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Brood Parasitism - Parasitism/Ammensalism/Commensalism?
Parasitism has the parasite benefitting while the host is harmed. In brood parasitism, the cuckoo lays its eggs in a crow's nest for incubation. How does this harm the host? Why is it not considered ammensalism?
If I see the fact, while laying its eggs, the cuckoo might break some of the crow's eggs, and in this way the crow gets harmed. Parasitism from here fits.
But, as the chicks grow, the cuckoo chicks protect the crow chicks from other birds or predators. Seeing this, yet commensalism fits.
So, if I have to finalise which species interaction brood parasitism comes under, what should I select?
And why is that interaction preferred over the other?

It's called brood parasitism because it's parasitism (and not commensalism/ammensalism). Because the Cuckoo benefits at the expense of crow (crow's time and heat energy, and the harm posed by hatched Cuckoo to the hatched crows)

As this question focuses only on crows as hosts, does not mention egg or chick eviction, and refers to the cuckoo chicks protecting the host chicks from predators, I think that OP is referring to a 2014 study in which carrion crows appeared to benefit from the presence of a cuckoo chick (from a non-evicting cuckoo species). I've posted more on this in my answer below.

The cuckoo chick hatches earlier and instinctively pushes the host eggs out of the nest. If you view this from the genetic perspective of the crow, it becomes the foster parent of offspring that does not carry its genes. The harm, therefore, is to the host's passing on of genes, rather than to the immediate health or well-being of the individual.
For more information see:

Brood parasite (Wikipedia)
The Ecology of Avian Brood Parasitism (Nature)

And it's not just the eggs - cuckoo chicks are also known to push live young out of the nest!

Various aspects of this question suggest that OP is not asking about cuckoo/host interactions in general, but about research published in 2014 which appeared to show carrion crows (Corvus corone corone) in an area of Northern Spain actually benefitting from the presence of a great spotted cuckoo chick (Clamator glandarius) in the nest.
Unlike other species of cuckoo, clamator glandarius chicks do not "evict" the host eggs and chicks by pushing them from the nest. Furthermore, they are actually notably smaller than the crow chicks, making it harder to compete with them for food and host-parental attention.
Based on a 16-year dataset of observations, the researchers found that the average number of crows successfully fledged in a parasitized nest was $1.584$, versus $1.379$ for an unparasitised nest, suggesting an advantage to the cuckoo chick's presence. This particular cuckoo species had other hosts in the region, notably magpies (Pica pica), and no such advantage was observed for magpie hosts.
When attacked, chicks of this species could secrete

a malodorous cloacal secretion ... a mix of caustic and repulsive compounds, dominated by acids, indoles, phenols, and several sulfur containing compounds ... that are known to repel mammals and birds

The researchers conjectured that this ability bestowed a degree of protection on the other chicks in the nest, by repulsing predators and causing them to abort their attacks prematurely. Experiments showed that crows, raptors and mammalian predators were more likely to avoid meat that had been treated with this substance.
Other experiments were carried out, such as introducing cuckoo chicks to unparasitised nests and observing the effect this had on crow chick fledging rates, which appeared to support the aforementioned findings.
Based on this, the researchers suggested that this relationship may be more mutualistic than parasitic. To quote the paper:

We believe that the outcome of this parasite-host interaction may depend on predator pressure and thus fluctuates among parasitism, commensalism, and mutualism. ... It has been advocated that interspecific interactions should not be strictly categorized as parasitism, commensalism, or mutualism (21), because costs and benefits for each partner may vary in space and time, producing variable outcomes depending on the environmental context.

However, these findings have yet to be replicated. In particular, a study was published in 2017 in which another research group studied great spotted cuckoo parasitism of magpie, blackbird and common crow nests in southern Spain. They had four years worth of data for the crows, and eight for the magpies. This group did not observe the same benefits in terms of predator repulsion, or in the average number of fledged crows.
With regards to the secretions, they noted:

Great spotted cuckoo nestlings do not excrete the malodorous secretion when they are scared in the nest (personal observation), as does happen with hoopoe (Upupa epops) nestlings that are capable of throwing their faeces and cloacal secretions directionally against the predator [35], but only when they are grabbed (personal observation).

this secretion did not protect parasitized blackbird nests

direct evidence of a predator releasing a cuckoo chick is also lacking today. During nearly 30 years of studying great spotted cuckoos, we have ... never found any injured cuckoo fledgling in either magpie or crow nests.

the protection of crow nestlings would occur only in the case that predators attack the cuckoo chick first, which presumably would happen only in a fraction of predation attempts.

They also criticised the experimental methodology, claiming that the relative developmental stage of the introduced cuckoo nestlings did not match that which would occur in the wild.
The autors of the original study wrote a response in which they put forward counterarguments to some criticisms (for example, the same size in terms of number of nests being smaller in some years than others). In the case of the introduced-cuckoo-chick experiments, I am not entirely convinced by the counterargument, but am definitely not an expert in this field.
The authors of both studies agreed that further research with more data on different populations was needed.
In the aforementioned response, the authors stated:

Interestingly, a positive effect of the presence of cuckoo chicks on magpie nest success was reported in a different population in southern Spain (Sierra Morena) where carrion crows are rare and are not an important predator of magpie nests

However, the 1998 paper they cited in which this was supposedly observed is not available online (not even behind a paywall!) and so I can't offer any opinion on this. I have, though, looked at some of the other papers that cite it and have not seen any reference to this beneficial effect.
In summary, there may, depending on further research, be evidence that this particular cuckoo/host relationship has commensalistic aspects which are more significant than the parasitic. Or ammensalistic, if the differences in crow chick survival rates are not statistically significant. But this is not guaranteed, and future research with other datasets may show that the relationship is mostly parasitic.
Sources:
Canestrari, D., Bolopo, D., Turlings, T. C., Röder, G., Marcos, J. M., & Baglione, V. (2014). From parasitism to mutualism: unexpected interactions between a cuckoo and its host. Science, 343(6177), 1350-1352.
Soler, M., de Neve, L., Roldán, M., Pérez-Contreras, T., & Soler, J. J. (2017). Great spotted cuckoo nestlings have no antipredatory effect on magpie or carrion crow host nests in southern Spain. PLOS ONE, 12(4), e0173080.
Canestrari, D., Bolopo, D., Turlings, T. C., Röder, G., Marcos, J. M., & Baglione, V. (2017). Formal comment to Soler et al.: Great spotted cuckoo nestlings have no antipredatory effect on magpie or carrion crow host nests in southern Spain. PLOS ONE, 12(9), e0184446.
The Sierra Morena paper I couldn't find online:
Arias-de-Reyna, L. (1998). Coevolution of the great spotted cuckoo and its hosts. In: Rothstein S. I., editor. Parasitic Birds and Their Hosts, Studies in Coevolution. Oxford Ornithology Series, 9, 129-142.


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Can 'hardware' thermalization explain memory decay?
Often we are able to memorize very precise bits of information (exact addresses, birthdays of inlaws, number of dirty socks under the bed), but over time our recollection tends to become fuzzy. We no longer recall the day and month a certain president was killed, only the year, or maybe the decade (despite being straight A students in junior high). Like the smoothing out of a delta function under the heat equation, instead of a pin-sharp value we're left with a range of values where the correct one is likely situated. However, most of the time we are perfectly satisfied with such approximate information and can work with them just fine (except in some extreme cases of function impairment, such as Alzheimer's or the aftermath of binge drinking).
Discrete data must be stored in low entropy structures in the brain that over time spontaneously shift to a higher entropy state. Meanwhile, our biology tries incessantly to slow down the decay by expending energy (with the frequently utilized neural pathways being better maintained than the abandoned ones). Even processes analogous to error correction take place, e.g. when we arrive at a certain lost piece of information by lateral thinking and piecing together available data.
My question is whether the fading of memory exactitude can be explained in terms of the thermalization of the digital-like structures where discrete information is stored, and if anyone can point me to studies in this direction.

Interesting point, but I think there is a simpler and possibly more widespread reason for the decay of memories. Namely, as new memories need to be stored in the same neural networks, the weights, timings and other properties of the network links are constantly changed. In other words, there is competition for the limited amount of memory. This re-use of the same networks for multiple functions and memories is the same reason we have redundancy in our brain - it's also largely why they are as fuzzy in remembering as they are. And since memories are recalled associatively, the more connected two networks that encode different memories, the more likely it is that activations of one will activate the other. But that also blurs the boundaries between specific bits of information stored. It's a trade-off between fidelity of the memory stored and recalled and generality of the recall and associations possible.

Good point. There are various theories on memory loss but I wanted to address the problem of organic decay specifically, which seems prevalent in some situations. In particular, older people suffer from memory decay more than young people, even though they're arguably faced with less new information and the corresponding need to free up space is also smaller, so your argument doesn't provide a full explanation.

No, you are right, it doesn't. But we could extend the point I'm making to older people as well: they have a significantly smaller number of neurons so that while there may be less new information to deal with, there is also more competition from the memories previously stored.
Also, on a different note, it could be that there is memory decay due to a greater inability to sustain the current memories - for example, because of lower production of certain crucial cell-adhesion and receptor proteins.

Great, I'm not debating all these phenomena you mention, in fact they're all organic ways of decay, but let's look at how they are essentially able to turn digital values into fuzzy feelings of what the value should approximately be. I'm convinced that only a small, high-level, conscious part of the human mind deals works digitally as an emergent feature of a larger, fuzzy mechanism (without breaking it all the way down to quantum mechanics).

