. Most computational studies are focussed on identifying gene interactions based on coexpression or co-occurrence. There is literature on computationally identifying AND/OR relationships between interacting genes. I don't have a specific example to provide but, for argument sake, if we did suspect that three genes are interacting in an AND like manner, how do we biologically validate this finding? I'd also appreciate if you may have comments on the usefulness of such findings, particularly, with regard to designing more efficacious combination therapies against a disease".
Thanks

I think that this is an interesting question, and could lead to lots of discussions of strengths and weaknesses of different experimental approaches, etc.  I think, for me, it would be helpful if you could provide either (A.) a specific 3-way interaction—that you have in mind, or (B.) a reference to a scientific publication that reported this type of experimental result (if either os these are possible). Otherwise any potential answers you get might be too general  OR, miss the mark.

Oh also, standard blurb RE: Homework questions would apply here (because this question sure reads like an exam/test), In other words, where is the evidence that you have tried to answer this yourself (and failed)?

Thank you for your feedback, I edited my question to add my "homework".

Hang in there, this answer will grow over time.
Just off the top of my head, I think we could write a small book (or a very long review article) to cover both the depth and the breadth of your question(s).
First, we need to define, and/or clarify, some terms.  The term interaction probably means different things to different authors at different times.  In fact, one author may use this term to mean different things at different times.  So I would like to propose that we make some distinctions.  For example, I would make a distinction between a genetic interaction between two genes (which is typically detected in one of the model organisms, using a genetic test between two loss-of-function alleles) versus a protein-protein interaction (sometimes called a PPI) between the two proteins encoded by those same two genes.  PPIs have been detected classically by co-sedimentation in a sucrose density gradient, or co-immunoprecipitation (co-IP), or by affinity chromatography.  More recently PPIs have been detected by mass spectrometry (MS) (sometimes coupled with affinity chromatography).  PPIs have been inferred by using proxy assays, such as the yeast two hybrid (Y2H) assay.
PPIs can also be detected by surface plasmon resonance (SPR) assays, and there may well be others.
So, when you say gene-gene interactions, what precisely do you mean?

I'm gonna try to cover as many scenarios as I can think of:

Gene interaction ( = co-expression):
This is probably the easiest to validated (e.g. by western blot like you mentioned) but the hardest to interpret. Without further analysis of the genes functions you have no idea what effect their co-occurring activity might have. If the genes are metabolic enzymes or part of a signal cascade it would be a good idea to check both their individual roles in these pathways, but also check for potential synergistic effects. The same is in principal also true for transcription factors, but in that case 'pathways' are often not  equally well understood, instead go for:
Gene interaction ( = on same targets):
In the case of transcription factors (but also e.g. Kinases/Phosphatases) that are co-expressed it might not unreasonable that they also affect the same targets. Here you need to again compare both individual effects (list of up/down regulated genes) with synergistic effects (e.g. geneA prevents normal function of geneB, geneC increases geneB function multifold). For transcription factor analysis you should generally analyse expression on the mRNA level (via qPCR) since the protein level introduces (at least) another layer of regulation.
Protrein interactions:
A good way to prove these experimentally is by using co-IP (immuno-precipitation) experiments: you use an antibody to retain a specific protein and all its (direct) binding partners. Then you show the presence of the partners you're interested in with a western blot.
One caveat for this method with 3-way (or higher order) interactions is that - depending on the binding strength of the proteins -  it can be very hard to prevent anything but direct interaction partners from being co-purified. If you want to absolutely prove that two proteins interact directly a yeast-2-hybrid (y2h) experiment is better suited.

Others have covered a lot more ground but I'll throw in a couple of approaches from the spectroscopy side since I've been looking at them recently.
Bioluminescent resonant energy transer (BRET) shows if proteins bind in vivo: "BRET measures the interaction of proteins using a bioluminescent donor fused to a protein of interest and a fluorescent receptor fused to its binding partner. The bioluminescent donor, usually a luciferase, does not excite the fluorophore using light, but transfers resonance energy through dipole-dipole coupling. To transfer resonance energy, the donor must be within 10nm of the receptor and in the proper orientation making the technique useful for measuring proteins in close proximity." (From https://www.promega.com/resources/pubhub/features/bret-nanoluc-luciferase-and-protein-protein-interactions/)
Surface plasmon resonance (SPR) also shows if proteins bind, but in vitro: "SPR is sensitive to changes in refractive index within about 150 nm from the sensor surface. To study the interaction between two binding partners, one  partner is attached to the surface and the other is passed over the surface in a  continuous flow of sample solution. The SPR response is directly proportional to the change in mass concentration close to the surface. Biacore systems can be used to study interactions involving (in principle) any  kind of molecule, from organic drug candidates to proteins, nucleic acids,  glycoproteins and even viruses and whole cells." (From the Biacore assay handbook)
These are both ways to look at direct interaction, ie binding. Functional interaction is a whole different story.


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Identify snails
Can you tell me what are these 2 kinds of snails I found?
The first is around 2cm shell diameter. The second is around 3cm shell diameter.
I found both of them in Normandy (north of France) 100km from the sea, and found 2 days ago (summer).

I've just edited the post

The first one is Cepaea nemoralis, the Grove snail, one of the most common snails.


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How does DNA codon (5`-3`) convert to mRNA?
There is a problem I stumbled upon when doing a lesson on molecular genetics (Grade 12 level).
The lesson contains many tables in this format:
I don't understand how it got to the mRNA codon considering how RNA polymerase creates mRNA. From what I know already RNA polymerase reads the anti-sense/template strand (3`-5`strand) and synthesizes mRNA in a 5`-3` direction.
For example, using the first column with the DNA codon 5`-TAC-3`, I would automatically convert it to 3`-5` complementary anti-sense strand because of the nature of the enzyme. It would be 3`-ATG-5`. Now using that anti-sense strand I would find the complementary base pairs and the mRNA strand would be 5'-UAC-3'. This is not consistent with the example given by the lesson. I can understand how to get to the answer (just find the complimentary base pairs of the DNA codon given) but it goes against what I know.
Now if the table said (3`-5`) instead of (5`-3`) it would make sense. Am I misunderstanding a fundamental concept?

In addition, I did some research and found this table. https://en.wikipedia.org/wiki/DNA_codon_table
With the example I mentioned, Tyrosine would be the amino acid if I was going directly from the DNA codon not methionine.

