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Why haven't modern grass based crops overrun wild grasses?
Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.
I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.
So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)
Edit:
I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

Which plants do you have in mind specifically?

@James my question is specific to grasses, though the rhetoric regarding GM plants depends on the particular GM technology being attacked.

There are something like 10,000+ species of grass. There are many GM crops and they have a huge range of modifications. If you're unsure about what your question is about, then please cite the article stating that GM crops will escape into the wild. Perhaps that will provide some insight. Currently the question is not clear enough to answer.

Ignore the GM part of my question if you must. My question is exactly as stated. Why are wild grasses still dominant in the wild when crop grasses are so morphologically superior.

The selection process employed in agriculture selects for high yield, disease and weather resistant crops. Not necessarily their invasiveness, which would probably be selected for in nature. Perhaps there are some examples where they have overrun wild plants.

Many of the popular grass varieties that are used in lawns are originally from Europe (namely the UK). They have quite a different and particular moisture requirement compared to the many different types of wild grasses that have evolved all across the world. Also cultivated species having had to compete less with other species for territory and resources can sometimes be less "aggressive". I think it's important to acknowledge there is a large difference between GM varieties cross-breeding with the non-GM varieties of the same domesticated species vs. competing with wild species.

Also, "morphologically superior" seems subjective when viewed from the standpoint of agriculture, but from a natural perspective, is not so subjective. Any favorable trait might also have an unfavorable consequence, faster growth could mean more water dependency, stronger stems could mean weaker defense against harsh winds and weather.

Crops are not superior in a whole range of ways, especially in things that deal with direct competition (like nutrient efficiency).  more importantly they are often worse at reproduction (wheat cannot even spread its seeds without human help), which is the ultimate negative selective pressure.

Modern grass crops (cereals) haven't run out in the wild is because that was the whole purpose of their development. What differs them from their wild counterparts are the domestication traits, like, seed shattering, uniform maturity, day length sensitivity etc.

Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.

This is only true under well resourced conditions, such as, irrigation, fertilizer, planned planting density etc. They grow faster and stronger because that is how they are bred. They are bred to utilize these resources better and produce better.

I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.

What people generally talk about here is the genetic transfer due to pollen contamination. But this is generally hard because of species differentiation. Even if that happens it will be with very low frequency compared to wild population. As far as I know modern crops do not and probably will not out compete wild plants under natural conditions.

So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)

Explanation above applies here too.

Edit: I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

That is generally due to seed contamination due to somebody threw a seed there. Or it is due to remnant seed from previous year's crop, these plants we call volunteer plants.

I believe the OP is referring to the fact all our crops have been genetically modified through artificial selection and selective breeding, often just through domestication alone. The vast majority of our crops are genetically modified in this sense.

In that case, true, they have been genetically modified.

It is a common issue in any scientific sense the colloquial usage of GM is completely unsound, there is no definition of GM that does not cover the either the vast majority of crops or such a small insignificant percentage that it you will likely never eat them anyway.

Exactly. I find it funny when people talk about GM (the colloquial use) to say they have been genome edited but fail to realize that what we have today is all GM via artificial selection, selective breeding, mutagenesis, domestication etc.


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Grafting vegetables onto fruit-bearing trees
There are multi-fruit trees with as many as 40 different fruit, but would it be possible to graft a vegetable onto a tree?
Or maybe something in between, like grafting onto an apple tree a fruits in the botanical sense, but one of those often eaten as savory food, similar to vegetables: tomato, squash, avocado?

Some vegetables are actually fruits (like apples and bell peppers), others like carrots and potatoes are root modifications. You have to clarify what vegetables and fruits you are interested in. The type of plant is also important.

For grafting to "take", the the two plants' vasculatures have to be organized similarly. This is not possible for two such differently organized stems as a pepper and an apple.
This is a cross section of a young woody stem (such as an apple, though this example is a tilia):

This is a cross section of an herbaceous stem (such as a pepper):

You can see there is dissimilarity in organization. Furthermore, herbaceous plant stems die back in the winter.
Even if possible, grafting an herbaceous (non-woody) stem onto a woody stem (e.g. apple) would not confer any advantage for the green pepper, a tender annual, and would be disadvantageous to the woody stemmed tree (pruning for no reason, when the branch would otherwise have produced apples, and the leaves performed their useful functions.

How about a tomato and an apple tree?

@DanDascalescu - how are a tomato and a pepper significantly different? They are both tender annuals in the nightshade family.

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Do microorganisms have complex social behaviors like dominance hierarchies, just as "higher animals" do?
I used to believe that dominance hierarchy (a.k.a. pecking order) exists in higher order animals and is associated with complex social behavior. See the wikipedia definition of dominance hierarchy and pecking order which is restricted to animals. For example, a pecking order can be an order decided by the brightness of feather, without straight competition or direct fight.
However, I recently came across some examples on the complex social behavior of microorganisms, dominance hierarchy of microorganisms and bacteria, dominance hierarchy and hierarchy of exploiting in bacteria, and pecking order of pastures and plants.
For  a specific example, here is a comment of a MIT paper published on Science about "social structure of microoganisms":

They reasoned social structure can reduce conflict within populations of plants and animals and determine aggression towards competing biological populations. "Think of a population of lions in the Serengeti or a population of fish in a lake," said Cordero. But could the same be true for populations of bacteria?

The answer to this question seems to be positive, according to the abstract of the Science paper:

In animals and plants, social structure can reduce conflict within populations and bias aggression toward competing populations; however, for bacteria in the wild it remains unknown whether such population-level organization exists. Here, we show that environmental bacteria are organized into socially cohesive units in which antagonism occurs between rather than within ecologically defined populations.

So I am very confused.

A better question than last time. Note that just because they used the words "dominance" and "hierarchy" in them, doesn't mean that the papers are talking about a social order. The first plant link is about genetic dominance/recession in alleles within the plant. Can I suggest you investigate the terms mutualism and antagonism in ecology?

@bob1 You are right that those two things are only distantly related. I will delete it.

Similar to my comment on your other similar question and also bob's...have you read the papers you cite for "dominance hierarchy"? What concept are they talking about? Does it relate to what you know about "pecking order" in social mammals? I think they are each clear about what they mean; the same words can be used in different contexts to mean different things.

Short answer
All of these papers describe competition; that's all they share in common. Competition is ubiquitous in nature; it need not even involve organisms that have ever encountered each other: when you put two organisms together that use some of the same resources, competition occurs. Just because competition occurs does not mean "complex social dominance hierarchies" occur. Just because someone talks about a "hierarchy" it does not mean that hierarchy is the result of a social agreement for weaker individuals to defer to stronger ones to avoid conflict; "hierarchy" just means "we are putting these entities in an ordered list"; the order and meaning of that list depends entirely on the conditions and criteria used to arrange that list. When someone says "hierarchy" or "order" you have to read what they mean by hierarchy/order and not assume that it is related to any other hierarchy you have read about before. If you have some sports teams, you could rank them according to their win/loss record, according to an Elo-based ranking system, according to how much you like their team colors, according to a weighted average of expert/sportswriter opinions about how good the teams are, etc. The teams don't even have to meet each other for most of these measures, they certainly don't need to agree among each other about who is stronger for you to be able to put them in a hierarchy according to your preferred criteria, and even if you think you've designed the best hierarchy possible, their pairwise interactions may not be what your hierarchy predicted.
Long answer
The type of dominance hierarchy described on Wikipedia is an evolutionarily stable strategy among social animals. In short, by establishing a hierarchy, fighting is limited. Fighting is costly and dangerous: wounds that may seem minor can result in deadly infections, and any effort towards a fight costs energy/calories.
Your question cites several other situations where authors have used "dominance hierarchy" or "pecking order" to describe the results of competition, but not all competition needs to have this social deference-to-established-strength aspect.
With respect to the specific papers you talk about:
https://royalsocietypublishing.org/doi/epdf/10.1098/rspb.2003.2338
This paper is about competition among yeasts. It does involve interference competition and exploitation counter-strategy. However, there is no complex social hierarchy, this is all competition happening on a molecular level. Species/strains that produce and are resistant to a toxin get the benefits of the toxin but also carry the costs of producing it. The authors study a system where growth patches are isolated and from each other and strains spread from patch to patch. When present in the same patch, the toxic strains can often defeat the sensitive strain. However, sensitive strains can be successful in places where the toxin producers are absent, and since they don't need to bother to produce toxins, they grow and spread faster. Depending on the parameters of the environment, the increased growth ability comes into an equilibrium with toxin production.
Nothing social needs to happen for this to occur, none of the yeast strains in these models are behaving in any different way, it's merely a result of the cost-benefit of producing a toxin.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106711/
There is absolutely no intraspecies social competition in this paper. They have squid and bacteria that have a symbiotic relationship. If you take the bacteria from one species of squid, it can survive in other squid species, but it doesn't do as well as the bacteria native to that squid, and vice-versa. The closer the squid are phylogenetically, the closer their bacteria are, and the more similar cross-collaborations are better than dissimilar ones. The "hierarchy" here is completely environment-dependent; from the perspective of the bacteria, you have a different hierarchy for each squid species.
https://onlinelibrary.wiley.com/doi/full/10.1046/j.1420-9101.2003.00545.x?sid=nlm%3Apubmed
In this paper, they study a slime mold that produces a fruiting body to spread. The fruiting body consists of a stalk and spores; in their terms, they call "dominant" strains the ones that produce more of the spores. However, the stalk is important for effective reproduction. Therefore, strains that produce more spores are "cheating" a bit, and this strategy is only effective when other strains are present to make up the stalk. This is a complex interaction, but doesn't rely on any social hierarchy; the "hierarchy" here is simply the ratio of spores to stalk produced by each strain, in other words, the level of "cheating". Being "high" on this hierarchy aka a "cheater" is only good when there are lots of non-cheaters around.
https://www.jstor.org/stable/3565800
Here they are growing plants together in a plot. They rank these plants according to how they grow in competition with other plants. There is no social interaction here at all. The paper shows how hierarchies can be non-linear due to different demands for resources that appear when different species compete. Therefore, Plant A might outgrow Plant B, and Plant B outgrows Plant C, yet Plant C outgrows Plant A if each are isolated in a bi-culture. Real ecosystems contain more varied conditions than an experimental plot, so in the real world you'll find different niches where each plant exists. Despite using the term "dominance hierarchy" these authors aren't talking about anything but relative abundances in different co-culture scenarios.
The last link is to a book on plants; I won't address it directly here, because it's unclear what part of the book is being referenced, but I am guessing it's describing something similar to the Aarssen article.