My understanding is that there are two major reasons for not being able to recall where your socks are or when your anniversary is:

The information was not committed to short term memory in the first place when you initially encountered it, so there was never anything to remember.
The information is intact, but you are not able to effectively retrieve it, because other memories compete and act as noise when you try to remember a certain specific one.

Neither of these scenarios involves actual loss of long term memory, which is more commonly a result of concussions, or other sorts of serious brain damage.

Discrete data must be stored in low entropy structures in the brain that over time spontaneously shift to a higher entropy state

How on Earth could you possibly know that? You are overextending physics to the workings of the brain and there is nothing that says this is necessarily so. Memory decay is not fully understood but it is known that the more features(i.e sound ,taste) are used when forming the memory and the more it is associated within an existing knowledge framework, the higher the chance that the memory will persist.

What exactly are you disputing exactly? Information is pretty much synonymous with low entropy (i.e. ordered) structure. E.g. a magnetic tape whose domains are collinear is seen as holding information, whereas a random distribution of the domains corresponds to no information. It takes a lot of data (i.e. high entropy) to describe a randomly ordered structure. Roughly, total degrees of freedom = useful information + entropy. Finally, the second law of thermodynamics states that entropy spontaneously increases.

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After doing brush I feel hungry?
Why I feel hungry after brushing my teeth in morning?
I usually have my dinner in between 9 to 10 at night and then I sleep at 12. Sometimes I wake up at 6 in morning and then I go to brush my teeth. After brushing my teeth I feel hungry. Why I feel hungry after brushing my teeth? And this hunger is gone even if I take few(about 5-10) biscuits.
Now one day I woke up at 6 am and then I have not brushed my teeth till 11 am and on this day I was not feeling hungry till 10 am.
So is there any chemical in toothpaste which triggers hunger? One thing which I can notice is that before doing brush there is saliva in mouth whereas just after doing brush there is no saliva or very less amount of saliva in mouth.
Even after chewing a gum for 30  min I feel the same hunger. So is there any relation between toothpaste and chewing gum?

Correlation does not imply causation. Furthermore, you have presented an anecdotal claim. Do you have any evidence this is a widely experienced event?

@Singh try to keep anecdotal experiences out of the questions - only if its a widely held belief or experience should you be asking the question

I think your daily pattern has made your brain associate brushing your teeth as a precursor of your breakfast. Skipping this step will confuse your brain into thinking it's not time for breakfast yet. Same goes for chewing gum, the toothpaste smell will trigger your brain's association of brushing teeth with the breakfast to come.

Sir I think you are right because when I was in school then my school timing was from 7 am to 12:30 pm but always I wake up at 6 am and after that I brush take bath then I get dressed and take my breakfast and then go to school. So the time in between my brushing and my breakfast is small and so I think you are correct. Thanks for your answer.

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Identification of a mysterious lifeform, what is this?
For the third time in a row, I found a mysterious life-form inside my house. I live in the Netherlands in the Eindhoven region, in a city called Oss near a forest area. Before I set it free outside, I put it in a jar to make a few pictures for identification purposes. What is this creature?

How big is this bug? Do you have a photo where the markings on the back can be seen better?

Wow, the site is getting bigger, we actually already have a question about this insect (or a very close cousin), voting to close as a duplicate.

@Chris The creature is about 3~4 centimeters long, including the legs. If I'd have to estimate the body, I'd say roughly ~2 centimeters. terdon; It does not seem to be the same one?

@terdon I think so, too. Its hard to say which one exactly from the images since the back is not clearly visible.


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Method for preparation of LB agar plates with Ag+?
I need a method for preparing LB agar plates with 1 mM concentration of AgNO3.
I can not seem to find a method online, does anyone know of one that I could use?
Here are my main questions regarding the method:
a. Do I add the silver before or after I autoclave?
b. do I add the silver in a liquid form for powder?
Thanks.

Why do you want to add silver ions to a agar plate? Besides this: LB medium contains sodium chloride - which will react with the silver ions and form silver chloride which forms an unsoluble precipitate. Additionally silver chloride is light sensitive and will stain the plate black eventually.

Yes, that is true. However, bacteria which are silver sensitive still can not grow on the plate given these conditions. I am in need of growing silver resistant bacteria on an agar plate, and this is the method in which I want to do it. AgCl precipitate will occur, however some Ag ions will still remain in the agar.

If you consider the solubility product of AgCl (which is around 1,88mg/L at 25°C) and the fact that you add 10g/L NaCl, I doubt that there are notable amounts of Ag ions present in the medium. Aren't there any protocols available?

What you could try (and what I did a few times with antibiotics) is to dry the plates and then plate the solution on top of the plate. Then the ions are at least available at the surface layer.

I have done this before. Although the amounts of silver ions available may be minimal, silver sensitive bacteria can not grow on the plates. I have tried concentrations from 1mM - 10mM. The plates were prepared by a different person in my lab. However, I can not currently contact this person for instructions.

Ok, practice beats theory here :-) Can you make a few plates where you add the silver before autoclaving and a few where you plate it on the surface and the compare it?

Sure, here is a picture of what I have seen in the past

Shoot it didn't work, just a sec.

https://docs.google.com/document/d/11qCvylNhwn1XQ_FDEPQZhsojjEmsHmY-6rxG3RJ86q8/edit?usp=sharing

Let us continue this discussion in chat.

You add the silver after autoclaving. Just make sure that you make your stock concentration of silver in sterile water to avoid unwanted contamination. Do it in liquid form; it is easier to dilute from a stock.

Yes, this is what I found to be the standard when working with silver

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Why did evolution fail to protect humans against sun?
Experts recommend that people apply sunscreen every two hours throughout the year, even in winter.
Especially phototypes I - III are supposed to be most vulnerable to harmful UV radiation, so especially these phototypes should take care to keep applying sunscreen and to use at least SPF 50. This, at least, is what European health agencies tell us.
Native to Europe are phototypes I - III. This means that these phototypes evolved in these precise conditions. Isn't evolution suppose to lead to best adaptations to the precise conditions native to the area an organism evolved in?
So, by this line of argument, phototypes I - III should be well-adapted to the levels of Sun radiation present in Europe. They should not have to use sunscreen there. When traveling to areas that are significantly higher in Sun radiation, such as equatorial areas, they may have to start using sunscreen - but not in areas they are native to.
Yet European agencies keep telling us that especially phototypes I - III should use sunscreen while in Europe.
Where is the error in my thinking?

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Skin cancer typically results from a lifetime of sun exposure, and is usually seen in older individuals. 90% of new melanoma cases are diagnosed in people over 45. Nearly 95% of melanoma deaths are observed in people over 45. Simply put, humans' currently level of adaptation to the sun is "good enough" - the vast majority of people do not have their reproductive fitness affected in any way by how they handle sun exposure. There is little selective pressure that would result in someone with better sun adaptation being more likely to pass on their genes. Evolution won't typically operate on traits that are only meaningful after reproductive age, as "selective pressure" refers to selection for reproduction specifically.
https://seer.cancer.gov/statfacts/html/melan.html

Although in species where parents and grandparents spend many years raising children, there's more selective pressure to keep them healthy later in life. Contrast this with species like spiders where the female eats the male after mating.

Where children need a longer period to become mature though, it's older siblings and the rest of the tribe who provide significant extra care.  Children really don't create an evolutionary pressure for grandparents to stick around.

@Barmar It's possible that pressure could even operate in the other direction - children without strong family structures may be less likely to survive, but more likely to reproduce. It's not hard to imagine that the child of a two-parent household might be less likely to experience teen pregnancy than the child of a parent who dies early and tragically to cancer. Social effects could actually select for unhealthy parents/grandparents in humans. I wonder what the net effect is.

@Graham While grandparents might not be directly involved in raising children, they often provide an advisory role to the parents, so it's useful for them to be around. Grandmothers, in particular, aid the mother during childbirth and afterward. While "it takes a village", grandmothers often have an outsized role.

@Barmar - I actually was going to comment what Graham stated; I don't see any evidence that selection pressure favors longevity in families at all. In fact, I saw something refuting that last night (I'm not sure where, but it did strengthen my suspicion.). It doesn't matter how many kids one has, which might be why you think grandparental childcare involvement selects for longevity. It doesn't. If you have evidence to the contrary, would you please provide it? Thanks.

Scientific American: The Evolution of Grandparents  @anongoodnurse

Longevity is probably selected for in some cultures, and against in others.  There's no reason to think one paradigm is true globally.

@Barmar - That does not support yopur position. Reread the article.

@Ryan_L Except in talking about cultures, you're looking at fairly short-term things. Evolution needs hundreds or thousands of generations to produce effects as significant as this.

I find your question to be fine for this site, and you've provided the asked for sources, so it's fair to give you an answer.

Where is the error in my thinking?

The error is in thinking that evolution is somehow directed towards the greater good. It's not. It's the result of random mutations.
Evolution doesn't make us perfect for the environment in which we evolved. We will never be perfect in any way, let alone every way. You're only addressing the risks of UV light, but people can come up with any number of imaginable "deficiencies" in humans that make us "imperfectly evolved".
That we're imperfect in no way means evolution has failed us somehow.  Evolution doesn't occur to select for perfection. Evolution doesn't happen for any "reason" at all, in that it's not directed by a goal; evolution simply happens because DNA is mutable.  If a mutation is harmless or beneficial in an environment, it will be passed on and likely persist. If it's harmful, depending on the degree to which it's detrimental, it will not be passed on. Sometimes in an particular environment, a mutation is both (e.g. sickle cell trait.)
If we're "good enough" overall to reproduce, if we're able to survive and pass on our genetic material, then that's what's going to happen, regardless of our perceived imperfections.
Also, somewhat aside to your question are the benefits of UV light to humans. We know that UVB allows us to synthesize Vitamin D, which is critical for survival. There are other possible benefits to UV light as well. It might well happen that we'll discover more concrete benefits.
The question which has been linked to as a duplicate discusses evolution in more detail (and more helpfully). This is only a fairly quick answer.