The table you reproduced shows the DNA sequence on the bottom or antisense strand of the gene, but the 5’->3’ notation refers to the coordinates on the top or sense strand.

Your reasoning is correct and the table is wrong. The mRNA will have the same base sequence as the sense DNA strand (with T replaced by U).

I have upvoted this answer, but would add that — although it is not the poor poster's fault — the term ‘DNA codon’ is non-standard and I can see little point at all in a table of this sort. Perhaps for mRNA codon v. tRNA anticodon, but not for this.


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Can someone ID this moth seen in Bellandur, Bangalore?

Picture taken near Saul Kere. You may need to zoom in.

It's the Indian Lily Moth
(https://en.m.wikipedia.org/wiki/Polytela_gloriosae).

That looks like a plausible ID. The site generally prefers the key details of the answer to be contained in the answer itself, not just at the link. What are the distinguishing features of the Indian Lily Moth, and how would you tell it apart from similar moths?


text:
What is the physical reason that a weak muscle means that its antagonistic muscle will tighten?
I've read online (probably from these two sources Athlean-X and Mike) that when one has a tight muscle that the antagonistic muscle tightens up as a defense mechanism. What I am trying to understand is why the body does this. From my intuition it seems that tightening up just makes the tight muscle vulnerable to wanting to stretch it and snap it, so I can't imagine how tightening is a good idea biologically. Furthermore, even if I choose not to stretch it (which is the instinct) it doesn't inform me what the real issue is nor does it seem as a way to defend anything. Thus, how is tightening up defending anything? How does this (perhaps from an evolutionary perspective) make sense? Why does this happen?


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How having sickle cell trait would provide resistance to malarial parasites?
It's mentioned in my textbook that subjects with sickle cell trait develop resistance to malaria. I've read a few research papers predisposing involvement of macrophages and papers asserting involvement of the heme oxygenase system rendering me confused; so what actually causes this resistance. And is this resistance also present in the subjects with sickle cell anemia? Also some African tribes are generally mutated to provide malaria resistance. See this https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499995/

Possible duplicate of Why do heterozygous individuals have increased resistance to malaria?

@DeNovo I was having a hard time understanding it; another approach to answer the question would be appreciated.

In someone with sickle cell trait (a heterozygote), red cells are typically normal. When those red cells are infected with P. falciparum, though, they sickle and are easy for phagocytes to capture and kill. This makes it hard for the parasite to reproduce and cause significant disease.

I would not consider it a duplicate the linked question does not address the mechanism of resistance.

@John the answer goes through it in good, simple detail.

@DeNovo No it doesn't, it completely glosses over what it is about sickle cells that actually makes them detrimental to plasmodium infection. "the chances are bigger they will be phagocytized" is the sum total of the explanation, without even a mention of why the chances are higher.

I would say that there are at least 2 explanations:

Higher levels of free heme in the blood of individuals with sickle cell anaemia/sickle cell anaemia trait. Free heme is toxic to Plasmodium.sp Science. 1981 Nov 6;214(4521):667-9., detailed mechanism is described here: J Mol Med (Berl). 2008 Oct;86(10):1097-111. This effect is also observed in people with other diseases affecting stability of erythrocyte's membrane, such as thalasemia or spherocytosis.
It is also possible that, when erythrocyte's membrane is prone to disruption, Plasmodium.sp  antigenes are present in higher concentrations and may be faster presented to the immune cells.

Sickle cell anaemia is where the red blood cells become sickle shaped hence since Plasmodium infests itself in the red blood cell for oxygen, it doesn't survive because sickle celled RBCs carry less volumes of oxygen.

do you have a source for this?


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I am trying to identify this little "bug"
I am trying to identify a bug. I find this little guy in Paris, at the rooftop near plants, in the streets without plants. I let one on my t-shirt, and it was trying to unpick it. I took a picture :

I think remembering having seen such bugs in old closets, on clothes, when I was kid, but I am not sure.

The focus isn't the best, but it looks to me like a lace bug (order Hemiptera, family Tingidae); not knowing the French fauna forbids further depth from me.


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Stained chestnut tree leaves
The leaves of the chestnut tree in our back yard have, for a while, developed these stains on them:

..which don't appear to be a normal feature of this tree's leaves, at least according to the pictures on Wikipedia (I'm no botanist).
Also, the grass at the bottom of & around the tree does not (no longer?) grows around its root:

Its fruit, on the other hand, appear to me to be healthy:

We've only moved here for a few months, so am not sure whether it has always been like this or whether the tree only got infested in the last period.
Does the leaves' degradation + non-fertile ground around its root, signal that the tree is sick? If so, is there some "medicine" I can get for it myself, or would I have to speak to the administrators of the garden? Thanks in advance for any thoughts!

This looks like Horse Chestnut Leaf Miner (https://www.rhs.org.uk/advice/profile?pid=533).  It is very common, and infects most of the horse chestnut trees around here.  Some years are worse than others. It has been spreading for the past few years.  It doesn't seem to seriously harm the tree, but there is no cure I have heard of.  The link I posted from the RHS offers some ideas about collecting the leaves and composting them in sealed bags, until the moth larvae have died. Occasionally, trees have been found that are genetically resistant to the disease.
Don't worry about the grass, the tree needs the light and water from that bit of soil, but you could try some bark mulch around the trunk to cover the soil, and keep the moisture in.

That's indeed what it appears to be - thanks so much!