Ok very detailed answer. Much appreciated. I get your point, especially your interpretation on those articles. So are you suggesting that microorganisms do not have complex social behaviors?

@HighGPA "Complex" is... often a meaningless word, unless you specify ahead of time what you mean by "complexity" and how to measure it. Also, no matter how you define/measure it, it's usually used in relative terms. The same is true of the word "social", as you can use it to refer to the types of relationships that form among humans, or use it to mean generally "interactions between two or more organisms of the same species".

I also agree with you that fighting in costly. However, I would like to point out that your "complex social hierarchy" is also determined by competition, for example, that peacocks competing the brightness and largeness of their feather. Such feather is also very costly to grow. So I wonder if there is a clear cut between competitive hierarchy and dominance hierarchy.

@HighGPA The peacock example is better defined by sexual selection than "pecking order" or a dominance hierarchy; I don't believe they participate in those social structures.

Well I thought the alpha peacock get more sexual and material resources?

After reading your answer, here is my understanding: the cited articles are mostly about direct competition, and the order determined by direct competition is not "dominance hierarchy"; however, if some orders in bacteria is determined by signaling, without any direct competition for resources, then this could be called the "dominance hierarchy". Is my understanding correct?

@HighGPA I believe peahens form harem groups during breeding season; as such, there is not so much an "alpha peacock" and a bunch of subordinate males, but rather a single male peacock and the peahens that choose to mate with him.

For "dominance hierarchy" I think you can apply that label to whatever you want, as some of these papers have, but when doing so you need to explain what you mean. Just because they say "dominance hierarchy", whatever the form, does not mean it comes with all the baggage of "dominance hierarchy" used in another context. I understand this may feel messy and confusing, but...well, welcome to biology - this sort of thing is common. It's incredibly important in understanding biology to know what terms mean as people use them, and not to overgeneralize.

Let us continue this discussion in chat.

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Why don't the female lions in a pride help their male lion to protect their children from other males?
I watched a dozen of videos taping the fights between male lions; none of them involve female lions assisting in the fight. It is also known that the male lion who take-over the pride will kill all the under-age lions.
Why don't the female lions help their male lion such that their offspring won't be eliminated?
From an evolutionary perspective, the female lions will surely fight for their children as raising a new child is costly. Though they will most likely not fight to death. Even if a lioness does not have any child yet, her older sisters might already have a child so help defending the entire pride is the optimal strategy. In this case, the younger sister might only contribute half of their strength comparing the older sister, as the child is only her nephew and not her direct offspring.

if they don't fight they just have offspring with the new proven more successful male instead of propping up a weak male. lets the males fight and take the winner.

@John Good point!

Alright, after watching a few more documentaries, here is what I found:
Lionesses do try to expel nomadic males, even if the male lion is not in presence.  On the other hand, I am still yet to find a single video taping the male and females collaborating to expel the invading lions.
When invading a pride's territory, the nomadic brothers will usually not attack first, even if there is only one "lion-king" in the pride. The nomadic brothers might think that the females will help the lion-king to protect the territory; otherwise the brothers will just simply attack as it is a 2 to 1 odd.
The nomadic brothers will usually disrupt the pride's food-supply first. As the pride usually have many cubs to feed, it consumes much more food than the nomadic brothers, and the lion-king is then forced to launch his attack first.
The fight between male lions are usually not lethal possibly due to male lions' body structure. Most of time the nomadic brothers are expelled, but sometimes the lion-king is wounded or expelled from his own territory.
After being wounded, the lion-king cannot protect his cubs. The nomadic brothers then start to find and kill the cubs. The females do sometimes try to protect their cubs, but their attacks can only lightly wound the male lions as males are well-protected by their hairs. In contrary, the males can one-hit the youngsters.
Cubs close to 2-year-old do try to run away and the females do sometimes help them by providing them food, even if the females seem to be obedient to the new dominating males. In this video the lioness even decide to run away from the original territory to raise-up her children and half-children: https://www.youtube.com/watch?v=eMgPf83uDec.
After all cubs are killed or expelled, the females lose the motivation to fight against the invaders, and the new pride is formed.

Interesting summary! What do you mean with 2 to 1 odd?

@KaPy3141 For example, the invading nomadic brothers are two male lions, while the defending pride only has one adult male lion. Even if it is a 2:1 odd, the invader will not directly attack the pride.

Oh I get it, thanks!

This looks like it could become a good answer, but answers are expected to include supporting references (primary literature is best) — links to videos are not sufficient (and are also unstable). Without that support, your answer is indistinguishable from opinion and thus inappropriate for this site. This is a good example of how to format references. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.

Usurpers and attackers would be useful vocab here. I didn't understand WHY the lionesses don't affront the challengers. just the outline of what they do.

" The male lions as males are well-protected by their hairs." I think that's the key information here, presumably the females are scared of the males because of their size and added protection. It's a good question, I hope someone can theorize why 2v1 fights are preferred over 2v7 to protect cubs. perhaps 2v7 encirclement can result in fights to the death because the adult females die, and 1 adult female is more valuable than a cub to the population.

@LifeInTheTrees Dear Trees, I agree with your terminologies. I directly copied and pasted the terminologies from those famous documentaries.

The prides mostly comprise at least 10 individuals, up to 40 and 1-3 alpha males. The average pride, both in Kruger NP and the Serengeti, consists of 13 members. In Kruger, the average composition of 14 prides totalling 181 lions was 1.7 adult males, 4.5 adult females, 3.8 sub-adults, and 2.8 cubs (including yearlings).
In larger prides, it is rare for the whole pride to be together, but individuals or small groups, typically of three-five members will scatter throughout the pride’s territory for days or weeks at a time, especially in dry environments or times where the number of prey are in small supply.
The mortality rate for the mature males is about 4/1 when they wander in between territories, and when they mount a challenge, it's often as a group of three or four bruising males.
There can be fights of a 270kilo alpha vs 2-3 challengers of 200-250kg, and the question suggests "shouldn't 2vs7 and 3vs8 lion fights happen? to protect the cubs?", including 100-150 kilo females. The females have a very vulnerable neck so a 7v3 serious fight could easily end in the death of 2-3 lions, weak hunts and hunger. That is why they are probably scared to mount a defense.
Animals tend to avoid potentially mortal fights, and the territorial fights are too life-threatening and vicious for the females to risk getting involved in. Prides usually have two alpha males so the strategy of challenges is very dynamic. It's best to find someone who has read a book about social organization of lions.

I've seen a video or two where the lioness will fight a male to protect the cubs.
And another thing, when a nomadic male or males take over a pride by force, it isn't considered a new pride being formed, it's actual meaning is the pride have new resident males.
Remember a pride is a pride without any males being part of it. Prides are so,
consisting of females only, the males that are there are residents of any said pride. So a pride of lions is so without a male unless they are male cubs of the lionesses within a pride.

And another thing, you all can watch every video ever made but until you go out into the bush and spend 35+ years observing Lions your answers are just guesses

I’m watching one right now on Disney plus and I was literally wondering the same thing as you until it showed that two out of a pack of 5 male lions initiated a fight and to protect her daughter she charged and fought one of them which inspired the other females and they all started to fight. They don’t show much of the other lion fighting thr prides male but I can assume they did.

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What species is this fly?
I am looking for an ID of this fly at genus or preferably species level.
Location: The Netherlands.
Size: approx. 7-8mm
Habitat: indoors, attic.
Timing: usually appears late winter, early spring

Apparently, this is a Pollenia sp
https://forum.waarneming.nl/smf/index.php?topic=447650.0.
One of the common species from this genus, Pollenia rudis, is often found overwintering in groups in attics and is therefore known as the cluster fly or attic fly.


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Why did animals evolve genders?
The majority of animals have two genders, and both are needed in reproduction. It seems like it would be more advantageous for creatures to be hermaphrodites, since they could mate with any member of their species instead of needing to find a partner of the opposite gender. Why did animals evolve to have genders instead of being hermaphrodites?

The title is a bit misleading. Hermaphrodites still have genders, if you consider the reproduction system. The title looks more like that you ask for a reason for meiotic reproduction, as opposed to mitosis, which is an interesting question, too.

Even yeast have a gender or mating type, called as A type or α type

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Does Yerba Mate contain Beta carbolines like harman and norharman?
I know that this is true of (roasted) coffee but haven't been able to find any reliable information about mate in its smoked or steamed state.  Thank you.

After a bit of research I can say that Yerba mate does not contain beta-carbolines. Now, I don't know if this makes you happy or sad but the tea has many antioxidant properties which makes it good for health. You can find a list of the components in Yerba mate in paper 1 and this article.

Hi. I'm the OP.  I just wanted to thank you for your answer.


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Evolution of bee hives
How do the instinct to create a hive appeared in bees? Is there some evidence of
"intermediate" hives? With this questions i mean all the factors necessary to build a hive, including the social structure, the producing of beeswax and architecture.