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Besides the arguments already mentioned in the previous answers, the human body has developed numerous ways to protect itself from the harmful effects of sunlight and ultraviolet (UV) radiation.

Melanin Production:
Melanin is the main pigment in the skin that absorbs UV radiation to
keep it from damaging its structure. So, if the skin is exposed to UV
rays, it is going to make more of this pigment, making the skin
darker, or tanned, which is a way of a protective response to the
deeper layers of the skin from getting damaged. This process helps absorb and dissipate UV radiation, reducing the risk of DNA damage that can lead to skin cancer.

Epidermal Thickening:
Another defense mechanism is the thickening of the outermost skin layers (epidermis) in response to UV exposure. This thickening serves to attenuate UV penetration to deeper skin layers, thus providing an additional barrier against potential damage.

DNA Repair Mechanisms:
The human skin protects its genetic material from being damaged by
DNA repair. These mechanisms are the body's way of dealing
with and repairing UV-induced damage by the sun. This includes repair mechanisms like the photolyase repair mechanism, which specifically repairs pyrimidine dimers of the DNA which are generated by UV exposure.

Inflammatory Response:
The acute response to excessive UV exposure is sunburn. This reaction is part of the body's inflammatory response, which serves to alert the immune system to potential damage and initiate repair processes.

The best natural sun protection is melanin. But melanin makes it harder for the skin to produce vitamin D. In places with lots of UV radiation black skin is an evolutionary advantage, and the weaker vitamin D absorption is no big problem because there is so much UV radiation.
Now if you live in northern areas, your sun protection isn’t as good as it could be, but lots of melanin would reduce vitamin d absorption too much, because there isn’t enough UV radiation around. So there is a balancing act: Better sun protection would hurt your health in different ways.
Also careless sun exposure was very much a thing say 1980 to 2000. Many people have wised up to the dangers and will avoid roasting themselves on the beach. So hopefully cases of cancer etc. will go down in the future. And health agencies are much more risk averse nowadays, and to some degree they have to because people get older and more survive to an age where skin cancer actually hits them.

Sources to support your opinions?

I think the answer has to be something like this. There must be a reason why those of us with pale skin lost our pigmentation so quickly, and that means there must have been an evolutionary advantage to being pale in temperate regions that offset the disadvantage of being more susceptible to skin cancer.

@N.Virgo The distribution of melanin correlates with the geographical height. People have a lighter skin tone the further north you come. Increased Vitamin D production might be the reason.

There are some excellent answers already referencing melanin. I used to live in the Solomon Islands, and noticed that the people from the West of the islands, and also in the East of PNG were much darker than the neighbours: in fact they were among the darkest people I ever encountered anywhere in the world. I found this article useful: The Case of Melanin in Melanesia. It includes a map showing ultra violet levels, and it is quite clear that the high UV levels are correlated with the regions where skins are very dark.
I recall Tim Flannery writing (alas, the book was lost during a move) that there are reefs in that area of the Western Solomons with an abundance of seafood, but that the optimum time for harvesting was also the peak for UV, hence greater selection pressure for melanin...

To add to other answers, there have been behavioral changes in many societies with paler skin phototypes that have increased the risk of skin cancer. Laying on a beach or in a park to get a suntan is an activity that's only become common in recent decades, for centuries Europeans avoided working outside around the midday sun during summer (such as sleeping in the shade) and when working outside wore clothing that covered up most of the skin along with wide brimmed hats or other head covering (have a look at typical medieval peasant dress). That was enough to mitigate most of the risk of skin cancer, but not in more equatorial countries.

And yet we have the song: Mad Dogs and Englishmen go out in the Midday Sun.

@SimonCrase a phase coined by Rudyard Kipling, so fairly recent all things considered.

One could theorize that migrating to colder climates required having warm enough clothing to survive winters there.
With more protective clothing, melanin production was a waste of energy and actively hampered vitamin D production in an area that already had lower UV radiation flux

@Crazymoomin Do you have a citation for the Kipling claim? It floats around on the Internet, but the closest I can find is this one from Kim "Only the devils and the English walk to and fro without reason...and we walk as though we were mad — or English.” All the evidence I've seen points to Noel Coward.

@SimonCrase Not anything better than you have found. However attributing it to Coward instead makes the argument for the recency of such behaviour even stronger!

Because cancer wasn't likely to be one's cause of death. Look at this comparison between 1900 and 2022:

Cancer used to be the cause of 5% of human deaths. Nowadays its at 24% thanks to us conquering diseases like tuberculosis and influenza. Similar data is available for the UK in the 1850s:

Cancers were relatively rare. While the Victorians did not possess sophisticated diagnostic or screening technology, they were as able to diagnose late stage cancer as we are today; but this was an uncommon finding. In that period, cancer carried none of the stigma that it has recently acquired, and was diagnosed without bias. For example, in 1869 the Physician to Charing Cross Hospital describes lung cancer as ‘… one of the rarer forms of a rare disease. You may probably pass the rest of your students life without seeing another example of it.’

Evolution can't solve every problem all at once. Cancer was simply too far down the list of causes of mortality for it to enact sufficient evolutionary pressure. We also have evidence from the Tasmanian Devil population showing that immunity to certain types of cancers can evolve very quickly if necessary:

Devil facial tumour disease (DFTD) is an aggressive non-viral clonally transmissible cancer which affects Tasmanian devils, a marsupial native to the Australian island of Tasmania. The cancer manifests itself as lumps of soft and ulcerating tissue around the mouth, which may invade surrounding organs and metastasise to other parts of the body. Severe genetic abnormalities exist in cancer cells—for example, DFT2 cells are tetraploid, containing twice as much genetic material as normal cells. DFTD is most often spread by bites, when teeth come into contact with cancer cells; less important pathways of transmission are ingesting of infected carcasses and sharing of food. Adult Tasmanian devils who are otherwise the fittest are most susceptible to the disease. DFTD is estimated to have first developed in 1986.
...
In 2016, devils are endangered as the localised populations were shown to have declined by 90 per cent and an overall species decline of more than 80 per cent in less than 20 years, with some models predicting extinction. Despite this, devil populations persist in disease-stricken areas. The devils have, in a way, fought back the extinction by developing the gene that is immune to face tumors. The genes have already existed in the Tasmanian devil as part of their immune system. They increased in frequency due to natural selection. That is, the individuals with particular forms of these genes (alleles) survived and reproduced disproportionately to those that lacked the specific variants when disease was present.

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Do all Fungi have similar cells?
I know that most fungi are not differentiated into tissues. And tissues are groups of specialised cells aiming to perform a collective function. Does it, then, follow that most fungi do not have distinct cells for distinct functions, and that all their cells are essentially the same? I am slightly skeptical of arriving at that conclusion; but if it is true, then I believe that it would be reasonable to say that there is no difference between the cells that give rise to spores and those who don't. How is it possible, though, for cells to be structurally similar but capable of performing varying tasks?
To summarise,

Do tissue-less fungi have no dissimilar cells and all are exactly the same in all respects? I believe that the answer to this question would also be applicable to other multicellular organisms as well.
Can it be possible for two structurally similar cells in fungi to be adept at two different tasks? This too seems to be extendable to incorporate all other multicellular organisms.

No. Only a small group.

@Marzipanherz I did not know that. My textbook didn't mention it, perhaps to be in accordance with the naive standard that I happen to be with respect to the study of Biology. I think I should edit my question to reflect what you made me to learn.

@Marzipanherz Done. I hope it's answerable now. Thanks for feedback. :)

@MartinKlvana I would be very grateful to you if you could add a full answer. It's been days and there's no answer still. Thanks :)

Months now......

More than 2 years now... I'm still waiting.

You are an unusually patient and (gently) persistent user!


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Do ant pheromones indicate the direction to go?
I know that ants communicate with pheromones but I am wondering if these pheromones can indicate in which direction to go. For example the ants leave pheromones to indicate a food source and when they find food they eventually create a "highway" of ants running to the food.
If I disturb the ants while they're going to the food source in such way that they don't know anymore in which direction is the food will they choose a direction randomly (nest or food) or will the pheromones also indicate in which way to go to get the food?

I think the ants usually start at the nest and they know which way is away from the nest.

I guess they know where they're going depending if they have collected food or not, that's why I specified "If I disturb the ants...". For example if I blow air on them so that they fly away 15-20cm so that they are close enough to the pheromone trail to get back on it right way but since they flew in the air they have no idea about the orientation they're looking compared to before I blew on them.

@shigeta is correct.  Trail disruption is actually a method of controlling ant populations.
For an example, see http://www.ncbi.nlm.nih.gov/pubmed/20077128

I have ants in my kitchen and this is a reproducible result :)

Great ! Now I have to apply this in my house...

Pheromone sensing in ants is pretty cool.  The results from this paper indicate another way of potentially controlling ant populations on a larger scale (similar to introducing sterile insects): http://www.cell.com/abstract/S0092-8674(12)00523-5?switch=standard

Of course, that sort of control is far off, and what the paper really shows are the channels mediating pheromone detection and somehow, courtship behavior, in fruit flies.  Also, look up "male-male chaining in Drosophila" on YouTube.