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Automating figure-making with PyMOL
What I want to do
I have a list of almost 200 PDB entries that I need to visually inspect. Luckily, the thumbnail image displayed on the PDB website (examples with RCSB or PDBe for a well-known structure) is enough to figure out whether I want to exclude an entry for subsequent use of the resulting cleaned-up list of entries.
Now, looking up these entries one by one on the website is easy to do, but is very slow and error-prone. I need to be careful copy/pasting accession codes, and it takes a lot of time to go to my list, copy an accession code, go to the website, paste, search, and have my answer once the result page has loaded fully.
In other words, I'm lazy and I think my time would be better spent doing something more interesting than copy/pasting 200 times.
Attempt at a solution
I figured it shouldn't be too difficult to use PyMOL with a bit of scripting to automatically fetch each entry and generate a small image (faster than ray-tracing, which I don't need for this quick inspection). Here is my attempt:
pdb_entries = ['1m18', '1eqz'] # The real list has almost 200 entries, but 2 are enough to test the script

for entry in pdb_entries:
    cmd.fetch(entry, async = 0, path = "./pdb-files")
    filename = "./pdb-imgs/" + entry
    cmd.png(filename, width = 600, dpi = 100, ray = 0, quiet = 0)
    cmd.delete(entry)

Problem
When I save this script as fetch-all.py and run it from within PyMOL with the command run fetch-all.py, the structure files are correctly downloaded in the ./pdb-files directory and images with names matching the PDB accession codes are generated in the ./pdb-imgs directory. So, it seems everything works. Except these images are just black, not showing anything of the structure.
I tried to add cmd.center(entry) and cmd.show("cartoon", entry) before saving the PNG files, but it did not change anything. I also looked up the help page for cmd.png(), thinking I was missing something, but I couldn't find anything I would be obviously missing there.
Any idea? Thank you all in advance.
Edit: I forgot to mention that this problem of black images happens with the latest PyMOL (2.2.0) and also with an older version (1.7.4).
Edit: when I run the commands inside the loop one by one at the PyMOL prompt, everything works fine, I get images correctly saved. It seems it doesn't work in the context of the loop only. I double checked the loop syntax and it looks fine to me (but I might be missing something; I don't know python very well).
Edit: I also tried cmd.save() instead of cmd.png(), but it did not solve the problem.

Could it be that as all your structures have different x, y and z coordinates. Therefore whereever pymol is centered  it isnt in a position where the protein is?

Therefore could be fixed by aligning all the structures so they all appear in the same x, y and z range

I tried to add cmd.center(entry) in the loop that processes each entry, to make sure that each entry gets properly centered before saving a picture. That didn't solve the problem.

Have you tried using cmd.orient ?

I just gave it a try, it did not solve the problem of the black images.

Were you able to fix this problem

I ended up using ChimeraX instead, which I found easier to use overall. I abandoned the idea of generating pictures and browsed the models interactively in ChimeraX (this is slower than looking at pictures, but being able to rotate the model was useful in some cases).

I’m voting to close this question because it is not concerned with a biological problem.


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What is this Las Vegas area weed?

This is a picture I took of my mystery weed out by Pittman wash in Henderson NV earlier this year. From my experience this last year, I assume that the plant turns red later in the year and loses the bottom leaves. The plant typically seems to grow no more than half a foot tall but can grow a couple feet wide at or near the top.
Edit: I wasn't able to get a background but here are more pictures

The spindly nature of those stems makes it hard for the camera to find a focal point.  Maybe try getting down low and have the camera focus on the basal leaves, and if the depth of field is good we'll be able to see the stems as well.  If you are taking photos with a phone be sure to sit down (for steadiness) and tap the image where you want it to focus -- sometimes they need a little guidance!

@BryanHanson Thanks, I'll take a better picture when I get a chance later today.

If there’s a lot of that plant around, you might pick one of the stems, and bring it home and photograph it on a neutral surface. Might be easier to get focused there.

@BryanHanson idk if these are better but I picked one and took some pictures.

Those are helpful, thank you.  Not a lot of plants generally w/o any leaves (ignoring the tiny basal leaves that are probably from when it sprouted).  Someone will know this plant, I may have time later to dig through some field guides.

Alright, after a lot of searching, I have a proposed ID: Eriogonum deflexum known commonly as skeleton weed or little desert trumpet.  I feel pretty confident of the genus, less so on the species (there are several close candidates).  The family is buckwheat or Polygonaceae.
This plant has basal leaves as yours does, has pretty much leaf-less stems and relatively infrequent flowers, which look quite a bit like your picture.  Reading various descriptions it seems the plant is somewhat variable, it often looks like your pictures but sometimes has more flowers and sometimes the plant is more dense, rounded, shrubby and taller (it probably depends on the moisture and soil quality).  It is a desert species, preferring scrubby areas and washes, widely distributed in Western US deserts.
CalPhotos has a picture which looks to be a good match (credit: Jean Pawek; also, CalPhotos has many other photos).  This photo by Hank Jorgensen looks like a good match too and shows flowers which look similar to yours.
If you see the plant again, bring a picture on your phone and check the flowers carefully. Also the leaves should be hairy/wooly.

Yes, the leaves are frequently wooly. Thanks!

Great! I've been semi-obsessing about this!  Found it by browsing a field guide to San Diego county plants and fortunately it was there.


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Is marriage with half-cousin's daughter more risky than marriage with others?
I want to know is marriage with half-cousin's girl more risky than marriage with a non-family girl?
Also I like to know if her parent are cousins(but from mother side), does it add more risk to this marriage or not?

The answers are yes and yes. However, I will have to dig up some sources before I can answer.

The marriage is obviously not an issue. The reproduction can be an issue.

Why is a girl connected with a girl? And she in turn marries a guy?

@TheLastWord it's an awkward diagram, but if you read the text of the post (her parents are cousins), you'll see that the lines connecting the family on the right side of the figure and the family on the left side of the figure are parent-child relationships, like all the black lines connecting boxes in this figure. The girl at the base of the figure is the child of the boy she is connected to with the black line and the girl she is connected to with the black line.

@TheLastWord: The (right side)girl is her mother and she is cousin with her father.

The medical term here is consanguinity, or a consanguineous union. The risks of consanguinity are well studied, and based on the principle that children born to parents with shared genes are more likely to be homozygous for recessive alleles. Population level measurements of specific risks for, e.g., fetal loss, major birth defects, or other problems vary depending on the population studied. Many of these studies look at first cousins, where typical numbers are between a 1-5% greater risk for major birth defects and 4-5% greater risk for late miscarriage or death of a child before age 10. The data on earlier fetal or embryonic loss isn't conclusive.  You can read more about this in the review I linked to at the end of this answer. The specific risk for a specific individual isn't on topic here, since it is a personal medical question. If you are looking for an answer to that question, I'd suggest scheduling a visit with a medical geneticist.
Your diagram depicts marriage between half first cousins once removed, with an expected shared percentage of genes of 3.125%, equivalent to second cousins, which fits the definition of consanguinity generally used in the medical literature and allows application of studies that use that definition. The fact that one of the potential parents in this marriage was also the product of a consanguineous union may increase the risk.
Consanguinity is an important risk factor for many birth defects and other diseases (see Cecil Medicine Chapter 41 and this review)

Thank you De Novo, but I can not understand why relationship between the girl's father and mother affects on her marriage, when that relation doesn't any issue with the boy who likes to marry with. I mean, why relationship of the right side family, can affect on this marriage when the boy has no relationship with the right side family?