Welcome to BioSE. You will have better chance of getting good answers if you include more specifics in your questions, e.g. some background and your reason for asking. In this particular case; Are you asking about the evolution of sociality in bees in general, or something more specific only dealing with hives?

I'm assuming you mean the distinct architecture and regular hexagonal shapes in bee honeycombs?
In fact, Charles Darwin spent a good bit of time with honeycombs.
First of all bees and wasps have a common progenitor and wasps also build combs and nests, albeit of paper/celluose as opposed to wax.  He was interested in how the perfect hexagonal lattice formed in the wax.

Darwin tried three different experiments with bees’ cells at Down that he reported in Origin. In one, he put a thick block of wax into the hive. ‘The bees instantly began to excavate minute circular pits in it: and as they deepened these little pits, they made them wider and wider until they were converted into shallow basins, appearing to the eye perfectly true or parts of a sphere, and of about the diameter of a cell. It was most interesting to me to observe that wherever several bees had begun to excavate these basins near together, they had begun their work at such a distance from each other, that by the time the basins had acquired the above stated width (i.e. about the width of an ordinary cell), and were in depth about one sixth of the diameter of the sphere of which they formed a part, the rims of the basins intersected or broke into each other. As soon as this occurred, the bees ceased to excavate, and began to build up flat walls of wax on the lines of intersection between the basins, so that each hexagonal prism was built upon the festooned edge of a smooth basin, instead of on the straight edges of a three-sided pyramid as in the case of ordinary cells.’ (Origin, p. 223.) The cells were built up in a hexagonal shape when their bases intersected with those of other cells; but the pyramidal bases were apparently not built, since there was no pressure to accommodate cells on the other side of the wax, which was a thick block.

This seems to have a built in burrowing behavior in how the lattice forms that eventually turns into hexagonal shapes.
BTW this topic is very similar to the evolution of spider webs, which is also fascinating.

I remember an episode of a German science show talking about this. If you do an experiment with bubbles. Eventually several bubbles will share boundaries and a hexagonal form will emerge.
Following this it is no instinct but the best way to create boundaries.
They had a more scientific explanation for this.
There you go:
http://www.exploratorium.edu/ronh/bubbles/bubble_meets_bubble.html
And I quote:

If you take two sheets of clear glass or plastic separated by about one-half inch, soak them in soapy solution and then blow bubbles between the sheets, you will get many bubble walls. If you look closely, you will notice that all of the vertices where three bubble walls meet (and there are always three,) form 120 degree angles. If your bubbles are of uniform size, you will notice that the cells form hexagons and start to look much like the cells of a beehive. Bees, like bubbles, try to be as efficient as possible when making the comb. They want to use the minimum possible amount of wax to get the job done. Hexagonal cells are the ticket.

-
I just noticed I was answering to an answer. My answer to the question would be that almost every animal on the planet builds nests. If you are a termite you can use mud. If you are a wasp or a bee you build nests in the air or at least not in the mud. That means you have to carry your material through the air. The less the better. Efficiency dictates that you build your "hive" or nest as compact as possible. That means spherical shape which has the most volume vs surface ratio and the hexagons inside follow the same rule. Use as little material as possible or you are outcompeted by bees that do.
Also it's a lot more efficient to "manage" a cluster vs nests cluttered all over the place. Again no instinct just necessity which eventually evolved into instinct. Because all other instincts became extinct.


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Are there any sustained efforts to model existing ecosystems?
Are there any ongoing, sustained efforts to obtain enough data about an ecosystem or part of one to build a viable computer simulation of it? All I can find (e.g. in Brazil or by google) appear to be sandboxes for demonstration or experimental purposes.
What I envision is a true model that can predict the future development of an existing system, and of course run simulations to predict the impact of certain external changes: Deforestation, temperature and precipitation patterns, introduction of non-native species etc.
Such a model would require a fairly detailed and complete biological inventory as well as detailed knowledge of the species' interactions, and a detailed map of the physical and chemical makeup of the location or region (water, ground, atmosphere, radiation). This would obviously be a vast undertaking, but with the potential of tremendous insights. Last not least, such a model would be a tremendous planning tool.
Are there any projects attempting this?

https://madingley.github.io/about/

The two hyperlinks both point to the same page. Is this a mistake?

@acvill Thanks for the observation. Fixed. (The google program, which is freely available at github, looks like a lot of fun.)

Such a model would require a fairly detailed and complete biological inventory as well as detailed knowledge of the species' interactions, and a detailed map of the physical and chemical makeup of the location or region...

I suggest reading about the The Simons Collaboration on Computational Biogeochemical Modeling of Marine Ecosystems (CBIOMES).1 This collaboration has produced ample research concerning the modeling of marine microbial communities in terms of spatial composition, metabolic interactions, nutrient flow, and seasonal variation.
Here are the research efforts highlighted on their website:

Developing New Computational Modeling Frameworks

Developing a New Trait-based Understanding of Microbial Communities Based on Metabolic and Elemental and Macromolecular Constraints (led by Zoe Finkel/Dal)
Constraint-based Modeling of Marine Microbial Community Metabolism and Physiology (led by John Casey/MIT)
Statistical Modeling of Microbial Communities: Niches, Traits, and Interactions (led by Andrew Irwin/Dal)
Thermodynamically Constrained Metabolic Networks for Ocean Modeling (led by Joe Vallino/MBL)
Models of Marine Microbial Biogeography and Biogeochemistry (led by Mick Follows and Stephanie Dutkiewicz/MIT)

Collecting and Compiling Relevant Datasets

Ocean Color and Biogeochemistry (led by Shubha Sathyendranath/PML)
Data and Tools to Define the Biogeography of Marine Microbes (led by Ginger Armbrust/UW)
Microbial Growth, Interactions and Biogeographies from ‘Omics’ Data (led by Jed Fuhrman/USC)

Bringing Together Models with Data

Advanced Statistical Analysis of Marine Microbial Systems (led by Christian Müller/Flatiron Institute)
Unifying Data and Models through Biogeography (led by Chris Follett/MIT)
Data Assimilative Modeling of Marine Ecosystems (led by Chris Edwards/UCSC)
Statistical Network Inference and Time Series Analysis (led by Jacob Bien/USC)

Concerning specific geographic sites, one of the best understood marine ecosystems is the San Pedro Channel off the coast of Los Angeles, which has been studied since 1998 as part of the SPOT project.2 Sampling efforts from this site include sensors that capture continuous in situ measurements of dissolved oxygen, fluorescence, temperature, salinity, and pressure, as well as monthly charters that collect seawater to measure nutrients (nitrate, nitrite, phosphate, silicate) and chlorophyll at 12 discrete water column depths. Peruse the publications section of the SPOT website to better understand the ecological and geochemical research that the SPOT project has enabled.
If you are further interested in the global effort to characterize and model the dynamics of marine microbial communities, I recommend a 2015 review by Fuhrman, Cram, and Needham3, which discusses methods to analyze microbial networks through space and time.

References

https://cbiomes.org/
https://dornsife.usc.edu/spot/
Fuhrman JA, Cram JA, Needham DM. Marine microbial community dynamics and their ecological interpretation. Nat Rev Microbiol. 2015 Mar;13(3):133-46.

Depending on how you define "model an ecosystem" the answer is somewhere on the spectrum from "yes, it's routine" to "no, that's impossible."
Let's start with the positive side. Ecosystem modeling based on inventories of species, information about their interactions, and spatial and environmental context are routinely used for analysis, prediction, and recommendation. For example, the Ecopath software tool, developed for modeling marine fisheries, appears to have been in pragmatic use for three decades by a wide community involving many different categories of stakeholders.
Now to the negative side. There is an inherent issue of scale and stochasticity in any question of ecosystems, not to mention their entanglement with scale-free and chaotic processes. Indeed, two of the prime examples of inherent unpredictability due to chaotic dynamics are population growth versus ecological limits and weather prediction. That doesn't mean we can't learn quite a lot about a system, though, as chaotic systems still operate within regions of the model space that can often be well-characterized and have high predictive value.
So, what to make of these apparently contradictory positions?
The takeaways that I would recommend are:

Ecosystems can be and are modeled effectively, but the models must be carefully formulated with respect to the questions that are being asked.
In modeling an ecosystem, more detail is not necessarily better, as the wrong type of detail can ruin the predictive power of a model.


text:
How to retrieve full gene names list and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any)?
How to retrieve full gene names and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any other software or language)?
Is it possible vice versa: having full gene names or IDs get HUGO names or the other annotation data?

Try DAVID. It has a gene ID converter option. There are many other Gene ID converters.

I'm voting to close this question as off-topic because it is not about biology.

I would recommend just downloading the database, which HUGO allows you to do free of charge.
The HUGO website has a "downloads" tab at the top that takes you to the following page
http://www.genenames.org/cgi-bin/statistics
You will see a table of statistics relating to how many protein- or non-protein-coding genes there are catalogued, etc.
Under the tables is a section called Complete dataset download links -- this is the section you want (unless you only want a subset of the data - but why not get it all!)
This plain text file (once uncompressed) can be loaded into R (or any other language) to be parsed and analysed as per your requirements.
It is worth updating the version you download quite regularly, as they update the HUGO database with new/updated info quite regularly.

Install bioconductor and use this library: http://www.bioconductor.org/packages/release/bioc/html/biomaRt.html
You can access BioMart which lets you translate between different ID types


text:
Amino acid compatibility
The (human) genetic code encodes 20 amino acids. They form a protein using peptide bonds. Each amino acid has a carboxyl group (COOH) and an amino group (NH2) that can potentially form a peptide bond.

Source: The Culture of Chemistry
Does this property of amino acids means that each amino acid can form a peptide bond in any combination? In other words, are there certain amino acid doublets in existence that never pair up?

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center.