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Why don't all ants have wings?
Since the new queens-to-be have wings, it means that ants either evolved from insects that can fly, or insects that can fly evolved from ants, or that we have a case of parallel evolution (which is unlikely).
Now, what evolutionary benefit is there to not have wings?

I think, "common" ants just don't need wings for their daily life... Here you can find the reason why males and females have.

I know why the wings exist to begin with, thus the exact wording of my question.

Sorry then, I misinterpreted you. Though in this case I guess your question is rather philosophical... Maybe it's because of the principle of laziness: don't do what you don't have to do.

Certainly ants evolved from insects that could fly.  All the earliest wasps (ants are specialized wasps) could fly.
Building and maintaining wings is expensive in terms of energy.  That's an obvious evolutionary advantage to not having wings.  So if there's insufficient benefit from having wings then there's selective pressure against having wings.

You could say that ants evolved the ability of having wings only when needed

Building on Noah Snyder's answer…
Having wings could also be expensive in other ways. For example, energy aside, maybe the growth of wings relies on some special nutrients, which were scarce in the environment of the first ancestors of modern ants. So the ant colonies that grew smaller wings (or no wing at all) thrived.
Having wings could also cost them their lives. Maybe the workers in ancestor colonies used to be small and had a tendency to get stuck in spider webs (not having enough in-flight momentum or brute strength to break off the web), and somehow the queens and drones are less affected (because they don't tend to go to the same places as the workers to begin with, maybe; but that's unlikely: I see plenty of queens stuck in spider webs in Hong Kong in the mating season).
In fact, I believe the nutrient-driven path is quite likely. When you think about it, there is a huge behavioural component to this trait. If I remember correctly, all female ants are equal at birth. Whether a certain female becomes a worker, a soldier, or a queen depends on what it is fed as it develops. So the scenario could be that some ancestor colonies arrived in a place that didn't have an abundance in nutrients for wings. Some of those colonies tended to reserve the said nutrients to the reproductive casts (queens and drones), and this strategy proved successful, so the trait got amplified over time. So it becomes a matter of less wings, not smaller wings.

To add to that, one other factor which may have prompted the evolution of winglessness is competition and niche differentiation. The ancestors of ants were winged predatory wasps, and the first ants were also predatory, but wingless. There could have been an advantage in specializing on ground-dwelling prey, which could have been more efficient to hunt/handle for wingless individuals.

When is it good to have wings?
When you need to move a great distance in as short a time as possible with minimal risk.
Clearly wings would have enormous benefit at a time when you need to get far away from the nest really quickly, perhaps at a time when you believe the weather would be particularly favourable. This benefit increases exponentially when procreation is involved.
When is it bad to have wings?
Almost any other time.

When it is raining.

Rain and wings just do not go well together. If you get hit by a raindrop while wearing wings you are basically stuck where the drop lands until it evaporates completely.

When it is windy.

I rest my case.

When you are under attack.

Agility, while wearing wings, just cannot be considered one of your evolutionary advantages.

When you are trying to gather/carry food back to the nest.

Surely an ant trying to carry a piece of a leaf, however small, would consider wings a severe burden.

When times are hard foodwise

The protein investment in wings would surely be better spent on survival when food is scarce.

Encounters with birds suck

Wings make you incredibly easy to grab hold of in mid-air, unless of course you can shed your wings when stressed, and many ants can (while obviously butterflies and moths cannot).
Wings or No Wings?
Surely my arguments suggest that having no wings would be a serious advantage in almost any situation except on the rare occasion when you need to move a long way really fast. Clearly the ant has an amazing skill to only have wings when they are needed and not at any other time.
Added after a number of comments
You have to remember that much of an ant's work is maintaining the colony as a collective. Preserving its cohesion, feeding the young, caring for eggs. The whole point of having a colony is to have far fewer individuals spread out, in danger, gathering food. This is to reduce the risk of complete colony death, which is essentially the death of the queen and therefore the gene pool of the colony.
You have to look at each ant colony as a single individual when you look at them on an evolutionary scale. In this way the life or death of one, or even 1,000 ants is not important, it is the survival of the colony. From this perspective, wings are dangerous for all my reasons above. The only time they are of value is during diaspora and that is the only time ants have them, which I think is incredibly clever.
Evolving a detachable appendage to an ant is like humans evolving detachable breasts at menopause. An astonishing achievement even humans have failed to achieve.

It could easily be good to have wings when under attack - if you can fly away from a conflict that's a whole extra dimension of escape routes compared to those available to a flightless animal.

Many smaller winged insects use the wind to aid dispersal, see this paper for example. Wings are extremely useful in many situations, hence their evolution despite the major energy investment.

Also flying could easily improve foraging or hunting success at a greater rate than the increased protein cost of growing and maintain wings. Unless you can provide some referenced support for your reasoning I think I disagree with almost all your points, so -1

@RichardSmith - I thought we were talking about ants. Flying away is a huge negative in a "Colony" species.

@StephUnna - Wind dispersal would only be of value during a diaspora. At any other time, wind would just scatter the colony.

@RichardSmith (Also ...) - If they could evolve to fly in formation, thus preserving the colony then I would agree. Keeping together is much easier when everyone walks and you can smell/taste where your colleagues have been.

@OldCurmudgeon it wasn't clear until you added that last section that you were only talking about ants; it sounded like you were making general statements about when it's good to have wings and then specialising the case for ants.

@OldCurmudgeon and all your points about colony living being better without wings are disproven by wasps and bees, which have the same colonial constraints but retain wings throughout their adult life stage.

@RichardSmith - Wasps and bees are what ants would become if they had wings. Wings would enable them to feed off the far more cost-effective nectar and pollen rather than the leaf cellulose they actually feed on. Essentially, if ants had wings we'd call them bees.

That's my point exactly - your arguments for wings being bad for ants either apply equally to wasps/bees and are therefore invalid, or would only apply once ants had lost their wings, and therefore don't explain why they don't all have them.

@RichardSmith - interesting discussion - my arguments do not apply to bees because bees, although still a colony species like ants, feed primarily on nectar and pollen, a much richer foodstuff that can support powerful and robust flying mechanisms and sufficient brain power to find your way home and communicate 'good' locations. Ants feed primarily on the cellulose of leaves or what fungus breaks it down into. This is an energy-poor foodstuff that cannot support the energy required to fly[citation needed].

@OldCurmudgeon so you're assuming the move to leaf cellulose as a food source must have predated the loss of wings - if not, there was another driver for loss of wings. You're right about one thing: [citation needed] :)

Note that ants communicate the location of important places (like food source) via pheromone trails. It's not possible to follow pheromone trails while flying, so they couldn't use flying for foraging.


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What happens to an ant colony when the queen dies?
Does the colony collapse? Do workers keep following the last orders? Or can future queens replace the dead one? I'm guessing this might also depend on each specific sub-species.

Not ants unfortunately, but with bees if the queen dies the workers start rearing some larvae under queen-developing conditions. They're not normally as effective as 'proper' queens and you might end up with several at once, but you get something. Leaving this here in case someone feels like looking up whether similar processes occur in ants (although if I get time to I will try to do it myself at some point).

http://www.antweb.org/antblog/2010/12/can-ant-colonies-reproduce-and-sustain-with-no-queen-angela.html has an interesting answer (basically, they struggle but should survive by turning workers into temporary queens). That said, I'd like to have community experts confirm this, or detail whether it's species dependant before making it an official answer.
@arboviral: looks like it works just like bees if this is true.

Does your second question assume ant workers follow orders given by a qeen? I am not an ant specialist but how would that happen physically?

@BagiM: not sure if I've imagined this or read it somewhere, but I thought pheromones were used to spread general orders, influencing behavior throughout the colony.

Not really my field, but I can point to this review which discusses a couple of different ways in which ants organize their communities:
Heinze. 2008. The demise of the standard ant (Hymenoptera: Formicidae)
I know that in some species there can be several queens per colony (so more robust to queen deaths). In many species, workers can start laying eggs if the queen dies, but these will develop as males (since they are unfertilized). However, in some species (e.g. Platythyrea punctata) the workers can reproduce by parthenogenesis which can stabilize the colony to some extent after the queen dies.


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Why do ants dig surface paths?
A few days ago I observed a corridor built and used by ants that went over a path in fields:

Why do they build it? It seems it doesn't bring any considerable protection from the surrounding environment and it certainly costs them a lot of work.
The picture was taken in the morning when the temperature was low so there is no ant activity visible.

How is that "protected"? It looks to me like there is a natural "cliff" which the ants are simply walking along.

@terdon No, I'm quite sure they built it for some reasons. I've seen many of these structures on that place. You're right, I don't know if it's for their protection or for anything else.

I mean I do not see any protection. Since there is no wall on the "southern" side, there must be a difference in altitude between the "north" and "south" areas pictured. If the ants were creating this path by walking down it, there would be walls on both sides. At best, perhaps the ants created the path just by walking down it, if there is a difference in altitude that is exactly what would result with no active effort from the part of the ants other than the act of walking. That is how paths are formed after all.

@terdon The location is completely flat, and the ants walk inside the structure, so they're covered from both sides. Most these structures have only the side walls, but it looks like this one is being covered from the top as well at the ends. I'll try to find the place again to see if they'll eventually cover the whole path.

Well, that's the thing, It can't be flat, if it were there would be no wall or the wall would be higher than the surrounding area which is not the case. The overhang would be created naturally by the ants' walking down the path and does not imply that it was done on purpose.