@Hasani it suggests both potential parents are part of a subpopulation with a higher rate of consanguinity and less genetic variability. This means there is a slightly higher risk that the potential parents are both carriers of the same recessive allele for some disease. Empirically, when there is more than one consanguineous union in the family tree, we see a higher rate of birth defects and other diseases than you would expect form the expected shared percentage of genes alone.

Dear De Novo, May you explain how percent the risk of this marriage is more than a non-family marriage?

@Hasani the specific question about the risk of defects in your child should be asked in a visit with a doctor, ideally a medical geneticist. I've edited my answer to include more about what studies have reported in general.


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Unknown Insect identification
Found this bugger crawling across my laptop.  Any help identifying would be appreciated.  After a bunch of googling it appears to be close to a lady beetle larva.  I am located in north east USA.

It looks most like a common Green Lacewing larva - Chrysoperla rufilabris. Lacewings are considered a benefit in the garden because they effectively feed on aphids and other soft bodied garden pests. Here are some links that may be of further help.
https://bugguide.net/node/view/16103
http://www.uky.edu/Ag/CritterFiles/casefile/insects/lacewings/lacewings.htm
https://greenmethods.com/chrysoperla/


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Can animals train to be noticeably stronger, faster, more agile... than other animals of the same species?
Humans have a huge variation in physical ability because of exercise differences. Olympic athletes are a number of times stronger than average people on the street. It seems that variation in animals is very small, but I am wondering if one could force an animal to follow a specific program and eat specific food to get a lot stronger, agile, etc. than an average animal of the same species.

When I visited the Cheetah Outreach Center in South Africa, the guides there told us that their captive cheetahs couldn't run nearly as fast as wild ones, and that wild ones were much more muscular than the ones in the center; their point was that actually having to run full-out or starve caused much more rigorous training than occasionally jogging after a fake rabbit on a string. That's supported by this article:

The cheetahs being studied didn’t come close to the speeds reported for wild cheetahs — the zoo animals reached 38 mph (61 kph), while the greyhounds topped out at 43 mph (68 kph).
The researchers said this was probably because the captive-born cheetahs have never really gotten the chance to let loose in the wild and run full throttle.
"They have lived in a zoo for several generations and have never had to run to catch food. They have probably never learned to run, particularly," Wilson said.

Cheetah Speed Attributed To Animal’s Ability To ‘Switch Gears’ While Running

In other words, animals in the wild are training like they are Olympic athletes,

@ArcanistLupus It's almost like they trained as hard as if their lives depended on it... :)

I once visited a zoo that had a large enclosure for cheetahs, and “feeding” the cheetah entailed hooking meat on to a zip wire running across the enclosure’s longest side. The meat hook was then propelled at high speed along the zip wire and the cheetahs had to “chase” it in order to eat. The idea was to simulate hunting to provide physical exercise.

Related question https://biology.stackexchange.com/questions/40367/how-do-crocodiles-stay-fit

Can animals train to be noticeably stronger, faster, more agile.. than other animals of the same species?

Yes, of course!
Humans are animals, so yes! But even in non-human animals. You can look for example in a tutorial on how to train a dog (or a horse) for specific skills (speed, high jump, long jump, etc...).

It seems that variation in animals is very small

Such a general statement can only be wrong. Consider dogs as an example. The fastest dogs go at 72 km/h (~45 mph) while many dog breeds barely reach 5 km/h (~3 mph; and they're all considered as the same species). So, there is a lot of genetic variation among dogs.
Now when it comes to variation caused by training it is a little harder to estimate. Consider having a look at Guy and Snow (1977), McKeever et al. (1987), Evans and Rose (1987) and Rivero and Piercy (2008). For what it is worth, note for example that trained racing horse can go up to 70km/h while most horses can go only up to 40-45 km/h. There are a number of studies showing the effect of training on horses.

I don't think that dog breeds are a great example. Clearly, breeds differ substantially due to genetic differences. It doesn't take much thought to understand that certain anatomical features would be better suited for fast running, say. However, the OP is looking for differences due to training/exercise/diet. It doesn't matter that they are in the same species, the differences are still due to non-training related causes. Therefore, I think that it would be better to use an example of variation within a breed (Although, even this could be partly due to genetic differences)-

@Eff Highly agreed! If you want to use dogs as an example then take two same sex pups from the same litter and provide a life of luxury to one but take the other on for police K-9 training and five years later let them play and I am positive you will notice great differences.

@Eff The claim I was responding to was It seems that variation in animals is very small. I indeed considered a case where a fair part of the variance is likely genetic. I never meant that the observed difference between a chihuahua and a greyhound is caused by training. But I very much agree that this is a confusing phrasing, so I clarified that I talked about genetic variance and added a paragraph with papers on the effect of training in horses. Thanks for your comment!

@Remi.b Okay, there is no disagreement then. And yes, your edits clarify things a lot.

Definitely when it comes to horses. They are selectively bred for generations to work in different sports: dressage, show jumping, endurance, racing and so on. As one example: to train a horse for olympic level dressage takes ten years or more in order to build muscles and coordination.
Some example of horse sports, several of them describes how horses are trained:
https://en.wikipedia.org/wiki/List_of_equestrian_sports#Olympic_disciplines

Welcome to Biology.SE! Thank you for answering the question. I'm not sure, though, what the link to a list of horse sports does to help support or add to your answer.

Even our ordinary trail-riding horses will be out of shape in the early spring, and will get tired doing rides that they can easily handle later in the year.

Wild animals may have less variation in traits such as speed of running, if they predominantly eat similar diets, and if the slow ones are regularly getting eaten and failing to breed. Wild animals likely run at around the optimal speed for their environment.
The process of training implies some level of domestication - humans protecting the animals, perhaps modifying their diet, and expecting them to perform a service in return.  In this situation, the animal's day-to-day activities would likely change, together with the change in diet.  Animals' physiology tends to be able to change substantially in response to these kinds of environmental and behavioural changes (phenotypic plasticity).
So I guess the answer is yes to whether animals can be trained to perform differently, but the question of whether they would want to is maybe open.