Right, so any amino acids may be chained together. The limitation is that the function of a protein depends on which amino acids are in your polypeptide chain, and in what order. The cell mediates this on multiple levels: http://en.wikipedia.org/wiki/Protein

Exactly what is the question? Whether all amino acids are "compatible"?

I edited the question to prevent closure. I think it is a valid question with enough background. It was just formulated a bit unclear

Short answer: there are no restrictions in principle on which amino acids can follow which. That means that in principle you can have polypeptide in any configuration: AAAA, WQWQWQ etc.
Problem is that polypeptides must be functional and, because they are in aqueous solution, it puts restrictions on how polypeptide form secondary and tertiary structure. It means that having very rigid hydrophobic surface is energetically unfavorable. If cell where to produce such polypeptide, it might be either degraded or cause problems for cell, such as aggregates or other form of toxicity.
That means that polypeptides has more restrictions than just linkage (C-N bonding) order. And of course it has been studied: Probabilistic analysis of the frequencies of amino acid pairs within characterized protein sequences.
Authors analyzed protein databases to find out which doublets of amino acids are more and less common. First of all, not all amino acids (of which there are 20 considered) have same occurrence, e.g. P(L, leucine)=0.096, P(W, tryptophan)=0.0118.
And, of course, not doublets are equally distributed (16 pairs out of 400 were picked as statistically significant):

I think this is the better answer.

To answer your question: No, there are no restrictions to what amino acid is next ("a nearest neighbor") to its N-terminal or C-terminal neighbor.


text:
To which negatively charged components of the cell envelopes do the crystal violet complexes bind in gram staining?
The gram positive have negative components in the peptidoglycan layer in the form of teichoic acid phosphodiester bonds, and the gram negative have negative components in their outer membrane in the form of lipopolysaccharide. Is that where the crystal violet binds?

The gram staining relies on the differences in the bacterial membranes. The gram positive bacteria have a thick peptidoglycan layer on top of the cell membrane, the gram negative bacteria have a lipid layer on the outside followed by a thin peptidoglycan layer and then the cell membrane. See the image for clarification (from here):

Crytall violet dissociates into a positively charged dye molecule (CV+) and chloride (Cl-). The CV+ travels between the membrane layers (outer and inner membrane) and is trapped there by the addition of iodine. This is used to form large crytal violet-iodine complexes which are retained during the destaining process.
In the destaining process, the peptidoglycan layer of gram positive bacteria is dehydrated and therefore shrinks which prevents the staining from being washed out. In the gram negative bacteria, the outer lipid layer is removed and the peptidoglycan layer (which is much thinner) exposed which allows the removal of the stain. The teichoic acid is important for the rigidity of the membrane but not for the binding itself.
References:

Gram staining
The Gram Stain after More than a Century
Use of the Gram stain in microbiology


text:
Why my base-quality in alignment is not perfect?
I have a fasta file with some DNA sequences. I would like to simulate next-generation sequencing reads from it. I'm doing it without any base error and mutation error.
wgsim -e 0 -r 0 sequence.fa seq_0_1.fq seq_0_2.fq

To my knowledge, this is a perfect simulation. Next, I give the paired alignments to bwa for alignment.
bwa mem -M sequence.fa seq_0_1.fq seq_0_2.fq > P0.sam

Now, I check the ASCII of base quality (column 11 in the SAM format, the specification is here).
head -n 3 P0.sam | cut -f11

IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII
IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII

According to this page, the ASCII (in order of quality) is:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}~

Question: My experiment is supposed to be perfect, so my base-quality metrics are expected to appear near the right-end of the list (like x,y,z). However, my metric I is no-where near the top of the list. In particular, I'm unable to achieve anything from J to ~. Why?

When fasta reads are aligned they are by default assigned the phred score of 40, which in phred+33 encoding is represented by I. Phred+33 uses ASCII characters from ! to I:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHI

Phred+33 was originally used by sanger machines but it is now used by all popular platforms such as Illumina, Ion-torrent (also Ion-proton) and Roche 454. Since most platforms now use phred+33, most aligners also assume it by default. You can specify other quality encoding formats if you want (such as phred+64 or Solexa).
Have a look at wikipedia page on FASTQ format for the different quality encoding formats.


text:
What significance does the moon have for the development of life on earth, and for earth's ecology?
Planets like Mercury and Venus do not have moons, and they do not appear to harbor (higher) life (forms). How significant is it for the emergence of life on a planet that it has a moon? How does it affect the planet's ecosystem, especially seasons and periods?

This question is too broad, and to a large extent off-topic for Bio-SE.

This question appears to be off-topic because it is about astronomy, not biology.

"our" moon certainly affects tides and so the animals living near the sea shore like barnacles have to face both high tide and low tide during which they become dry.

Out of curiosity, has this been posted on Astronomy SE? The moderators might take it, although I believe it's a duplicate of something.

Pluto does, in fact, have moons.

The part of the question which asks about the ecosystem is utterly on topic, and also interesting. If I'm not mistaken there are theories which attribute the genesis of life to the moon (via tide pools).

Another factor is that the moon stabilizes the earth's rotational axis. Without the moon the axis would significantly tilt over geological periods of time, causing large-scale climate change. So this is an interesting question straddling astronomy and biology. I'd vote to re-open, but I can't.

This question is indeed off topic here but the reason these planets don't have moons is pure chance. Different moons have different origins, some could be meteorites or other drifting bodies that were captured by the planet's gravity, others could be pieces of the planet itself that were spun off before it solidified or from an impact event. Others could be mass ejected from the sun which was captured by the planet and so on and so forth. Whether any of these events occurred in a planet's history is down to chance.
As for ecosystems, since the only planet we know of that has one is the Earth, we have no idea how other ecosystems would be affected by the presence or absence of a moon. The absence of tides would be the most obvious effect but you could also get tidal effects if you have an erratic orbit around the sun or if you have other large bodies close enough to affect you.


text:
Burns' "To a mouse" - what species of mouse?
What's the most likely mouse species Robert Burns is referring to in his poem "To a Mouse, on Turning Her Up in Her Nest with the Plough".
Burns farmed near Ayr, which is on the Firth of Clyde in Scotland. So the mouse of his poem would have to live in that area in the late 18th century. The creature obviously was living in an open field in December in a nest made of "leaves an' stibble [stubble]". From the poem's title it appears like the nest was constructed underground. "Sleekit" refers to sleek coated as in shiny fur. A clue to the mouse's diet is given by "A daimen icker in a thrave", ie grain. According to Wikipedia: "Scotland has no population of the Edible or Hazel Dormouse, or of the Yellow-necked Mouse, and the Harvest Mouse's range is limited to the southern part of the country."
The poem is here: http://en.wikipedia.org/wiki/To_a_Mouse

Have you looked at the poem for more information about the mouse's habitat and behaviour?

I've tried to give a bit more information in my original question. Does that help?

Very much, thanks! Deleting my previous comments. Off topic but which word actually refers to grain?

"Daimen means rare or occasional, icker is one ear of corn, a thrave is a measure of cut grain". Taken from http://www.robertburns.plus.com/mouse.htm.

It could be Wood Mouse(Apodemus sylvaticus).

Courtesy : redbubble.com


text:
RNA migrating slower than DNA on Formaldehyde Gel?
So I ran into an interesting problem.  I'm getting a linear DNA band that is twice as long (4x bases, but as denatured probably only 2x) as an RNA band running at the same size in a formaldehyde gel.
Both sequences have been isolated an 100% confirmed.  The gel was run in MOPS buffer.  My experience, and all the publications I've found, show that if anything RNA should run faster.  Can anyone think of a reason why the DNA band and RNA band would be running the distance despite the DNA being twice as long?
I've read a lot of fun papers on drag factors in gel matrices now, but none of it leads to this confusing and repeated result.
Edit: Gel and Conditions
Gel was 1M formaldehyde, 1% agarose.  Run at 100V for 1.5h.  RNA was mixed in a RNA loading dye which contained 15.3% v/v formaldehyde, 41.3% v/v di formamide, 4.6mM EDTA, MOPS, and bromophenol blue.  We believe our RNA loading dye to be denaturing, and it ran at expected size with RNA ladder.
................(1)........................(2)............................(3)

Lane 1 is a DNA template plasmid, cut 1 location.
Lane 2 is the Template + DNase from in vitro transcription reaction w/o polymerase.
Lane 3 is the RNA + DNase from in vitro transcription reaction.
There are no other bands in the DNA lane, and it looks like if anything, the DNA is migrating much faster than expected, despite being sequence confirmed (both before the process, and gel purified out and confirmed again).

I've deleted my answer as it was useless. In the comments you said that you're running a denaturing gel. Have you considered polyacrylamide/ polyacrylamide-urea gel?

Interesting. Do you have a picture of the gel?

I'm trying to get an OK from the tech office to post an image now.

Maybe this is stupid but could it be that in the RNA (which I suppose is single stranded) there is only one phosphate backbone therefore less negative charges per length so that it migrates slower ?

Maybe your RNA does secondary structures...

@Pao I'm assuming that might be true for the RNA, but in a formaldehyde gel, how does that happen?

What's your agarose percentage, solution pH, voltage and running time?

Well, did you add denaturing agents such as SDS or urea?

@Kendall Gel was 1M formaldehyde, 1% agarose. Run at 100V for 1.5h; updated question

@Pao 15.3% v/v formaldehyde, 41.3% v/v di formamide; updated question.  Think that should be denaturing, and does SDS actually help denature RNA? That's probably off topic though.

Since RNA and DNA of equal sizes and equally denatured would have pretty much the same charge and almost the same mass, why wouldn't they run at the same rate? Never run both DNA and RNA on the same gel, so I don't know what's supposed to happen.

They are not of equal size, that's the question.  The RNA is 1/2 the length of the DNA.

Then off the top of my head, maybe the RNA isn't being fully denatured for some reason. That lane also looks very overloaded, could that alter the migration rate?