@terdon The surface that surrounds it flat, the structure is not. I'll try to make a better picture.

I wonder if this might be an extension of nest-building behavior.  the dirt that runs along both sides of the path looks like debris from nest cleaning.

It kind of looks like there is a wall on the bottom side but it's really hard to see the edge of it as it blends in, making it appear flat.

I don't have it with me, but the book Adventures among Ants by Mark Moffett, which I highly recommend if you're even vaguely interested in ants, describes the creation of paths such as this. Some ants apparently build underground "highways" of a sort, and such a sunken path is indeed an intermediate step in the construction of such. I can't remember the specific reasons given in the book but I expect protection (if not from the elements, then from other insects and rival ants in particular) and efficiency (it minimizes ants wandering around for that bit of their journey) would be involved. Given how short the path in the photo is it might also be an underground path that the ceiling caved in on for a section.
I am not saying that this is what your photo shows, or even that the ants you were looking at typically make such paths, and I realize that I am technically not even answering your question, but I hope that a confirmation that this is a phenomenon that happens and the recommendation of a book that will answer your question is a decent start.
EDIT - Found the book !
The ant species described in this section is the Marauder ant, a species from India so probably not the one you saw. But the motives described in the book could be transferrable. A few quotes from the chapters "Roads" and "Defense":

Marauder colonies maintain a fast, steady, well-protected flow of food and labor on their trails. Whereas small ant colonies, like people in small societies, are able to access and distribute the supplies they need without roads, larger groups depend on an infrastructure so complex that in the marauder ant it rivals human highway systems.(...)
Marauder colonies avoid both gridlock and species confrontations, like that with the Diacamma worker [an encounter described at the beginning of the chapter where killing that errant worker of another species involved major disruption in the flow of traffic], when trails are in good shape. Highway construction efforts are part of the society's logistics, providing supply lines for fresh combatants on the front lines as well as streamlined routes for bringing home the plunder[2]. Trunk trails are well looked after - that's how they can be distinguished from the fleeting paths created by raids

The note after "plunder" points to the following:

The lower cost to ants of sticking to clear paths rather than going over rough ground is addressed in JH Fewell 1988, Energetic and time costs of foraging in harverster ants, Pogonomyrmex occidentalis, Behav. Ecol. Sociobiol. 22:401-408.

A description of the building of the trails, which matches some of how the picture looks like:

Each worker size class participates in the creation of the roadways. All the castes eliminate surface irregularities along a trunk: while the medias[medium-sized caste] and majors[big ones] chisel out embedded roots and pebbles, minor workers[little ones] extract grains of soil, establishing the road's slightly concave shape in cross-section. The dross is discarded along the edges of the trail, where it accumulates in embankments(...). When the ground is moist, the minor and media workers build up the ramparts into a complete soil cover, or thin-roofed arcade, fabricated from soil extracted from the trail surface or from mining shafts - blind-ended tunnels near the trail used specifically as quarries.

Giving some reasons for their existence:

To what use is all this effort? Not, it seems, as protection from the elements. The earthworks fall apart in rain, and disintegrate when the earth is dry. Arcades are thin enough to puncture with a tap of a finger, which means a route is weatherproof only when it travels through an underground tunnel, perhaps dug and then abandoned by other animals. Alternatively, near the nest the ants may make a subterranean route of their own: over time, construction crews can scratch away so much soil from the trail surface that the highway sinks from view, at which point the ants seem to be able to construct a thicker, rainproof cover that becomes flush with the surrounding land.
The main function of this relentless building is defense. Because trunk trails extend for dozen of meters, they travel through territory controlled by other ant species. Marauder ants must therefore be organized to protect the trunk trails from aggressive neighbors or even from hapless passerby such as the Diacamma.(...)
...after an arcade has been completed[,] the Diacamma workers could now walk over the trunk trail, blissfully ignorant of the industry below them. if a trail should sink underground, it is as protected as a passage in an army bunker, safe even from human footfalls.
Bulwarks constructed over trails and provisions prevent battles among competing marauder ant colonies as well. Where they are absent, combat can last a day and engage thousands of minor workers, which pour along the line of contact between the armies.

Are there trees ? The only thing this seems to stop is leave litter and small grains from blocking the path when there is a slight breeze. They build other structures for rain and seem to build less of these where there is shade and more where there is sun and nothing much to eat or hide under. But thats just from a few observations walking larve areas. When ita going to rain they take sticks and thing and make a cone structure around the entrances. Initially the just clear paths and collect food. Thats from the karoo eastern cape south africa, dry lands with large areas that get really hot and some patchs with trees (acacia karoo, thorn tree small leaves) have more ants.


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What kind of spider is this, please?
I've found this spider in my bathroom today, never seen one like this, especially since I'm living in part of Europe ( Bosnia, Balkans ) that isn't known for being promised land for spiders. This one was somehow aggressive, when I touched him with an object, he immediately launched himself from the roof using his net, and when landed, he raised his "bottom"?! I've sprayed him with some water, and removed him as seen on picture, didn't want to kill him, but I'm interested if this is some venomous kind, because his head was blood red, and I've never seen this in my region

To me it seems to be an Araniella Cucurbitina ,also called a cucumber spider. It grows upto 4mm to 6mm. This type is native to the UK and they have venom which is not considered dangerous to humans.

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looks more like a kind of sac spider to me


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Evidence of condition-dependent sex-allocation in regards to humans
Coming from zero background in biology, I am looking for expert opinion on evidence regarding Trivers-Willard hypothesis (1973) and humans.
In short the hypothesis states that
if

"Condition" of offspring during their whole life are correlated
to that of their mother during pregnancy
Males have better on average better reproductive success (more genes in next generation) than female when in "good condition", and vice versa if you compare male/females in "bad condition".
Females objective is "eventual reproductive success" down the
generations.

Then it makes sense for females to vary sex ratio, more males when in "good condition" and more females when in "bad condition".
I think it is safe to say that plenty of evidence exists on assumption one. The second assumption seems more nuance in todays environment, but one would imagine that during most human history it does hold true. On the third one I think is safe to assume it is true based on the theory of evolution by natural selection.
Any (rigorous) reference (articles, researchers, journals) or comments would be superb!
Reported association that I am already aware of are:

Reduced gender ratio at times of war and famine (Ansari-Lari & Saadat, 2002; Song, 2012; Valente, 2015) and after natural disasters (Fukuda et al. 1998).
Darwin (Descent of man); Norberg, 2004; Almond & Edlund, (2007); Hamoudi & Nobles, (2014) divorce or "unmarriedness" correlated with lowered gende ratio.
Negative association between parents age and gender-ratio,  Jacobsen, Møller, & Mouritsen, (1999).

Have you looked at http://www.ncbi.nlm.nih.gov/pubmed/?term=trivers-willard+human+%22sex+ratio%22 ? -  although  see @Remi.b's comments about statistical issues ...

Yes, I've looked around but have not found anything that seems to settle the debate. But most things I find point towards the same direction as Trivers-Willard. For example: http://humrep.oxfordjournals.org/content/13/8/2321.short

Interestingly Darwin had spotted a pattern: excess of male over female births is less when they are illegitimate than when legitimate - The Descent of Man

@snoram Be sure there has been a lot of work on the evolution of sex-ratio since Darwin made this claim. You could start with West and Sheldon 2002 for a review but you will very likely have to start with a very introductory course to evolutionary biology (such as Understanding Evolution for example) as you were unfamiliar with the term 'fitness'.

The paper you link to does not mentions humans specifically, but they state "the extent to which data on mammals fit this prediction is disputed". I wonder how much that has changes since 2002.

I am not aware of any such evidence in humans but I know little about this literature. If you happen to have data showing that, then it would probably be a relatively big thing! Below is a series of comments that might be of interest.
Evidence from Hyena
The evolution of the sex-ratio variation in hyena have been quite extensively studied. This very short article (not peer-reviewed) cite a number of key papers on the subject.
Logic behind the second assumption
In case clarification is needed. The variance in fitness is indeed often higher in males than in females. The reason is that females (by definition) produce the larger gametes, the one that don't leave the body and therefore often pay a much higher cost when reproducing than males do. As such, females are the limiting factors. As a consequence, males compete a lot to access females and "good males" receive a lot of mating opportunities while "bad males" receive little mating opportunity causing the higher variance in fitness among males than among females.
Statistics
IMHO, there is a tradition of horrible statistics when dealing with human sex-ratio data. It is particularly the case as these papers are often published in journals where reviewer have little knowledge in statistics (e.g. medicine). Typically, "windowing" data is generally a very bad idea and previous papers in the field have reported very bad interpretation from data due to cherry picking specific ways to classify observations. Please be cautious in your statistical analysis!
About the post
The formulation of the hypothesis is clear enough but some sentences are misleading

it makes "natural selection" sense for females to vary sex ratio`

This sentence sounds very wrong. You should rather say "females that are able to vary the sex-ratio among their offspring will be have a higher fitness".
Note that I said "among their offspring" because while this would cause variation in sex-ratio in the population, genotypes are selected based on their ability to vary the sex-ratio among their offspring and not in the population. In fact, any given individual, would appreciate if all the other would produce the exact opposite sex-ratio than the one they actually produce among their offspring.

better chance of reproductive success

This sentence a little clumsy as well and should be replaced with higher fitness

Great. Thanks! But not sure I understand your last comment "replaced with higher fitness". The second assumption (as I understand) is that at some point on the "fitness scale" males start to have a reproductive advantage over females.