One could argue that it isn't a matter of wild animals having "less variation" but rather that the variation is harder to observe because the weaker ones are so much less likely to survive.

There are actually two questions here:

Can animals train to be noticeably stronger, faster, more agile...
than other animals of the same species?'

As a couple of others have stated, yes.  This is, in fact, evident in horse racing, dog racing, dog agility course competitions, and a few other similar competitions.  If animals couldn't be trained to become stronger/faster then those sports would not exist as they are.

Is there natural variation in strength/agility/speed/etc in animals they way there is in humans?

This question is implied by your statement "It seems that variation in animals is very small..."  In fact, statistical analysis asserts that virtually every measurable difference between organisms falls on a Normal Distribution (see also Bell Curve).  However, this only works if we compare like populations, or "apples with apples".  For example, I certainly would not compare a bull dog's running speed with that of a whippet (racing dog similar to a greyhound, and a cool Devo song).  But if I compared all whippets then they would be normally distributed.  Now, if I had a trained whippet vs a non-trained whippet then we are again going to run into problems (see point 1).
Here is the thing with the normal distribution though, 68% of the population lies within 1 standard deviation of the average.  This means that over 2/3 of the population is pretty close to average.  Further, 95% of the population lies within 2 standard deviations of the average.
Here is a slightly more realistic example of this:  The average height of men worldwide is roughly 5'10" and the standard deviation is roughly 3".  Thus 68% of men worldwide are between 5'7" and 6'1" tall.  (Yes, I'm rounding these numbers a bit but you get the point.)  You can do something similar with weight, strength, etc, though certain attributes are difficult to measure.
What does this really mean?  Well, the natural speed of say a cheetah in the wild is normally distributed.  That is, if we could measure them all.  However, in the wild, not all cheetahs survive.  As part of survival, only the fastest and strongest survive so what we actually have is a much smaller set.  This is why animals might appear to have less variation.
If you look then you can see the variations in nature.  Go to a park and stop and look at the pigeons.  Some are actually quite fat while others are not.


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Are red blood cells prokaryotic?
After searching "do antibiotics impact the immune system" I found out that antibiotics target prokaryotic cells. It all made a lot of sense thinking about all those yogurt recommendations you get after taking antibiotics: the collateral damage is on the prokaryotic cells that live with us, but are not "us" as such.
Except I remembered human red blood cells don't have nuclei, so where's my confusion?
(I'm only a biology enthusiast.)

Are red blood cells prokaryotic?

No!

There are many more differences between procaryotes and eukaryotes than just the presence of a nucleus. See DeNovo's answer for more information.
The terms procaryote vs eukaryote refer, not so much to the physiology of the cell but to a specific evolutionary lineage. Eukaryotes are individuals that belong to the monophyletic group of Eukaryota aka. Eukarya (see here for an intro to phylogeny). As such whether or not a eukaryotic loses its nucleus and start looking exactly like a E. coli won't change anything to the fact that this cell is still in the Eukaryota lineage.

When differences between prokaryotes and eukaryotes are taught in an introductory biology course, a generic prokaryotic cell and a generic eukaryotic cell are typically compared. Cells in a complex multicellular organism, like a human, are quite diverse. Human red blood cells are one example of a highly specialized cell with a mature form that is quite different from the typical eukaryotic cell. Keratinocytes in the epidermis are another example (see Ross Histology, Ch. 15). In both cases, these cells produce large amounts of a single protein, eventually, at their most mature stage, stopping protein synthesis, extruding their nuclei and most other organelles.
The absence of a nucleus or other organelles, however, does not necessarily make either of these cells more susceptible to antibacterial antibiotics. Antibiotics are targeted toward things that bacteria have (positive differences), rather than the absence of typical eukaryotic structures. Almost all antibacterial antibiotics have one of three targets (see Goodman and Gilman Chs. 48, 52-55):

The bacterial cell wall or membrane
protein synthetic machinery
specialized metabolites required by bacteria

There is (almost) no overlap between these structures in bacteria  and structures in any of the diverse array of human cells. The one partial exception is a similarity between the mitochondrial and bacterial ribosome, that may, for example, be responsible for some of the toxicity of chloramphenicol (G&G Ch. 55).

"antibacterial antibiotics" - never heard antibiotic qualified in this way. What's an example of an antibiotic whose intended target is a microorganism other than a bacteria?

@bishop antifungal and antiviral therapies both qualify as antibiotics. They have different targets, based on the properties of pathogenic viruses and fungi.

No.  Prokayotic cells are full organisms with their own DNA, red blood cells are not.

It's also hard to even call them living things, since they do not do most of what living organisms do. They are just half dead components with a single purpose: zombies so to speak.

Good answer. I expanded  a bit on the details.

@DanielGoldman thats not true. They consume organic matter, they reproduce, they have their own genetic instructions that produces proteins. What don't bacteria do that you would not consider them alive?

@JamieClinton he meant mature RBCs, which don't do what most living organisms do. They fulfill more than a single purpose, but otherwise, he's exactly correct. Once they reach maturity, they don't synthesize any more protein and can't reproduce.

Gotcha. Although I wouldn't call a cell in a multi-cellular being a 'living organism' regardless.

@DeNovo Even mature RBCs are living cells. They metabolize fuel and use the energy for repair and various other cellular reactions. They maintain their own membrane and ionic concentrations. They are no less of a living cell than the neurons in certain insects which lose their nuclei.

@forest I'm fully aware of the full range of erythrocyte behavior, which
is why i emphasized that they have more than one purpose. I was explaining Daniel Goldman's comment.

Not even an answer.

True; they do serve other purposes, but I don't think I would call [mature] RBCs alive. "Zombies" is still more appropriate.

@DanielGoldman how about a post menopausal female mammal?

@De Novo.  This is just what the world needs more of.  People openly saying that women who are not breeding are things. I wish I could delete my answer.  It disgusts me that it's being used to treat half the species like garbage.