Some sources note that old formamide or formaldehyde may cause issues in the gel. pH may also cause mobility issues if it's too acidic.. as for optimizing the gel, I see some resources using a 1% agarose gel with 2M formaldehyde.. i believe here and they also suggest running the gel in a 1x MOPS buffer for 10 minutes during prep. It's still confusing, though. You could try a different denaturing method, and see if you can repeat the result.

+1 for the "overloaded" explanation. At least for SDS PAGE gels, overloading a well results in the lane "blobbing" and travelling slower than expected.

@Kendall That's a good idea.  We're giving it another go.  Oddly enough the RNA seems to be running the right size, it's the DNA that's migrating to far.

Do you see the correct size bands for the integrity of RNA?  28S, 18S and 5S bands?

The inclusion of formaldehyde in the gel and buffer is to keep the RNA denatured (ie after heating the sample to melt the double-stranded stem-loops, just prior to loading the gel), in the hope that the RNA will migrate through the gel with an Rf proportional to its molecular weight (approximated here by its length). Therefore the correct size markers would also be made of RNA (and prepared the same way, by heating).
It is difficult to predict, a priori, how a double-stranded DNA fragment would migrate under similar conditions, without also including a lane of ds DNA size markers.
In other words I would only use DNA markers for DNA and RNA markers for RNA. By repeating this experiment (1 lane of DNA MW vs 1 lane of RNA MW) at different voltage gradients and different concentrations of agarose, you might be able to plot two standard curves that would let you predict where your DNA fragment is expected to migrate relative to the RNA transcript, but without that data I would not assume that a larger DNA fragment would run slower than its RNA transcript.
Even if the dsDNA was exactly the same length as the ssRNA (and pretending that the MW of the dNTPs and NTPs are identical), the DNA's MW would be twice as much as the RNA, but the negative charge on the DNA would also be twice as much.

Instead of a standard curve, why not just run two ladders on your gel? 1 DNA and 1 RNA.

@user137 Exactly, that is the immediate practical solution.

While I agree with everything you mentioned, it doesn't really address the issue.  I've been working on a standard curve. It is odd that the DNA is migrating much quicker than expected, as you point out it should be slower for the same length, doubly so for twice the length.  And yet under multiple conditions I am seeing the same thing.  Might be  the long poly-A tracks in the DNA, I don't know.  At this point it's not as import for the project as it is a curiosity.


text:
Is this plant in my urban garden poison ivy?
Is this plant in my urban garden poison ivy?

Toronto, Ontario area.
July 19, 2023
Full shade
Three leaves; toothed but not serrated.

Possible Answer: (I can’t post an answer due to the question being closed)
I suspect it is Boston Ivy (Parthenocissus tricuspidata).

Eastern Poison Ivy vs Boston Ivy
Boston Ivy: A deciduous woody vine native to east Asia, introduced in North America. Established in numerous scattered locations, mostly around urban areas. It is a close relative of the native Virginia creeper.
Middle leaflet has no stem or a short stem not much longer than that of side leaflets.

Related: Vine has simple and compound leaves

Virginia creeper has leaves in 5s, not leaves in 3s. Definitely not virginia creeper.

Almost certainly Toxicodendron (poison ivy) genus; I think Toxicodendron rydbergii (western poison ivy). Leaves are in threes, with the central one longer than the others. Leaves are variable in toothing and serrations on the same plant. This one will be a shrub rather than a climbing vine.
Incidentally, the other, dark-green leaved, plant in there is common ivy (Hedera helix).


text:
Do Vaccinium membranaceum plants need a minimum amount of darkness per 24 hours?
I have Vaccinium membranaceum (black huckleberry) seedlings growing in a greenhouse. I have the option of providing fluorescent light to the plants 24 hours a day.
However, it has occurred to me that plants like Vaccinium membranaceum might require a minimum amount of darkness per 24 hours.
What darkness requirements do Vaccinium membranaceum plants have?

This is likely to vary greatly given that some Vaccinium species grow under thick (shaded) canopies while others are capable of growing in clearings and forest gaps. So, they would experience different amounts of light to begin with. Are you instead thinking that perhaps temperature differentials or time spent respiring might impact the plants?  What research have you tried to do on this topic on yoru own?

Some plants are long day plants -- they require a certain number of days longer than a certain number of hours.
Some plants are long night plants -- they need nights that are longer than a certain number of hours.
See this for more details: http://www.biology-pages.info/P/Photoperiodism.html
Other plants are day neutral.  They bloom when triggered by other stimuli such as it being warm enough.
If you don't care if they bloom or not, then you can give them 24 hour light.  They should grow somewhat faster.
However, you may need to check what triggers them into dormancy.  E.g. Spruce start going into dormancy when days get shorter than about 10 hours (Varies by species, and provenance)  Reforestation growers trick them into going dormant in August with black tarps in mid afternoon.  They can then plant them with minimal stress, and they take off in the spring.

Please add citations or additional support to backup some of your claims. Thanks.

Can't.  First year botany lecture 45 years ago.

My old plant physiology textbook is at the office and it has been 15 years since I had the class so going a bit off memory here...  But yes, they do have a circadian rhythm and benefit from having a dark cycle.  There really isn't any need or extra benefit from having them under more than 16 hours of light.  I can dig out specifics from my textbook and old class notes later if someone else doesn't chime in with more info...

Recalling info from memory is much better reserved for a comment on this site. Answers should be complete. I recommend that you find your textbook and provide direct evidence (either a quote, citation, etc.) to support your claims. Thanks.

What's the title of the textbook? I'll order a copy.


text:
ID: Serated-leafed seedling
A seedling has popped up in one of my planters (acid soil; Toronto, Ontario).
What is it?

June 4, 2020:

June 20, 2020:

it's a kind of tree, perhaps a kind of oak. https://ask.extension.org/questions/332861

@com.prehensible The leaves look opposite. Are there Oaks with opposite leaves?

Yes i wasn't that convinced either that it's an oak, it just has a lot in common and also some differences. You could tell straight away from it's woodyness and toughness if its a tree by feeling it, if its twiggy its a tree, time will tell.

An extension of com.prehensible's comment -- your sapling could be a bur oak.  It is older than the seedling pictured below, but retains a similar cotyledon.  The range of this species includes Ontario.

bur oak seedling
Photo by Todd Dwyer, via Flickr
(please ignore the image artifact -- an effect of resizing)

Your photo appears to show the tree at a stage after the seedling shown above and before the more mature sapling shown here:

bur oak sapling
Photo by John T. Fowler, Alamy Stock Photo

Thanks! For what it's worth, an aquaintance had this comment: "...I don't think it's an oak of any species, since it has normal cotyledon (seed) leaves above ground. Oak cotyledons are modified to store food for the seedling, so they don't resemble leaves and usually don't emerge from the acorn. I don't think the example photo posted to Stack Exchange is an oak either." ... Food for thought?

Seedling emergence patterns - PDF: "...the cotyledons remain underground and the stem (epicotyl)
emerges above ground. This pattern is called hypogeous. Large seeded plants like
Kentucky coffeetree and oaks tend to have hypogeous germination."

..."the first photo is not an oak. The second one (the older plant) is an oak, but the bristles on the leaf lobes mean it's not a bur oak."

A diagram from The Woody-plant Seed Manual - United States Forest Service -- Google Books link here.

@Wilson it sounds like your acquaintance is quite knowledgable! I don’t suppose you can convince her/him to make an account on biology.SE? ;)

With regard to the seedling being an oak, just gently excavate around the stem - the acorn will still be there to identify. You can do this without hurting the roots.

The hairy stem and leaf pattern remind me of elms. Wikipedia has an example of american elm seedlings which look quite similar to what you have to me:


text:
What species of mulberry is this?
I have several mulberry seedlings that have popped up in my garden.

What species (or hybrid-species) are they?
Details:

The location is Toronto, Ontario
The date is July 18th, 2019
I have several different kinds of cultivated and uncultivated mulberries in the surrounding area that could have been the parents. I would list their cultivars and species names, but to be honest, I don't have much faith in them (I think they might just taint our analysis/identification).

Note: Here are some close-up photos of the plant in the bottom-right of the above photo:

https://i.sstatic.net/qi6dJ.jpg
https://i.sstatic.net/JlNh0.jpg
https://i.sstatic.net/rP2M8.jpg
https://i.sstatic.net/yWQGg.jpg
https://i.sstatic.net/vkH80.jpg
https://i.sstatic.net/ZJTx2.jpg

Even if we restrict ourselves to Morus rubra, the native species, versus Morus alba, the species introduced from China, and ignore possible hybrids, I think you may have to wait for the trees to be larger for an ID.  I found a relevant paper (Nepal, M.P., M.H. Mayfield, C.J. Ferguson. 2012. "Identification of eastern North American Morus (Moraceae): Taxonomic status of M. murrayana." Phytoneuron 2012-26: 1–6.) which contains the following paragraph:

Salient features for correct identification of M. alba and M. rubra
Morus rubra can be easily distinguished from M. alba using
  morphological characters of the leaf, bud, branch, bark and
  infructescence. Leaf characters present a challenge because of the
  tendency for leaves of juvenile shoots to converge in morphology among
  these species. Nearly all of the unique characteristics of M. rubra
  fail in juvenile leaves. Leaves of M. rubra (5–40 x 3–28 cm) are
  larger overall than those of M. alba (2–20 x 1.5–18 cm). In M. rubra
  leaves, the adaxial (upper) surface is rough and dull green (vs.
  smooth and lustrous) and the abaxial (lower) surface is usually
  densely hairy with erect trichomes evenly distributed (soft to the
  touch); the base is often cordate (heart-shaped); the apex is acute,
  acuminate to subcaudate; marginal teeth are often pointed; and the
  color of the main veins is more or less like the color of the lamina
  on the underside. Leaves of Morus alba are usually deep green and
  lustrous adaxially and have few hairs concentrated along the main
  veins on the abaxial surface; the base is rounded (vs. cordate); the
  apex is obtuse; the marginal teeth are fewer, relatively larger, and
  rounded; and the primary veins (underside) contrast more with the leaf
  surface than in M. rubra. The winter buds of M. rubra have bud scale
  margins with a darker (almost black) apical band, while in M. alba,
  the bud scale margins are uniformly brown. Morus rubra has grayish
  bark with flattened, thin plates that peel outwards in age. Morus alba
  bark has thick and solid ridges that are more of a reddish tan
  coloration. The orientation of branches in a mature M. rubra is
  somewhat planar (flat) and spreading like an umbrella. In M. alba the
  orientation of branches is more erect or spreading, and the plants
  appear more rounded or bushy as a result. The fruit of M. rubra is
  longer and narrowly cylindric, while in M. alba it is typically ovoid
  or ellipsoid.