You are misusing the terms "fitness" and "reproductive success". reproductive success is the realized number of offspring of an individual for a chosen duration (often the whole life). Fitness is a function of survival and reproductive fitness and is generally defined as (but might differ slightly from one model to another) the expected lifetime reproductive fitness of an individual. Therefore "Better chance of reproductive success" translate into "higher fitness" and we usually use this expression.

Fitness just means good health. Agreed? (I checked the dictionary). By saying "better chance of reproductive success" I mean exactly higher expected number of offspring.  Good health causes "Better chance of reproductive success" not the other way around.

You are getting confused with the use of the term fitness in the sense physical fitness and in the sense "biological fitness" (which is just termed "fitness").  In evolution, "fitness" does not mean "good health". In evolutionary biology we sometimes talk about "overall health" of an organism (which would mean something like "physical fitness") as an extremely multivariate trait that is eventually (but not necessarily) a good proxy for fitness.

I will do some small edits to my original posts based on your comments. But to clear I never used the word "fitness" (nor do Trivers and Williard) and use instead "condition" for something like "physical fitness".


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How high into the air are spores of molds commonly occurring?
I understand so far that most of the air surrounding us contains mold spores so that given the right environment and a food source they start to grow. I assume this is true for air close to the earth. But how high mold spores are still common?
To clarify: I don't want to grow mold, I want to know how high into the air on earth mold spores are usually common.

You can grow molds in space if you give the right condition. You need to add details to your question; details about different parameters that you want to consider. Are you asking about natural distribution of fungi?

You can have a look at this article.

@WYSIWYG: Seems this article checks for the distribution of fungi growing at the ground in mountain-areas with higher altitude. I'm asking for the spores distributed through the air, to which altitude above ground they are still available.

Air currents can carry bacteria and mold spores into stratospheric altitudes.  Early balloon collections found bacteria and mold in air samples at a little above 71 thousand feet altitude.  There were only a few colonies, but we also know that our bacterial media often do not allow many microorganisms to grow.
More recent studies of the atmospheric microbiome have indicated that a wide variety of bacteria and fungi can routinely be found in the atmosphere thousands of feet up.  Modern measurements find about 10 million living microbes per cubic meter.
Sandstorms or jet streams are known to be able to move living bacteria long distances.  Spores are often of about the same size and I see no reason why we will not find that they do the same.

I remember reading in an HHMI bulletin about a rate infectious disease in babies. Apparently the pathogen is carried by seasonal air currents over very large distances. I am trying to remember more details.

Ohh yes. It is the Kawasaki disease but the hypothesis is still open as the causative agent is not yet identified.

Small addition: This article talks about Aspergillus spores being carried to Caribbean from Africa, by dust storms. However it also mentions that that dust free wind does not have spores. Perhaps you would like to add this in your answer.

Stratospheric altitudes sounds scary. Anyways, for all europeans like me: 71000 feet = 21640 meter.

thanks @Mnementh - i should convert everything to metric but I was lazy and just copied the reference

No problem, different countries have different units. This needed only a quick Google, Google puts that on the result-site. I added it in the comment for convenience.

forgot to say thanks for the additions @WYSIWYG - helpful as ususal!


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Recommendation for a molecular biology book that explains how we know what we know
My background is in math and I know very little about biology.  The few biology books that I've looked at seem to explain what is known (or what is believed), but don't really explain how we know what is known.  For a specific example, when I hear that "DNA makes RNA and RNA makes protein", I would like to know things like:

How do we know that DNA makes RNA?
How do we know that RNA makes protein?
How do we know that there is such a thing as "protein" in the first place and how do we know what it is?
How do we know that there is such a thing as RNA and how do we know what RNA is?

Can you recommend any books that do a good job of explaining how we know what we know in molecular biology and genetics?

so basically you want a biology textbook and possibly a book about the history of cellular biology. You may want to google Francis Crick and the origins of the "Central Dogma of Molecular Biology" which is will show you how transcription (DNA->RNA) and translation(RNA->protein) were discovered. This slideshare will help you with proteins, https://www.slideshare.net/sabarnisarker/history-of-protein-discovery, The trick isthese are not single discoveries but a series of many many discoveries and experiments building our understanding.

The following wikipedia articles give an overview on the various discoveries that lead to our understanding of genetics. https://en.wikipedia.org/wiki/History_of_molecular_biology
https://en.wikipedia.org/wiki/History_of_RNA_biology
https://en.wikipedia.org/wiki/History_of_genetics

@John Those slides about the history of protein discovery are great, thanks.

@Adrian Thanks, good to know about.  While learning the history of the discoveries can be very enlightening, and might be the best approach for me, I'm not only interested in how it was done historically.  What I would most like to know is, in hindsight, what would be the simplest or most direct way to go about discovering these things.

Just about every molecular biology book that I've seen covers the basics of the history, including providing answers to your questions, via a summary of landmark experiments in the field. I've always fantasized about teaching a "History of Molecular Biology" course, where we read the original papers, but I'm neither employed as a university professor nor confident that others would find that anywhere near as interesting as I would.

You may want to try A History of Molecular Biology by Michel Morange, it is currently in its third edition, It will not cover everything (proteins are discovered much earlier), you are asking for a wide swath of biology, but it should get you started.
The Eighth Day of Creation: Makers of the Revolution in Biology is also a good read.  It is also funny to hear Crick bemoan his misuse of the word dogma that has been immortalized by his discoveries, he used it in the title becasue it was "catchy".

As a master of science in molecular biology. I would recommend getting the two books.
Biochemistry by Stryer
Molecular Biology of the cell by Alberts et al.
Those two together are the course books used for several semesters worth of molecular biology and biochemistry, covering the central dogma plus quite a lot more. They are very well referenced and are worth every penny.

While I'd agree to some extent (I know them well; we used both at undergrad), I think OP wants a book which actually describes and explains the key experiments in terms understandable to a relative newcomer, rather than simply referencing them.


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Function and Characterization of poly(T) and (AT)
I came across three terms; "poly(T)45", "poly(A)45" and "(AT)15". Can anyone explain what they are? I know the number refers to strand length, possibly poly-T is a strand of thymine monomers and that ss(AT)15 refers to a 30-base (dAdT). I assume this refers to a single that looks like this;
dAdT-dAdT-dAdT...repeated 15 times.
In that case, what is the d?

Did you try finding an answer? Please share it and see our homework policy. Homework is not implied to be Home assignment only. Thank you.

Homework tag and explanation added

Poly(T) is an oligonucleotide with only repeating thymine residues. These are generally used as primers in Reverse Transcription PCR, as mature eukaryotic mRNAs have a Poly(A) [adenosine] tail added to them as a post transcriptional modification in order to protect against mRNA degradation. You would also sometimes see this referred to as an oligo dT. It could also be the primer for some paired end adapters used in next-generation sequencing (NGS)
The 45 generally would indicate the number of residues in the oligonucleotide.
Poly(A) could be a primer for a paired end adapter for NGS, however I would need to see the context of where you saw the terms to be sure.
d = Deoxyribonucleotide, in other words you are dealing with a DNA oligonucleotide (though Thymine is also an indication). Technically the d refers to the 2' Carbon on ribose having a hydrogen instead of a hydroxyl attached to it making it deoxyribose.
Without the d it is a Ribonucleotide, indicating that you are looking at an RNA molecule and that the 2' Carbon on ribose has a hydroxyl group.
You will sometimes also see ddN (N for any base). This indicates a chain terminating dideoxynucleotide which has a hydrogen on both the 2' and 3' Carbon instead of hydroxyl groups. The reason this molecule is chain terminating is because you need the 3' hydroxyl in order to link to a 5' phosphate group to form a phosphodiester bond, which is needed to continue the elongation of the nucleic acid molecule.
As for the ss(AT)15, I think you are correct in saying that this is a 15 pair repeat of AT so a 30 nucleotide oligonucleotide. Though it didn't say dAdT, you are likely correct that they are deoxyribonucleotides as they use thymine instead of uracil as the base.
Just in case, the ss stands for single-stranded, which is often the case for oligonucleotide primers for PCR reactions.


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What exactly happens during the crossover
My knowledge of biology is rather limited, but I think I have a grasp of some basic concepts. For me (as a person close to math) a chromosome is a sequence of elements from the set {A,C,T,G} of some (arbitrary?) length. In humans, there are 23 pairs of chromosomes, and during meiosis each of these pairs produces a singe "mixed" chromosome.
Q1 In each pair, do chromosomes have to be of the same length? If yes, does it mean that this length is the same for all humans? Do chromosomes in different pairs have different lenghts?
Now, we have two chromosomes from the first pair and they get mixed during the meiosis.
Q2 In which exactly place do they get mixed?

if chromosomes are same length, I expect they exchange pieces of the same length only as well; however, if they are of different length, do they exchange pieces of different lengths? e.g. suppose first chromosome in a pair has length 100, second is 105 (I do understand that in reality the numbers are much bigger). Can that happen that the new chromosome is created using the first 10 elements of the first, and the last 80 of the second (so the first 10 of the first replace the first 25 of the second), with the total length of 90?
how many exchanges may happen in a single meiosis, namely can that happen that chromosomes exchange several separated pieces from the middle?

I guess, that this process may not be understood completely yet, so I'm rather looking for an answer either "No, it can't happen at all, we know that for sure", or "this we don't know yet, perhaps it may happen".  Thanks.

Q1 In each pair, do chromosomes have to be of the same length?

Yes, approximatively.

If yes, does it mean that this length is the same for all humans?

Yes, approximatively.

Do chromosomes in different pairs have different lenghts?