@swbarnes2 That's not at all what I'm saying. Many attempts to define life start by considering reproduction. I was pointing out the problem with that, exactly because it is ridiculous and disgusting to consider an infertile individual to be a non living thing. I'm honestly shocked that someone would somehow interpret my comment as the converse (because these people are useless garbage, we can safely say that's a good way to classify cells). How would anyone think that?

@DeNovo: Although I'm just as surprised by swbarnes2's response as you are, I don't think your comment actually made that much sense even when taken as you meant it. Daniel Goldman didn't even bring up reproduction at all. I don't think it's controversial that some parts of the human body aren't alive (consider e.g. hair); someone can reasonably suggest that another part might be borderline without you needing to jump straight to a reductio ad absurdum counterargument.

@swbarnes2 As a species, we are able to reproduce. Individuals who cannot reproduce do not mean that they are not alive when, as a species, they are able to. Just think about a colonial organism such as ants. Their species can reproduce, letting them all be classified as life, even the drones.

To be clear, I never stated that a mature RBC was a zombie, simply because it cannot reproduce.

But they could have been said to be such before they threw out their kernels.

No, they are matured (broken) reticulocytes without the net structure and ribosomal DNA, which themselves are matured (broken) normoblasts that have lost their nucleus.
So basically they're the left over plasma membrane of a once-alive eukaryote cell, now filled with mostly hemoglobin, and little else.
(The above is not necessarily true for all animals, some have nuclei, but it's the case for mammals, and thus humans.)

Erythrocytes have very complex metabolism and maintain internal homeostasis. It's not fair to say that they are "once-alive, filled with hemoglobin and little else" considering they are still living cells.


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Can a viable embryo develop from the fusion of two egg cells?
For a zygote to form, two haploid gametes undergo meiosis and fuse during fertilisation. Since two egg cells (or even two sperm cells) are both haploid, is it theoretically possible for them to make an embryo (via experimental manipulation)?
I’m guessing that if such a thing were possible, the two egg cells could each come from the same organism or two different sources.
Would there be any side effects, such as persistence of mutant alleles due to a lack of genetic variation if both egg cells originate from the same organism?

Related: Is ovum + ovum fertilization possible for human?

Yes, it is possible to make a zygote from two ovules. Other more complex scenarios are possible as well. You might want to read this cbc article. If the two ovules came from the same organism, then the baby will very likely suffer from a number of diseases due to very low heterozygosity (same mechanism that is causing inbreeding depression and problems of consanguinity).
It is likely not possible to get a zygote from two spermatozoids though because you would lack mitochondrial DNA (mtDNA). There is a little bit of mtDNA in spermatozoids but they are generally not transmitted. Through experimental setup I imagine it might be possible. Also, spermatozoids are very small and would lack many of the ressources necessary to start a zygote.

This pretty much answers my question, thank you.

You're describing chimerism (distinct genotypes in a single organism; in animals, this arises when two fertilized eggs merge). This article suggests that "microchimerism" can occur during pregnancy when small quantities of fetal cells migrate through a mother's body. You can find additional examples from humans and other species at my first link (the Wikipedia article), but here's one more from The New England Journal of Medicine in early 1998:

A 3.46-kg infant was delivered vaginally at term; he had a normal
  right testis and an undescended left testis, with otherwise normal
  male genitalia. At the age of six months, the left testis was palpable at the inguinal ring.  Surgical  exploration  at  the  age  of  15
  months revealed a hernial sac containing an abnormal gonad and
  vas deferens. These structures were excised; they proved on histologic examination to be an ovary with a fallopian tube attached to a horn of uterus. Karyotyping of peripheral-blood lymphocytes then revealed two cell lines, one 46,XX and the other 46,XY.

No, he is not describing chimerism.  He is talking about two unfertilized egg cells being fused to form a diploid zygote (instead of a sperm fusing with an ovum).

Did he ever specify that the egg cells couldn’t be fertilized? I’m struggling to see that in the original text of the question, and my answer is valid in the sense that it provides an explanation for how two eggs might combine to form “a viable embryo.” A mouse study showed potential for egg-egg fertilization but wasn’t sustained beyond ex vivo POC. For now, bi-egg organisms (especially humans) require sperm.

Yes, he indicated the egg cells (or sperm cells) were unfertilized by the terms he used: "For a zygote to form..." -- a zygote is a fertilized cell ready to divide into an embryo, being diploid (having a full set of paired chromosomes). "...two haploid gametes..." i.e. sperm or ova having half the DNA ",,,fuse during fertilisation. Since two egg cells are both haploid, is it theoretically possible for them to make an embryo?"

In that case, I’ve answered both parts of his question in my original answer and response to your question – the mouse study I linked is the only evidence I can find of an egg-only diploid, and otherwise it doesn’t seem to be possible without sperm.

Unrelated... but please stop assuming I'm a "he".

Certainly – and your point is well-taken (any further discussion will use your pronoun of preference, as specified) – but it’s important to keep in mind that there’s no maliciousness, assumption of gender, or any other subtext to the use of the word “he” here. At University, my english professors were always adamant that we not use the androgynous/singular “they.” Instead, I was taught to choose a singular (gendered) pronoun and use it, whether or not it’s specifically applicable to the group it describes. In this case, we were identifying/referring to a (functionally) anonymous user.


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Viral susceptiility of Nose and eyes
I read that opening in our face like nose and eyes are one which get us infected with numerous communicable diseases like  cold , flu ebola etc.
Both these organs have preventive mechanism like nose hairs, eye lash , etc.
Which one of eye and nose does protect human better from airborne virus and bacteria?

Between the eyes and nose, which offers better immune protection

Neither. Both are mucous membranes lined by epithelial cells. Each is their own niche (and the nose has a number of sub-niches), with particular receptors, environmental factors, and immune factors that interact with pathogen factors. The interaction between the two produces the tissue tropism of a particular pathogen. Each is colonized with many commensal microbes, with some overlap (see Murray Medical Microbiology Ch 7 and this study of the eye). As far as "airborne" transmission, vs. inoculation by physical contact, the nose and nasopharynx are important structures in respiration. The eye is not.


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identify this ant queen
can anyone help me identify this ant queen, if it's an ant queen? I only assume it is because I caught another with wings which looks exactly the same. Thanks in advance..