This might be very useful for mature trees, but note the line "Leaf characters present a challenge because of the tendency for leaves of juvenile shoots to converge in morphology among these species. Nearly all of the unique characteristics of M. rubra fail in juvenile leaves."
There is also a recent, purely genetic analysis of the mulberries freely available at PLOS One but I don't think it's too helpful in this context other than it confirms that hybrids are common.
The Phytoneuron paper and a number of internet sites generally point to M. rubra being densely hairy on the underside of the leaves as one of the more important characters.  Your specimens appear glabrous, but the pictures though excellent may still not show tiny hairs well.  If we trust this character in the young plants then we would lean toward M. alba but as stated above, you may have to wait and see.


text:
What gives things their colour?
My 6 year old daughter asked me 2 biology-related questions yesterday and I tried my best to answer them with the aid of YouTube videos.  One of the questions (I may post the other one too) was

How do we see colour?

I showed her a video on YouTube where it was explained that light hits an object and if that object is a tangerine then that object will absorb all colours except orange and will reflect orange and that's why we see it as being orange.  I then repeated this explanation and she said.

But how do we see different colours?

I then showed her a video describing corneas, vitreous humours, lenses, optical nerves and so on.  I think I lost her.  I got a bit lost too.
Now I have two problems, which I'd like to ask to you all as questions

I do not know how to explain to a 6 year old how we are able to perceive colour.  Does anyone know how this can be explained?
I have never quite understood this idea that an object has a colour depending on the light that hits it.  Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.  What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours.  What is that something?

That "something" is just the absorption and emission of this light energy within the bonds and structures of whatever you happen to be looking at.

Also, related: http://biology.stackexchange.com/questions/1446/why-can-cones-detect-color-but-rods-cant?rq=1

this question has two pretty formidable parts - 1) how do we perceive color and 2) what optical properties of matter give them their color. @LanceLafontaine's answer does a good job with this. (2) is a very big question, depending on the level of detail at least as much chemistry and physics as it is biology.

my daughter asks formidable questions.  I just hope she doesn't ask me how babies get inside their mummy's tummy's.

I hope I'll have the time to whip up an answer later, but I just wanted to make the point that objects do not "have" color. We "perceive" them as colored. Try holding a gin&tonic under a neon (UV) light (it will appear bright blue) or placing a blue object under a streetlight (it will appear green).

But you see this is exactly what I don't get.  Holding a gold bar under neon lighting, I assume, produces a different colour to holding a silver bar under the same neon light.  Therefore, objects do have a property, lets call it shuyutokiwomatatalilibo, for the sake of argument, that makes it appear to have a different colour to other objects.

I do not know how to explain to a 6 year old how we are able to perceive colour. Does anyone know how this can be explained?

Well, depending on the depth you want to introduce her to, it can be difficult to explain to adults - much less children. You explained the basics well enough. Without going to the molecular mechanisms, here's a useful diagram:

Light will pass through the eye and Retina until it hits the Cones and Rods. That produces a reaction (which I'll address next) - which then causes signals to either resume or cease (Rods are, ironically, shut off by light - not turned on). These signals pass through Ganglion cells, through the Optic Nerve, and interpreted by the brain. When some cells are switched on, like a 3-Way traffic stop, they will prevent the information from other cells being transmitted.
A simple way of explaining it might be that inside our eyes are millions of teeny-tiny molecules that act like light-switches, and the brightness and color of light determine which of the "light-switches" are on or off.
If you want to go further into the actual mechanisms (or just have the background knowledge for future reference) the next diagram shows the mechanism itself (and the original in full-size since the one shown is squished if you prefer):

The big things to note above is the change from cis-Retinal to trans-Retinal which occurs after a Photon is absorbed. This causes signaling molecules to go a bit wild, open ion channels, and the depolarization of the membrane propagates the charge down the cell - much like a neuron.

I have never quite understood this idea that an object has a colour depending on the light that hits it. Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.

Well, let me stop you here. Low-light is a different situation than colored-light. Let's get the basics down:
Photons are absorbed by the electrons of the atoms that compose the molecules of an object. Whatever Wavelength of light is not absorbed by the electrons is reflected, and it's this Wavelength that we perceive as the color of the object as our Cones absorb the reflected light.
Photons can also be emitted when an electron moves to a lower-energy state. The Wavelength emitted by the electron is directly related to the difference between the High and Low energy states, as this diagram shows fairly well:

The emitted photons are the object's "Incandescence" - which is when an object produces a color of light by itself. The color you perceive is NOT going to change if the object emits incandescent light because the object is generating its own light. Neon signs are a great example: The gases being subjected to a current emit light, and will appear whatever color it's supposed to be whether or not it's a blue moon or sunset.
Photons which are reflected and not emitted - i.e. almost everything that doesn't have a power source - as I said above, are then absorbed by our Cones and our brain interprets the signals to produce a color.
The reason why objects that reflect light can change color is because not all environmental light is the same. Red objects will appear Black under Blue light because Blue light doesn't contain Red Wavelengths - there's nothing to reflect, so the object absorbs all of the available Wavelengths - the very definition of Black!
A lot of our color perception depends on ambient light, and most of the time - thanks to the Sun - that is a full-spectrum white light. Which brings me to answer the last bit of your question:

What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours. What is that something?

Yes, there definitely is something inherent in both objects. That is: Their electron configurations absorb different chunks of the spectrum, and accordingly reflect different chunks of the spectrum. Although that's still a bit simplistic, since metals have some unique properties that other Elements do not. Their electrons exist in more of an "ocean" than around central atoms, but that's a whole other question.
As a fun bit of Trivia to impress your daughter when she's old enough, it's always a fun fact to know that the color Yellow is completely constructed in your head.
The human eye only has Rho (Red), Gamma (Green), and Beta (Blue) color receptors which have the following absorption pattern (from photo.net):

What everybody sees as "Yellow" is actually when both the Green and Red receptors are activated at the Wavelength where they intercept above, which your brain interprets as "Yellow":

Because your brain does a lot of processing, despite having only three color receptors we can perceive millions of colors (and shades/tones). Now for a while everywhere you look you'll be utterly amazed at what's going on, and you rightfully should be. ;-)


text:
Flow cytometry issues
I'm having problems with data analysis here.
I have flow cytometry data being collected on a Fortessa, and when I import them into FlowJo 8.7, all of my fluorescence values are systematically 10X lower than they are on the cytometer. No idea what's going on here, anybody can help? If you want screenshots and photos of the data, I'm happy to post them up.

What is your fluorescent output?

The answer I have come to is the difference between FCS2.0 and FCS3.0 files. The binning pattern is different, and as such FCS2.0 files arbitrarily lowered my flow cytometry values compared to what I saw on the FACS DiVa software.
In the end, exporting with FCS3.0 was the way to go. If your software supports this, I'd highly recommend doing so!

I have this issue too with data from a Partec PAS III. I don't consider it a problem, as it's really just the x-axis which is one order of magnitude higher. At the end, all values coming from the machine are arbitrary values, so as long as the change is systematic, there's no problem.


text:
What would be the estimated cost sequencing?
I'm a newbie to the world of NGS, but I thought it might be a suitable and cheaper alternative to doing traditional Sanger sequencing for this particular application. However, I'm not so sure on how to approach calculating this cost, so I was hoping to reach out and see if someone could help here. This is for my grad school research project.
Problem Statement
I am about to make a rational library of ~1000 protein complexes belonging to the same family of proteins. There are 4 protein's plasmids to make per complex, and they are to be made by a combination of synthetic genomic cloning methods using cDNA, and multi-site directed mutagenesis on existing plasmids. Before testing their function as a complex, I need to verify that the cloning steps succeeded by sequence verifying each plasmid.
I could do traditional Sanger sequencing on each of the protein sequences, but given that each protein is ~2kb long, I would need 4 single direction sequencing reactions per plasmid to cover the CDS. In total, per protein complex, that's 16 sequencing reactions. At USD5 per sequencing reaction, each protein complex would cost USD80 to sequence. At 1000 sequences, that would be USD80,000 in Sanger sequencing.
I was thinking of doing something else - after creating the library, say in chunks of 384, send them for NGS on an Illumina MiSeq.
Request for Help
Given that:

I am not wedded to any particular NGS protocol,
Our only goal here is to, by one way or another, sequence verify the cloned plasmids.
1000 proteins is the right ballpark for the number of proteins that need to be sequence verified. 4 plasmids per protein complex.

What would be the appropriate sequencing strategy that could help us get way below 80K for sequencing costs?

How would NGS help you? Are you planning on mixing all 1000 plasmids together and trying to get complete coverage on all of them?

@MattDMo: Yes, that's the plan. It's 4 plasmids per sample, 1000 samples in total, each needs to have (at minimum) its 2 kb insert sequenced. But if we could get full coverage of the plasmid that's cool too.