Yes. E.g., in humans, chromosome 1 is 294 millions nucleotides long while the chromosome 22 is only 50 millions nucleotide long.

Q2 In which exactly place do they get mixed?

These crossover can appear pretty much anywhere. The probability of a crossover to happen at a given locus (locus=location on a chromosome) is not a constant throughout the chromosome though. In any case, the crossover always (almost always) happen at the same locus for each pair of the chromosome. In other words, if ~3 millions nucleotides goes from the paternally inherited to the maternally inherited chromosome, then ~3 millions nucleotides goes from the maternally inherited to the paternally inherited chromosome.

A good answer until the last paragraph. "the rate of crossover is limited to exactly 1 per chromosome" is wrong: the number per chromosome averages the same as the length in Morgans of the chromosome (higher in females), so more for chr. 1 than chr. 22.  "the crossover happens at the location at which spindle attach during meiosis" is wrong: spindle attaches to the centromere, not the crossing-over chiasma.

Yes, you're right. Thank you. I deleted this last paragraph.... but then I don't fully answer the question anymore...

Thanks for the answer, pretty much comprehensive. The last paragraph is confusing though: you're saying that the crossover can happen at any location of the sequence (with non-uniform probability, fine), but "in other words" you're saying about the length of the exchanged sequences - those two facts are important, but to me they are quite different. Could you elaborate? Also, rephrasing the last part of my question was: during a single meiosis, can crossover happen at two separate locuses?

@Ilya, the process can be thought of as having the two chromosomes laid out parallel to one another and aligned, at a random locus (same in both) both are cut and the loose ends are reattached to the other chromosome.  Hence the pieces exchanged are (approximately) the same size.  And yes, multiple crossovers can occur on a chromosome in one meiosis.  The longest chr., Chr. #1, averages 4 and a quarter crossovers in a human female meiosis (males average 2.9 crossovers on Chr. #1).


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What's the simplest set-up to demonstrate soiless plant growth to middle school students?
I'm looking for a simple, inexpensive way to demonstrate that soil is not needed for plant growth to middle school students.  I plan to germinate bean seeds in cotton, but where do I take it from there?


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Colloids in digestion
I am looking for examples of colloids involved in digestion for a cross-curricular (bio-chem-physics) lesson plan.  Although I have found references implicating colloids in both lipid and protein digestion, I haven't been able to identify which colloids they are speaking of.  Can someone provide specific examples?

Fat released from food will form macroscopic lipid droplets in the aqueous environment of the gut. In the small intestine, bile synthesised by the liver is secreted into the lumen via the bile duct. Bile contains bile salts which act as detergents to disperse the lipid droplets by forming micelles. I think this dispersion of micelles could be described as a colloid.
I have no idea what the reference to protein digestion could mean, although some hydrophobic proteins might become associated with the micelles that I've already described, and I imagine that bile salts might help to solubilise protein aggregates in the gut lumen by direct interaction - they, or their derivatives, are sometimes used by protein biochemists as detergents for protein solubilisation (e.g sodium deoxycholate.


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Prostaglandin F2-alpha production in men
I am trying to find information on Prostaglandin F2-alpha, specificaly production in men. Could somebody explain how this prostaglandin is produced? What types of cells are producing it, production signaling? Any books on this subject?

As I know:
One of the most important chemical mediators are prostaglandins that in vivo act on different cell receptors and have different effects on the body. Prostaglandins are twenty-carbon lipid molecules and structurally similar to cholesterol. Prostaglandins have different types, such as F2, E2 alpha, PGI2, and so on.
A phospholipase enzyme converts phospholipids of cell membranes into arachidonic acid. The arachidonic acid within the cyclooxygenase enzyme or Cox (both type 1 and 2) can be converted to prostaglandins.
PGF2alpha has functions in uterus contraction and bronchoconstriction, so I think both uterus and lung cells produce it.
I have no special information about production of PGF2alpha in men.

I think it is incorrect to say that prostaglandins are structurally similar to cholesterol.

PubChem is a good resource for finding out more about compounds of pharmaceutical interest:
http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5280363

This is more of a comment than an answer to the question. To make it an answer you should pick out some key points from the article and include them in your post.


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Examples of Vestigial Genes
I consider the existence of a broken GULO gene in humans to be the clearest evidence for human evolution - just what else is it doing there otherwise?
Are there any other examples of vestigial genes in the Human genome? Or perhaps vestigial proteins?

I think you are simply looking for examples of pseudogenes, right?

Yes, I guess I am :)

@Corvus pseudogenes do not express. I would assume that a vestigial gene is something that is expressed but is dispensable.

@WYSIWYG pseudogenes are often expressed. As described here and here. They just don't produce a protein. I guess they can't be strictly called vestigial genes, they might still have some effects.

@cagliari2005 By expressed I meant formation of the original intended product which could be ncRNA or protein.

@WYSIWYG great. just wanted to make sure :).

BTW, some examples of these would still be appreciated :D The wiki page above only gives one other 'disabled' gene comparable to GULO. Thanks

So, do we feel like we know what the OP means by vestigial genes? Are examples easy to find? @Tom, was the other vestigial gene you found on wikipedia the caspase 12 gene?

@Remi.b Yes, that's the one. I find these really interesting. On a more personal note, I have a number of intelligent friends influenced by the ID movement, so I always like to have as much evidence as possible :)  According to some, the 'difficulties' posed by the GULO gene/chromosome 2 merging has already been explained away.

Genes that were once functional but no longer are are called pseudogenes (as Corvus pointed out in the comments).
Many genes that are similar today (homologs) are hypothesized to have come from duplication events in the past.  In most cases, these duplicates diverge.  The divergence can happen in several ways:
1) one retains the original function while the other obtains a novel function
2) a dosage response occurs where both (keeping the original function) become necessary for that function
3) one retains its function while the other loses all functionality.
This third group are the pseudogenes.  This isn't the only way pseudogenes come to be, but it is probably the most well-characterized.
There are several resources for lists of these.  I'll just point you in that direction.  I assume you are interested in a particular group (i.e. genes important in development or patterning), so that you can dig more deeply into:

http://seqanswers.com/forums/showthread.php?t=32054
http://www.genomebiology.com/2012/13/9/r51


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Mathematical Modelling of Natural Selection
I'm a math undergrad looking for some papers on modelling the process of natural selection. The only paper I've been able to find is by the pre-eminent mathematician Herbert Wilf from 2010,
There's Plenty of Time for Evolution
Unfortunately, Wilf's model is extremely simplistic - he calculates the number of 'generations' required to spell out a 'word', if we allow each letter to 'mutate' with certain probability every generation, and we stop mutating a letter once it is correct (this is the 'selective' feature of the model). So to spell the word 'Evolution' by randomly placing scrabble tiles would require 5.4 trillion generations, but if we keep the correctly placed letters each generation and only allow incorrect letters to 'mutate', Wilf calculates we'd only need about 57 generations on average.
Wilf's model is a good first step towards modelling natural selection, but it's clearly only a first step. In particular, the fact that nature seems to know in advance exactly what letters it needs to keep in particular places and what it needs to throw out to construct a complex genetic 'word' is dubious at best.
As a young maths student the idea of the incredible complexity and diversity of life developing by a directed stochastic process gets me shamelessly excited :) I have been very surprised at just how little mathematical literature there seems to be on this topic, as I say, Wilf's one super-simplistic model is all I've been able to find. Can someone direct me to any other theoretical analyses of the power of natural selection?
Thanks

If you have a strong mathematical and theoretical computer science bend then you might be interested in: Ecology and evolution through the algorithmic lens

Mathematical and computational modeling of evolution is a huge field. To start you off with some broad strokes, there are two main approaches to evolutionary modeling with their own communities: frequency-independent and frequency-dependent models. Of course, in a real biological setting, the truth lies somewhere in between, but models are idealizations of key principles, and so the two extremes are good to study.
For frequency-independent selection, they key concept is the fitness landscape -- a way to map each genotype to a fitness. The population then lives in this landscape and agents with higher fitness reproduce better and so the population slowly movers over the lattice. Under reasonable macroevolutionary assumptions such as very rare mutations and asexual populations, the population will tend to be homogenous and can be just modeled as a single point in the fitness landscape with properly chosen selective sweeps to move the point from vertex to vertx (Gillespie, 1983; 1984).
The most popular concrete approach for frequency-independent selection is [Kauffman's NK model of rugged fitness landscapes] (Kauffman & Weinberger, 1989; Kauffman, 1993). Computer simulations tend to favor this sort of model. Wilf's model would be an NK model with K = 0, and fitness of 0 for incorrect letters and 1 for correct letters (to get the shorter walk). Related questions:

Is local equilibrium a reasonable assumption for evolutionary processes?
Structure of fitness landscapes in the NK model

The frequency-dependent selection approach is dominated by evolutionary game theory. A typical question for this field is the evolution of cooperation, and the most basic approach is to use replicator dynamics and look at evolutionary stable strategies. However, the field is in general saturated with all kinds of exciting models (both analytic and computational). A very friendly book-length intro is Nowak's Evolutionary Dynamics. For a genetle intro and connections to evolutionary psychology look at the slides in this post. A brief and sophisticated introduction aimed at mathematicians can be found in Hofbauer & Sigmund (2003). Related questions:

Sources for Algorithmic Evolutionary Game Theory
Why is 'Grudger' an evolutionary stable strategy?
How exactly are game theoretical evolutionary models described during implementation for computer simulations?
When does weak selection produce qualitatively different results from strong selection?