There is only one segment between the thorax and the abdomen and the first segment of the abdomen is not elongated, which indicates this is a Formicinae.
Because the head width is similar to the thorax width from top view, this likely corresponds to a social parasite ant from the genus Lasius.
See ref below:

Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


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The concept of high genetic load of disease and non-random segregation of deleterious variants
I'm new in this field. I was reading Shakeel et al. (2018) and came across the below sentences

The rate of emergence and distribution of deleterious variants in populations is important in determining the patterns of underlying genetic load for diseases, because the increased accumulation of genetic load of diseases due to non-random segregation of deleterious variants is so detrimental that fixation or near fixation of these mutations can play a significant role in the extinction of isolate populations with small effective population size.

I'm not sure to correctly understand the concept of the sentences, especially

genetic load of disease and its accumulation due to non-random segregation of deleterious variants.

Could you please kindly explain a bit to me about it?
Many thanks in advance

Can you please edit your post to link to the original paper?

Do you understand the definitions of genetic load, fixation, effective population size, non-random segregation and deleterious variants?

Hi, I added the link of paper. Yes, I knew, but not sure about genetic load and non-segregation in these sentences and totally the main concept of the text. Thank you in advance for any explanation and clarification.

Genetic load is the difference between the fitness of an average genotype in a population and the fitness of some reference genotype. Here the reference genotype would be a hypothetical genotype free from any deleterious mutations. They don't say "non-segregating" but "non-random segregation", likely referring to loci that are in genetic linkage, hence do not segregate independently. Does it help a bit? Do you manage to pinpoint to exactly what is unclear?

Thanks. Regarding, non-random segregation, as I searched it refers to non-random segregation of sister chromatids during meiosis. That's why I confused with its concept here. Any comments, please.


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Why the SNPs from the earliest human haplogroups are missing in people outside of Africa if they are infact the descendants of it?
The SNPs M91, P97, M31, P82, M23, M114, P262, M32, M59, P289, P291, P102, M13, M171, M118 from haplogroup A and SNPs M60, M181, P90 from haplogroup B are missing in people without recent African ancestry. Considering these are the earliest humans in Africa, perhaps someone could explain genetically why they don't exist in non African populations?

Sources:
Klyosov, A. A. (2011a). The slowest 22 marker haplotype panel (out of the 67 marker panel) and their mutation rate constants employed for calculations timespans to the most ancient common ancestors. Pro- ceedings of the Russian Academy of DNA Genealogy
Cruciani, F., Trombetta, B., Sellitto, D., Massaia, A., Destro-Bisol, G., Watson, E., et al. (2010). Human Y chromosome haplogroup R-V88: A paternal genetic record of early mid Holocene trans-Saharan con- nections and the spread of Chadic languages. European Journal of Human Genetics, 18, 800-807.
Simms, T. M., Martinez, E., Herrera, K. J., Wright, M. R., Perez, O. A., Hernandez, M. et al. (2011). Paternal lineages signal distinct genetic contributions from British Loyalists and continental Africans among different Bahamian islands. American Journal of Physical Anthro- pology, 146, 594-608. doi:10.1002/ajpa.21616

What do you mean by "Considering these are the earliest humans in Africa"? Who are "these"? Do you mean "Considering that the earliest humans arose in Africa"? And please provide links to the papers you quote and tell us whether any explanations are suggested there.

Without reading the link papers, I would assume that some african lineages carry these haplogroup. Not all. If this is true, there is really nothing surprising. If it is still surprising to you, can please explain why?

@David  honestly this question is not my own. I didn't find the papers my self, I only used google scholar to get some of the pdf.
The guy seemed adamant that the lack of these certain nucleotides were evidence for there being essentially a species discrepancy, with Asians and Europeans never having an ancestral background commonality with subsaharan Africans. A denial of the Out of africa theory.
I am just interested in how close or different, any of your arguments would be with the ones which I had posited in opposition.

Unfortunately, although this may be interesting, you really need to do the background research yourself if you hope someone here will take the time to consider your question. Of course, there may be someone familiar with the story, but the response so far isn't too encouraging.

It looks like the information presented in the question is not reliable.  Taking the first two Y SNPs mentioned, M91 and P97, it says these "are missing in people without recent African ancestry."  Yet Wikipedia says that M91 and P97 are defining mutations of haplogroup BT and that

Macrohaplogroup BT has been found in populations on every continent, since prehistoric times. It is the progenitor clade of the paternal haplogroups B and CT.

This implies that M91 and P97 are present in "people without recent African ancestry" (excepting back-mutations), in conflict with the assertion in the question.
However, this view has apparently evolved a bit, as the "haplogroup A" article says:

A major shift in the understanding of the Y-DNA tree came with the publication of (Cruciani 2011). While the SNP marker M91 had been regarded as a key to identifying haplogroup BT, it was realised that the region surrounding M91 was a mutational hotspot, which is prone to recurrent back-mutations. Moreover, the 8T stretch of Haplogroup A represented the ancestral state of M91, and the 9T of haplogroup BT a derived state, which arose following the insertion of 1T. This explained why subclades A1b and A1a, the deepest branches of Haplogroup A, both possessed the 8T stretch. Similarly, the P97 marker, which was also used to identify haplogroup A, possessed the ancestral state in haplogroup A, but a derived state in haplogroup BT.[5] Ultimately the tendency of M91 to back-mutate and (hence) its unreliability, led to M91 being discarded as a defining SNP by ISOGG in 2016.[43] Conversely, P97 has been retained as a defining marker of Haplogroup BT.

So this indicates that haplogroup BT, which includes most or all men historically outside of Africa, does not reliably display mutation M91, but does display P97.  I'm not going to research all the other SNPs (especially since the three references don't seem to be very relevant), but I think this much indicates the assumptions of the question are not coherent enough for a good answer.

This clears up a lot.


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The effect of sugar on rate of yeast Respiration
In my experiment, I am investigating the effect of different types of sugar on the rate of respiration of immobilized yeast (yeast trapped in calcium alginate balls). I am looking at glucose, fructose, sucrose and maltose.
Research leads me to believe that the disaccharides will perform the worst as they require enzymes to breakdown into monosaccharides and so will require more time to digest and this have a slower rate of reaction. In contrast the monosaccharides will work the best for the opposite reason.
Can anyone offer any insights into this hypothesis? Any helpful background theory that would support/discredit this.
Thank you.