Most NGS approaches should enable you to sequence all those plasmids at very low cost-per-base values (Please see here for more on prices). The challenge in sequencing them all, if there are sequences common to all your plasmids, will be to get adapters for each sample/plasmid so that reads can be mapped back to the correct plasmids.

Thanks Ankur - yes. These are a family of polymerases with 4 proteins. We are planning to make a rationally designed library of 1000 polymerase variants. 4 plasmids per sample, each of a different sequence, 1000 samples in total.

OK - as long as there are no sequences that overlap between those plasmids you should be able to get good depth of sequence for a grand or two I would imagine and then map back to the reference sequences to see if assembly has worked. NGS is defo the way to go.


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Quantitatively measure the impact of DNA vs epigenetics?
Background: While classical genetics deals with how DNA sequences directly code for traits, epigenetics involves chemical modifications to DNA and associated proteins that can switch genes on or off without changing the underlying DNA sequence (including DNA methylation, histone modifications, and chromatin accessibility, etc).
Question: Is it possible to quantitatively measure and compare the impact of DNA and epigenetics on expression? Which one is more important and by how much? If so,

What is the proportional contribution of epigenetic modifications
versus DNA sequence variation to gene expression variance in human
somatic cells, expressed as percentages of total phenotypic variance?

Example equation:
$\text{Total Phenotypic Variance} = \sigma^2_G + \sigma^2_E + \sigma^2_{G \times E} + \sigma^2_{\text{error}}$
Here, G means genetics, E means epigenetics, and the third term is covariance.
Example result: I wonder if there are already results like this: Genetic sequence variation explains about 25-40% of expression variance in a sample. Epigenetic variation accounts for approximately 10-30% of expression variance. The remaining variance is attributed to environmental factors, measurement noise, and gene-environment interactions
There are surely a lot of loopholes and drawbacks in this approach, so I wonder if there are better approaches. I think this quantitative analysis would be very important, because it can guide us in many areas. For example, in genetic engineering, we need to know if it is more efficient to edit the gene or to deal with the epigenetics.

There is extensive work attempting to decompose phenotypic variance into genetic, epigenetic etc. terms. Here are just three random examples from the last 10 years that I got by googling this:

https://www.nature.com/articles/s41437-019-0261-8
https://www.nature.com/articles/s41467-020-16520-1 (focuses specifically on DNA methylation, which is possibly dubious from a classic interpretation of epigenetics)
https://www.nature.com/articles/s41437-018-0114-x.pdf (theoretical review)

In some cases phenotypes show >50% of variance could be explained by epigenetic causes (see review). In other cases it is much less.
However, as always when considering these variance decomposition approaches, variance decomposition does not substitute for a causal analysis. Heritability is far too unstable of an estimator to be informative except in very well designed cases- that are more or less impossible to find for humans, because we can't breed humans for ethical reasons.
Epigenetic analysis only complicates this ambiguous approach, given its intimate relationship to both genetic and environmental contributors to phenotype.


text:
How to read this DNA inversion diagram?
In the following diagram about chromosome inversion, I don't understand:

Why do we need to take the reverse complement from step 1 to 2? Isn't inversion just reversing the bases in the region?
How is the bottom diagram derived? For example, where does the ACCCCACTC come from? I thought it should be: GACTGCCGT for 5'→3' and CTGACGGCA for 3'→5' (inversion of the sequences in the second step).

http://web2.mendelu.cz/af_291_projekty2/vseo/print.php?page=315&typ=html

Your misunderstanding probably stems from the differences of definition of inverse in bioinformatics (reverse) and cell biology/genetics.
What is shown in the picture is chromosomal inversion, in which the segment of DNA gets cut, flipped and ligated. Note that in the DNA, 5' would be ligated to 3' and vice-versa. So the 5' of the bottom strand i.e. T is ligated to the 3' of the top strand i.e. C. Similarly for the other ends. Therefore, you see a reverse complementation.
The sequence of the top strand however should have been 5'-TTAC-TGCCGTCAG-TAG-3' which has been incorrectly shown as 5'-TTAC-TGGGGTGAG-TAG-3'. That is a mistake in the picture.
Have a look at this picture [1]:

[1] Okamura, Kohji, John Wei, and Stephen W. Scherer. "Evolutionary implications of inversions that have caused intra-strand parity in DNA." BMC Genomics 8.1 (2007): 160.

That’s what I thought as well at first but if you actually look at the sequence of the red (flipped) bit, you’ll notice that it differs between the middle and the bottom picture: the red bit reads 5′→3′ TGCCGTCAG in the middle picture, but TGGGGTGAG in the bottom picture.

@KonradRudolph Oh! That seems like a mistake in the picture.


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How far does your center of mass move from stance to stance?
When the human body is perfectly centered, the center of mass is on the centerline around the belly button.  However, the human body is not always in this rigid posture.  We have many postures that we use.  How much does the center of mass shift, left to right, if we look at different stances.  I'm not so much interested in dynamic motions like walking, but rather static positions like:

At attention (obviously the center of mass will be very centered)
Weight shifted to one leg
A S-Curve, like from the traditional Greek statues

Obviously the center of mass will shift with respect to the ground, staying between the feet, but what I'm interested in is how it shifts with respect to the torso's centerline.

I'm voting to close this question as off-topic because although the question involves living things, it's not a biological question. This is a physics/mechanical engineering question.

@James While the calculation is pure physics, the numbers that would be needed can only be determined empirically based on how human beings carry themselves.  The only source I can think of to acquire such numbers would be biology.

This question is the field of biomechanics (video here). There is of course overlap. However, the simulations and measurements carried out in order to answer this question will be way more at the mechanical engineering end of the spectrum.

You can find the relevant math here:
http://hypertextbook.com/facts/2006/centerofmass.shtml
The key factors are the body mass distribution, height, standing center of mass, heartbeat, clothing, etc. You can approximate the center of mass for a given stance as:

In order to determine the center of mass of a person, we used the formula for torque:

$\Sigma\tau = r \times F$

The torques due to the weight on each end of the person were set equal to each other. The displayed weight on the scale was the force, and there are two different radii. The first radius is the distance to the center of mass from the person's feet, and the second radius is the length of the board minus the distance to the center of mass from the person's feet. The net torque of the system is zero and therefore the torques on the opposite sides of the boards must be equal:

$w_1\times x = w_2\times (l~-~x)$

where w1 is equal to the weight at the person's feet, x is equal to the distance from the person's feet to his/her center of mass, w2is equal to the weight at the head, and l is equal to the length of the beams. The resulting formula, when solved for the distance to the center of mass from the person's feet (radius one) is:

$x = \underline {~~~w_2\times l~~~}$
$\hspace {11mm}w_1~+~w_2$

After determining the location of each person's center of mass, the ratio of the center of mass to the height of each person was calculated using the formula:

$x/h$

where x is the location of the person's center of mass and h is the person's height.

That article had plenty of discussion of the center of mass from head to foot, but no content on left to right.  Part of this is because the study was done laying down, rather than in a standing position.

Its the same math. Just treat right as "head" and left as "foot". The fundamental problem is balancing two loads around a center of mass.

Its the same math, but different data.  I suppose that if nobody has ever done this study before, I can go gather my own data with this method.

COM moves both horizontally and vertically during gait. However, the displacement is much more higher in up-down than left-right shift


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Does the biosphere have infinite resources and are they infinitely renewable?
Does biomass represent all of the resources of the biosphere and therefore it would be theoretically infinitely renewable (as long as we have the sun) since all the biomass is part of the carbon cycle?
Also, should I consider resources like gold to be part of the biosphere and therefore all the resources would not be infinite nor infinitely renewable?

Assuming no one burned any fossil fuels, the carbon cycle isn't perfectly recycled. Some organic matter would get trapped as coal or oil. But thankfully we have solved that problem by digging it back up and burning it.

No, it is not infinite.
The sun has not an infinite mass neither does the earth. So energy is not infinite. But we probably don't really care about that as it applies at a scale we're not really concerned with. What is important at our scale is the rate at which is the rate at which the biomass we're destroying (eating, building houses with) is produced. The rate at which we consume this biomass has to not overpass the rate at which this biomass is produced. Than, practically speaking, biomass will be produced infinitely. Of course, ecosystem stability is not that easy but it is not within the scope of the post to talk about that.

Obviously not infinite, since the Earth has a finite mass, and the sun has a finite lifetime.  Also the Earth continually loses some (very small) fraction of its atmosphere & water to space, so eventually it would wind up like Mars (which was warmer, wetter, and probably habitable a billion years or so ago).

This is an interesting page. Mentions that the weathering of rocks will most likely deplete most CO2 from the atmosphere by about 600 million years from now. Some plants may survive for a little longer depending on what carbon fixation method they use. This would probably happen sooner than loss of atmosphere to space. I think the expansion of the sun will happen before then.

@user137 The Wikipedia article on Future of the Earth referenced above has so many faults, studded with facts, that it's not even wrong.