References
Gillespie, J.H. (1983). A simple stochastic gene substitution model. Theor. Pop. Biol. 23, 202.
Gillespie, J.H. (1984). Molecular evolution over the mutational landscape. Evolution 38, 1116.
Hofbauer, J., & Sigmund, K. (2003). Evolutionary game dynamics. Bulletin of the American Mathematical Society, 40(4), 479-519.
Kauffman, S. (1993). The origins of order: Self organization and selection in evolution. Oxford University Press, USA.
Kauffman, S. & Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Nowak, M. A. (2006). Evolutionary dynamics: exploring the equations of life. Harvard University Press.

Modeling evolutionary processes has a long history in evolutionary biology. Initially, these models were only theoretical or back-of-the-envelope quantitative (e.g., Simpson's Tempo and Mode in Evolution), but with the advent of cheap and accessible computing power, interest in stochastic models has greatly expanded.
The primary literature is vast, so I recommend a few books, which will give you a sampling of approaches and, more importantly, pointers to the relevant literature. If you are at a university, there is a good chance that your library will have one or more of these:

Otto SP and T Day. 2007. A biologist's guide to mathematical modeling in ecology and evolution. Princeton University Press.
Bolker BM. 2008. Ecological models and data in R. Princeton University Press.
Roff DA. 2010. Modeling evolution: An introduction to numerical methods. Oxford University Press.

And want to try your own models and you use R, there is an entire page of evolutionary biology packages. Many of these have built-in functions to simulate evolutionary processes:

CRAN Task View: Phylogenetics, Especially Comparative Methods

One thing to keep in mind is that simple models, like the one by Wilf and Ewens, often encapsulate the question at hand very well. Even though relatively simple, they are nonetheless very powerful. Wilf and Ewens wanted to prove a point about mutation, and they do that very well. It's easy to imagine way to extend their model to be more realistic, but as a start this is a very sound approach.
A rule of thumb for modeling is to make the model as simple as possible at first, including only the essential process or processes. Then gradually add complexity.

Nice answer (+1). I've been trying to find good intro's to modelling recently - just downloaded the Roff book and working my way through the introductory chapters, seems clearly written and informative so far!

I knew there must be some literature out there somewhere :) These look great - my library has them all so I'll take a look at them ASAP :D Thanks

thanks for the plug for my book, but I should point out that while it has useful tools for biological modeling, it doesn't explicitly cover evolutionary models

You might also have a look at some theoretical population genetics, which traditionally models selection as a diffusion process. The best introduction I know is chapter 15 of Karlin & Taylor's Second Course in Stochastic Processes (which, despite being only one chapter, makes up about half the book). From this, you can get results on hitting times, fixation times and other related distributions. Similar results are available in Durret's book, but he goes a bit deeper into the biological interpretations of his results.


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What insect is this? Found this at home, India

Found this insect in Kolkata India. Has a sting at its rear end. The wings are shiny.

Welcome to Biology.SE! Please edit your post to add an estimate for the size of this insect and the nearby environment as those factors can be helpful clues for identifications. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

That is a parasitic wasp in the family, Ichneumonidae. You can tell by looking for a cell in the forewing that looks like a horse head. The "stinger" is an ovipositor. These wasps lay their eggs in the larvae of other insects

I've been trying to work out which species of wasp in that family it is. Going by photos on https://www.projectnoah.org/spottings/17352592 it looks like this could be a female Xanthopimpla punctata ("Yellow Ichneumon Wasp"), but there seem to be a lot of very similar looking Xanthopimpla species it could also be.


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Correlation seen with low billirubin levels but not the gene that causes Gilbert's syndrome
I was reading the following study on associations between bilirubin and CAD (coronary artery disease). They looked at the bilirubin association, and the genes that cause Gilbert's syndrome, which increases bilirubin concentrations. Study here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648823/
The study states in the abstract:

"Both polymorphisms showed a strong association with bilirubin levels with higher levels for homozygote carriers of the minor allele."

But then goes on to say, a few sentences later:

"Logistic regression analysis revealed low bilirubin levels but not the UGT1A1 polymorphisms to be significantly associated with CAD: OR (95%CI) 0.90 (0.86–0.94), p=2.6×10−6 for men and 0.77 (0.68–0.87), p=3.2×10−5 for women, respectively for each 0.1 mg/dl increase of bilirubin."

How can we see a "strong association" between the gene that causes gilberts sydrome and bilirubin levels but not see an associatoin between the gene and CAD risk? If the study is stating bilirubin is significantly associated with CAD risk, and the polymorphism is strongly associated with the level of bilirubin, shouldn't it follow that we would see an association between the polymorphism and CAD?
My guess is that polymorphism correlation to bilirubin levels isnt actually all that strong, or that the association between bilirubin and CAD isnt all that strong, or both. Hoping someone could offer some thoughts on what they think is going on.
Thanks!


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What's the transposon difference between chimps and humans?
I was reading that humans and chimps share 98-99% of the same DNA sequence but I also read humans and chimps only share around 20% of the same proteins. Also, 45% of the human genome is transposable elements, It's 42% reverse transposons and 3% DNA transposons.
So, I wanted to know the difference between humans and chimps when it comes to transposable elements, especially reverse transposons.
Sources added:
Eighty percent of proteins are different between humans and chimpanzees. ncbi.nlm.nih.gov/pubmed/15716009 and Retrotransposons - In mammals, almost half the genome (45% to 48%) is transposons or remnants of transposons. Around 42% of the human genome is made up of retrotransposons, while DNA transposons account for about 2–3%.[3] [en.wikipedia.org/wiki/Retrotransposon]2

Do you have a source for your numbers?

Sorry, I didn't include the sources. Eighty percent of proteins are different between humans and chimpanzees. https://www.ncbi.nlm.nih.gov/pubmed/15716009 and Retrotransposons -  In mammals, almost half the genome (45% to 48%) is transposons or remnants of transposons. Around 42% of the human genome is made up of retrotransposons, while DNA transposons account for about 2–3%.[3] https://en.wikipedia.org/wiki/Retrotransposon

Note, saying "humans and chimps only share around 20% of the same proteins" is not quite right, the source you cite actually says that only 20% of proteins are absolutely identical - the remaining 80% are very similar, but have slight differences (based on the 1-2% difference in DNA sequence)


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Need either a [similar] ribosome to the following few | a heuristic for finding [similar] macromolecule given 20 others
Background :
Hi! I am running a small experiment dealing with structural heterogeneity of the ribosome, actually of ribosomes across all domains of life. It's entirely computational: I get cryoEM  samples(below) from PDB, parse the crystallographic profiles and see if I can enclose on physical clusters of proteins that persist across domains of life (i.e. uL4 reliably neighbors uL22 according to this ontology) and things like that.
So far I've been working with the following dataset of eukaryotic/eubacterial/archeal macromolecules and am feeling pretty shackled by it at this point.

Question :
I would be very happy to augment this dataset with any number of "similar" ribosomes to put through the algorithm, but I don't know much about exemplar species to draw from and decided to ask here if somebody would recommend some more or less well-studied species(or straight-up PDB IDs) that would make a good addition. If you could point a boy to where I can "just get more" that'd be even more awesome. I'm not a biologist by training so you probably know of some obvious resource I don't.
I have no other constraints on what the targets are. Thank you so much and stay safe!

 I realize that most of these listed here are like the go-to organisms in biological research.

If you have searched PDB (and that looks the case) you have what there is. I trust that you realize that a protein designated L4 in E. coli bears no relationship to the one designated L4 in eukaryotes. As far as I am aware there are very few similarities in structure between eukaryotic and prokaryotic ribosomal proteins, and in any case the nomenclature was in no way structural or functional, but based primarily on position on two-dimensonal electrophoresis. I am less familiar with the nomenclature of archaea ribosomal proteins, but these show differences from eukaryotes and eubacteria.

Thanks for the reply, @David. I should have included that, maybe, but didn't to keep it concise: I'm using the nomenclature system proposed by [Ban et al.] (https://bangroup.ethz.ch/research/nomenclature-of-ribosomal-proteins.html) which aspires to standardize on function and enables us to do actually run this study. That's the system in which I'm referring to uL22 and uL4 and all others. I figured out pretty quickly that chain ids on PDB have no particular rhyme or reason to them.

@David when you are saying that PDB is all that there is, do you have any species in mind that I can search on there to get the ribosome of or is it whatever?
My problem with the latter is most of the structures i see on there seem to be results of experimental depositions in which a ribosome just figures like Structure of a mammalian 80S ribosome in complex with the Israeli Acute Paralysis Virus IRES (Class 1), but is not the main model. I wouldn't want to dilute my sample with anything but ribosomal structures.

OK. Just thought I’d check. One way you might find ribosome structures in PDB is to search for a particular protein by number. It will also bring up that protein alone, of course. I wouldn’t have thought there was much interest in other species now, given the cost and effort involved, and the low publishability. There would have to be something special or different about the ribosomes. A recent review is the other approach, which I imagine you have tried.

@David, now we are talking. I can definitely relate to the point about the effort. It's been a pretty excruciating bead-stringing exercise wrt data-cleaning even before anything could begin to run.
What do you mean by the recent review, though? I don't think i have!

My internet connection is terrible this morning so I can do less than I intended, but I managed to find a 2019 freely-available review from Cold Spring Harbor Perspectives in Biology entitled "New Insights into Ribosome Structure and Function". I'd work back from the bibliography there (and also do the same from some of the more recent papers in your list). It would be worth your while glancing at the introductions to those papers to find out why the species were chosen. They exclude many of the usual suspects.

@David This is super generous, plenty to work with. Thank you kindly.