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Vibrio vulnificus from liquid soap
At some point between 2002 and 2006 I attended a departmental seminar in the UK on Vibrio infections, and particularly on the (then relatively unheard of) V. vulnificus, which causes necrotizing wound infections and septicemia when it enters open wounds. The speaker discussed two case studies: the first was of a case (possibly a cluster of cases) in a garage, I think in Australia, where the workers repeatedly topped up a liquid soap dispenser from a big bottle rather than replacing the bottle, and it had at some point become contaminated with V. vulnificus, which had survived in the soap, and infected an individual who went to wash their hands because they cut themselves.
The second case, which I only mention because it was part of the same talk and I have a suspicion the seminar speaker (whose name I can't remember) might have written papers on both, was about the rise in V. vulnificus cases in the Middle East (Israel, I think) which arose from a new trend for fish markets offering live fish in tanks at market rather than transporting them for a few hours on ice before sale (which was previously killing the bacteria, which occurred fairly ubiquitously in Israeli fish farms due to the high water table and high groundwater salinity).
This was a great seminar with two great stories that illustrate the ecology of Vibrios and I'd love to have sources for either, but particularly the first one. However, I can find no mention of either in the literature. Can anyone help?

The Isreali outbreak (associated with changes in fish marketing) was reported in Lancet a few times. It was particularly important for identifying biogroup 3. I hope that might be helpful, but I'm not sure it will be. Since it was an important epidemic, I wouldn't be surprised if it was discussed in a visiting lecture by someone who wasn't part of the Isreal Vibrio study group.
I'm not aware of a soap dispenser case for V. vulnificus, but soap dispensers have been implicated in the transmission of other pathogens. Could it have been some other halophilic bacteria, possibly another Vibrio?


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Help me identifiy this moth?
I found this moth in Bengaluru/India. Its body length was nearly 2cm. Brown colored with three yellow rings.

This looks to be a handmaiden moth (Syntomoides imaon) which has been observed in this part of India.

Source: India Biodiversity Portal


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Is there an existing database of mutation rates for mitochondrial loci?
I'm wondering if there exists a database of mutation rates (transitions and transversions) for both mitochondrial loci (such as cytochrome c oxidase subunit I (COI)).
Due to the use of COI as a DNA barcode to identify animal species, this gene has a relatively high mutation rate despite being quite conserved across major taxonomic groups. Thus, substitutions in COI are expected to become diagnostic of species much more rapidly (also because of the 4-fold lower effective population size compared to nuclear markers).
The reason I ask is because I am developing a simulation algorithm allowing a user to generate random DNA sequences under a specified nucleotide evolution model (e.g., Jukes-Cantor, Kimura-2-Parameter). I would like to be able to specify realistic mutation rates of transitions and transversions in order to closely mirror actual substitution rates in COI.
Any insight would be much appreciated


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With over 400 chromosomes, does mitosis in a species of butterfly happen in the same way as in humans?
The beginning of the Ars Technica article Gene editing crunches an organism’s genome into single, giant DNA molecule begins:

Complex organisms have complex genomes. While bacteria and archaea keep all of their genes on a single loop of DNA, humans scatter them across 23 large DNA molecules called chromosomes; chromosome counts range from a single chromosome in males of an ant species to more than 400 in a butterfly.

Thanks to @Remi.b for tracking down Lukhtanov (2015) The blue butterfly Polyommatus (Plebicula) atlanticus (Lepidoptera, Lycaenidae) holds the record of the highest number of chromosomes in the non-polyploid eukaryotic organisms.
Does mitosis happen in this species of butterfly cells, and if so, does the process that separates the pairs take place in a similar way mechanically to the way it happens in mammal cells such as the 23 pairs in human cells even though there seems to be almost twenty times the number of individual chromosomes?
Has the mechanics of this process ever been imaged or visualized?

above: from here and here.

above: " Image of the mitotic spindle in a human cell showing microtubules in green, chromosomes (DNA) in blue, and kinetochores in red." from here

For those who would rightly ask for a reference for the claim that there is a species of butterfly that has more than 400 chromosomes, consider having a look at  Lukhtanov (2015).

@Remi.b Thank you very much for tracking that down! I've added that back into to the question.

Mitosis was displayed in a lot of organism, also in organism with a very high number of chromosomes. Here's an example of the analysis made in a fish with an average count of 280 chromosomes. Look at the metaphasis of a cell with higher number of chromosomes (Acipenser transmontanus):

This doesn't mean that every chromosome is equal to others: there're microchromosomes, acrocentric chromosomes, meta, sub-meta.. So, the size required into the nucleus (because where're obviously talking about eukaryotic cells) isn't strictly connected with the chromosomes number.
The answer to your question isn't a clear "yes" : the high number of chromosome in a butterfly is connected with a karyotype instability, where some cells received a wrong number of chromosomes into an alterated mitosis. Actually isn't fully clear why and how these errors come out. Here's something else about butterfly karyotype and phylogeny.

Thanks for the explanation, link, and image! I just found and put an additional image in the question, and discovered the word "spindle" that I'd been looking for. Mechanically, if there were 400 pairs of chromosomes, I'm trying to understand if there would also be 400 pairs of spindles as well?


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What benefits do sloths and manatees gain from algae growth on their fur/skin?
Slow moving sloths and manatees have green algae growing on their fur/skin.  Are there any other animals that have algae growth on them, and does the algae benefit the fitness of these animals?

Source: Canadian Museum of Nature

Source: wildlife.org

Is there anything to suggest there is a benefit to manatees? My boat has a layer of algae on it.

@kmm 1: I seem to remember reading that the algae on manatees acted like a sunblock, but there were no references to this claim.  Unfortunately, I cannot remember anymore where I read it either.

I don't know about manatees, but sloths have a symbiotic relationship with the moths living in their fur because the moths supplement the sloth's diet with additional nutrients via algae. Sloth moths grow and die in a sloth's fur, decomposing to provide nutrients for the algae. The sloth then eats the algae. What the moth gets out of this is that its larvae can feed on the sloth's poop, and when they grow up, they make a home in the sloth's fur again.
Here's an infograph summarizing the relationship: http://www.pbs.org/wnet/nature/sloth-named-velcro-sloth-moths-mutually-beneficial-relationship/11159/