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Using the IMGT/GENE-DB service to find RSS
I'm trying to get the data for the Human and Mouse 12 and 23 Recomination
Signal Sequences (RSS), to run a classification algorithm on it. I'm not a
biologist, so I apologise in advance for my misunderstandings and
confusion.
A version of the data is available here, but I thought I would try to
get it from www.imgt.org, if possible. There is also another slightly
different version available for the mouse here.
I'm trying to follow the instructions at IMGT-FAQ to obtain Recombination Signal
Sequences for the mouse.
Here is what I have selected at the search page:
Identification:
Species : Mus Musculus
GeneType: any
Functionality: functional
MolecularComponent: any
Clone name: <blank>

IMGT group: IGHV
IMGT subgroup: any
IMGT gene: <blank>

I'm not clear what "Locus", "Main locus", and
"IGMT group" mean here exactly. Specifically, what is the difference
between "Locus" and "Main locus"?
I think, but am not sure, that IGHV corresponds to V genes in the
Immunoglobulin heavy locus (IGH@) on chromosome 14, where locus here
denotes collections of genes. Clarifications and corrections appreciated.
I would have expected that the IGH locus would correspond to "IMGT group"
entries like "IGHJ, IGHV" etc, and the IGK locus would correspond to IMGT
group entries like "IGK, IGKJ, IGKV", but no matter what I select for
Locus, it does not change the possible entries for "IMGT group".
Running the search gives
Number of resulting genes : 218
Number of resulting alleles : 350
As instructed, I went to the bottom, selected "Select all genes", clicked
on "Choose label(s) for extraction", and selected "V-RS".
I got

Number of results=98

The first few results were
>X02459|IGHV1-4*02|Mus musculus_BALB/c|F|V-RS|395..432|38 nt|NR| | | |
|38+0=38| | |
cacagtggtgcaaccacatcccgactgtgtcagaaacc

>X02064|IGHV1-54*02|Mus musculus|F|V-RS|295..332|38 nt|NR| | | | |38+0=38|
| |
cacagtgttgcaaccacatcctgagtgtgtcagaaatc

>M34978|IGHV1-58*02|Mus musculus_A/J|P|V-RS|554..560|7 nt|NR| | | |
|7+0=7|partial in 3'| |
cacagtg

Ok, now I'm confused. The lengths of the RSS should be 28 or 39. but I
counted lengths of 4,7, 31, 38, and 39. Are the results here not supposed
to contain the 12 and 23 RSS?
So, I must be misunderstanding things here. Possibly many things. Any
explanations and clarifications are appreciated.

I'm not clear what "Locus", "Main locus", and "IGMT group" mean here
  exactly. Specifically, what is the difference between "Locus" and
  "Main locus"?

From the same site:

A locus is a set of IG or TR genes that are ordered and are localized
  in a same chromosomal location, in a given species. […]
   A locus comprises the genes of different groups which participate
  potentially to the synthesis of a polypeptide of the same 'chain
  type'.

Main locus should have been Locus minus the orphons:

A chromosomal orphon set is a set of IG or TR orphons (genes outside
  from the main loci) belonging to a same group and localized on the
  same chromosome in a given species.

However the Main Locus and Locus have the same options; Options for the Locus should have been chromosomes. They must have made a revision in the site but forgot to change the help. I tried setting all the options except any in Locus and selecting all for the Orphons; it yields no result. It works only if you set any in Locus. So it seems Locus option is useless; you can set the Locus as any by default.
 For confirmation it is best to ask the authors.
From the changelog:

16 April 2012

Update of the IMGT/GENE-DB Query page:
The search criteria are organized according to the axioms IDENTIFICATION, LOCALIZATION and CLASSIFICATION of IMGT-ONTOLOGY.
  Addition of new search criteria:

MolecularComponent (IDENTIFICATION)
Locus (LOCALIZATION): includes main loci and chromosomal orphon sets
  Main locus: "all" value allows to search genes of all main loci.
  Chromosomal orphon set: "all" value allows to search genes of all chromosomal orphon sets

For details on the IMGT classification you should refer to this paper.
Fixing a Locus option does not change the IMGT dropdown box option but the results are different. If you try your example and set Main Locus as IGH and IMGT Group as IGKJ you would get no results. It is just a problem of the web interface. Apparently the search works fine.

Running the search
I searched with the exact same criterion as you mentioned and did not get any sequences smaller than 38nt. There must have been some bug which seems to be fixed.


text:
Prevalent large (>=90kDa) maintenance protein/loading control
I was wondering if anyone had recommendations for good, large (hopefully 100kDa+), control proteins that would be present in most mammalian cells.  I'm working mostly with tissue samples from humans and mice, and airway epithelium in particular if that matters.  So far the best I've thought of is HSP90, but that is far from ideal for a number of reasons.  My target proteins are between 125 and 210 kDa.  To improve resolution, we've run pretty much everything under 90kDa off the gel.
That removes the old standbys like actin or GAPDH.  I understand that the protein levels could vary between cell types for a good loading control target.  Bonus points if you know a good antibody clone to it.

How about RNA polymerase subunits - some of these are large. (In E. coli I used to use beta-beta prime for the same reason. Not particularly abundant but very distinctive.)

@alanboyd Not a bad idea, I'll give it a try.  Most of these will be testing effects from infections with RNA viruses, so this might look interesting anyway.

Vinculin!  I love our grad-students, I can't believe I didn't think of it last night.
Also, awesome chart, even if it's from a company.

Thats a pretty useful chart. Bookmarked for later use.

@Chris I thought about replicating it here, but it seemed too much like stealing


text:
Workflow for batch analysis of ROI in histology samples
This is a pretty big task, and I have several work-arounds, but I am looking for an efficient way to go from PAS stained slides of lung tissue to defined ROI's over the whole slide (presumably via BLOB detection).  I am hoping to get every airway epithelium annotated as an ROI so I can get colorimetric/masking data from the ROI.
That's the simply stated goal, but there are several issues along the way.  The imager we are using produces files in the MRXS format.  Satyanarayanan group's work at OpenSlide has been great in the initial hurtles of exporting the files into very large tiled TIFF files (~2-5GB each, under JPEG compression, generating a few hundred a week).  This has it's own bugs, but the mailing list has been solid.
Given a very large series of very large tiled TIFF files, what is the best way to train a BLOB (or other) detection method to find an ROI?  Using small images, I've gotten acceptable mapping with WIKA, but every time I try on larger images I run into errors and corruptions (when I don't run into memory limits).  Is ImageJ the best choice for this?  If so which plugins would you recommend trying?  I've used what comes FIJI and I've been exploring over others.  LOCI will load ~80% of the image correctly then run into tiling problems.  Given that you can't choose the ROI strictly on color, but human's can quickly ID it, I think a computer will be able to.
I have two systems I'm trying this on:
64-bit Ubuntu, 32GB RAM, FX-9590 processor
64-bit Windows 7, 16GB RAM, 2x E5430 processor

The Win7 machine is the one required for the imager, and I'm trying to do the analysis on the more powerful Ubuntu box.  Deroulers et al produced an interesting work on the subject, however, my group hasn't been able to implement the system as of yet.
I would prefer an open solution, but a proven solution with propitiatory software would also be acceptable.
I thought the over-arching question would fit here, but if people think I should break it up and put smaller questions on SO, I will.  I'm just not sure we're tackling this the best way from slide to graph.

@leonardo As mentioned in the question, I have tried FIJI.  Unfortunately I don't have a method that works to go from MRXS to an LZW compressed TIFF. I can go from MRXS to an uncompressed TIFF (5-10GB), then from that to an LZW compressed file, but that is a huge time hole. If you look at the paper, it's a known problem in the ImageJ world, and I think one that has no coordinated effort to solve. I was wondering if anyone else here has tried to tackle this, and we may end up publishing a methods paper if we figure it out.


text:
Why does hair turn grey or white, and why does it happen later for some?
The question is pretty simple: what is happening molecularly when hair turns grey or white? I would imagine that it is due to the lack of a particular compound. I'm also interested in why some people's onset of grey hair happens much later than others.

Each individuals hair colour is determined by the particular pigment they produce (called melanin - the same stuff in your skin that makes you tan).
As the body ages this pigment (produced by the melanonocytes - cells that reside in the hair follicle) is produced less and less, until the hair is no longer coloured, and appears grey.
This is unique to each individual because it is a genetic (and therefore highly heritable) trait. Because it is in no way linked to mortality there is no selection pressure against greying hair.
The reason that the pigment is not longer produced is the gradual depletion of the stem-cell pool with age. This is common to many tissues, hair follicles being just one. As the 'pool' of stem cells is depleted, the melanocytes are no longer replaced as frequently, and thus less pigment is produced as we age.

Are there ideas as to why the pigment production declines with age?

@RoryM - added reference to interesting review on the subject.

Thanks for the answer and the edit  (which is what I was most curious about).

Stress has finally been definitively shown to be a cause of graying hair.

As such, delay or acceleration of onset could be due to stress.

Work by Zhang et al. (2020) (postdoc in Ya-Chieh Hsu's lab at Harvard) showed that acute stress leads to hair greying through the fast depletion of melanocyte stem cells in mice.
Of note from their abstract:

hair greying results from activation of the sympathetic nerves that innervate the melanocyte stem-cell niche. Under conditions of stress, the activation of these sympathetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepinephrine). This causes quiescent melanocyte stem cells to proliferate rapidly, and is followed by their differentiation, migration and permanent depletion from the niche. Transient suppression of the proliferation of melanocyte stem cells prevents stress-induced hair greying. Our study demonstrates that neuronal activity that is induced by acute stress can drive a rapid and permanent loss of somatic stem cells, and illustrates an example in which the maintenance of somatic stem cells is directly influenced by the overall physiological state of the organism.

You can read a more complete summary of this work here.

The reason for this is that catalase, the enzyme responsible for catalyzing the breakdown of hydrogen peroxide on the surface of the skin, diminishes as we age.The "greying" is the the effects of bleaching of the hair fiber as result of the increased peroxide levels at the skin's surface.

Not exacly can you add any references for your claims ?

To reinforce the comment made by @L.Diago, I would suggest as a new user you consult the help on answering questions. The key thing about Stack Exchange sites is that answers are voted on in an objective manner. I do not know the answer to the question, but neither I nor the poster can judge if your answer is correct unless you provide evidence (references, preferably linked) in support. This is science. Nobody (or at least, not me) is going to accept it on your word, even if you are a Nobel Prize winner.

helpful link o you can properly flesh out this answer. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973559/