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Is the theory of evolution being disproved by bats?
For some species the Darwin's theory evolution makes perfect sense. I can easily imagine how, for example, the giraffe has evolved to its current appearance: the natural selection was favoring individuals that could consume more vegetable food from trees using longer necks, and some individuals were getting at birth necks longer than average by pure genetic randomness and the long neck trait was being propagated to descendant individuals by means of genetic inheritance. I have no problem with understanding this kind of evolution.
Now let's have a look at the bat and its relatives. The bat is one of the few mammals that have something to do with flying and the only one that took flying to the bird level. Paleontologically, first mammals date to the dinosaur era and initially looked similar to the present-day shrew (which looks much like a mouse). The question is: how in the world prehistoric mouse-like creatures could grow wings over time? It impossible to believe that some mouse-like individuals were getting wing-like limbs by mutation and the "wings" were growing out accompanied with the knowledge of how the "wings" can actually be used. Ok, then maybe first wings were tiny moth-size wings and then grew larger? But where natural selection would come into play in this case? Such mouse-like individuals would have no advantage over their wingless relatives and thus would not be able to transfer those wing-growing genes to their descendants, quite the contrary, such individuals with useless mutations that interfere with their ability to walk would be suppressed by natural selection and therefore "weeded out".
So what is the story behind the bat's wings and is the Darwin's theory really able to support it?

Darwin's theory was flawed and that's not a secret, but the contemporary theory of evolution is about as accepted as it gets. Species or traits which pose a challenge to it are nowadays more commonly regarded as a case which will be solved sooner or later (possibly by fossil findings) rather than a potential proof against the theory.

Please don’t cross-post. – If you’re unsure which site to post on, discuss this on the meta sites. FWIW Skeptics is a better suited site. A biology website is probably not the best place to question the basic tenet of biology, much like the Christianity Stack Exchange will not accept discussions about the non-existence of god.

@KonradRudolph: the cross-post looks like it may be closed as off-topic there.

http://www.sweary.com/dailyfun/wp-content/uploads/giraffes.jpg

@Mechanicals How do you figure that out? Two mods (me included) have commented saying that it’s on topic.

That's weird.  I added a comment here yesterday and it seems to have been deleted.  Is that possible?

Is the giraffe example accurate? Was reaching higher food sources indeed the mechanism driving the evolution of longer necks?

@DanielStandage... Maybe: http://www.wired.com/wiredscience/2010/09/giraffes-necks-for-food-or-necks-for-sex/

Never really fond of scientific fundamentalism  all theories are in need of continual questioning to keep them relevant. Socratic biology was at least as accepted for much longer than Darwin. In any case beginners often find that evolution in general is a lot more robust than it appears at first. This is not a difficult question.

Theory of evolution is not being disproven by anything and therefore it must not be being disproven by bats.

@Jerry yes, it is possible, in short if comments are straying too far away from the question they are pruned.

I think bats would actually be a good place to look to study evolution. Bats make up 25% of all mammal species, so there is a lot a diversity there. That diversity is direct evidence of evolution and speciation.

Take a look at this little fellow:

It's a flying squirrel — a shy little nocturnal rodent which lives in trees and, despite its name, does not actually fly.  It does, however, have a skin membrane called a patagium between its fore and hind limbs which allows it to glide from tree to tree and thus evade ground predators.
It's not hard to see how the flying squirrel's patagium may have evolved: after all, ordinary squirrels, to which the flying squirrel is indeed related, also spend most of their time in trees and avoid the ground, often performing quite impressive leaps to cross from one tree to another.  With sufficient pressure to minimize time spent on the ground, any little morphological changes that allowed longer leaps would be favored by natural selection.
Indeed, there are plenty of other groups of mammals which have independently evolved very similar adaptations to gliding.  Given how many small arboreal mammals there are, this is perhaps not surprising.  What's special about bats is not the fact that they possess flight membranes — it's that they're the only group of mammals, so far, to have taken the next step to actual powered flight.

Gotta love the way you started your answer. Thanks.

So basically, once trees evolved, birds (and bats) were inevitable.

I think sugar gliders (and the like) are different in that their skeletons dont indicate that they are gliders. The bone structure of bats have clearly evolved i.e. in forming elongated fingers to fit their wings.

try "flying" lemurs then, sugar gliders would the very start of the adaptations. you can also look at onychonycteris a late bad ancestor with short fingers compared to modern bats but far too long to serve any other function.

Check out this famous paper by Gould and Lewontin, the Spandrels of San Marco.  It's essentially a criticism of your question as it's not really the right question to ask.  You're engaging in what they call "adaptive storytelling".  The truth is that barring fossil intermediaries it's almost impossible to infer how a species transitioned from primitive ancestors.  Secondly you're assuming constant selective pressure over time. It certainly can be the case that traits evolve in certain environments but are conserved over time despite no longer serving their original function (why do flightless birds have feathers still? etc.).

Penguins would be pretty cold without their feathers.

Perhaps you didn't realise that bats' wings are equivalent to the front limbs of other mammals? They aren't extra limbs, just adapted ones, and the wings are formed from flaps of skin between the 'fingers'.
Taking that into account, I don't even see how anyone can think this is a challenge to the theory of evolution. It's obvious that increased skin webbing between fingers, eventually combined with increased finger length, provides an adaptive benefit to tree-dwelling small mammals. Initially it gives increased air resistance to allow controlled falling, then to allow gliding (like in flying squirrels), and in the most extreme cases to allow flying.
These kinds of questions are always about a failure of imagination, or a misunderstanding of the basic facts, and never about the theory of evolution being wrong. (edit: that doesn't mean the theory of evolution can't be challenged - it is a theory - but that this isn't a valid way to challenge it).

+1, I agree completely with you but I would remove or rephrase the last sentence. The theory of evolution is our current accepted model for the evolution of species. It is a scientific theory and hence it is falsificable. Maybe 500 years in the future strong evidence will have shown up that will make us rethink our current theory of evolution, much like some of Darwins' original points are now being refined. Assuming that any questioning of a scientific theory stems from misunderstanding it and that the theory cannot be wrong makes it become something more like a religious dogma.

By 'equivalent' you mean 'homologous', right?

@nico I certainly didn't mean the theory of evolution is immune to testing or falsification, but that saying 'I can't imagine how X trait evolved, therefore the theory is wrong' are not valid challenges to the theory. My answer was more of a grumpy tirade than a proper answer :)

@Mechanicalsnail yes, but given the asker thought bats' wings were an extra limb, I went for non-technical vocabulary.

@RichardSmith-Unna: I think the technical term for the OP's line of reasoning is Argument from Personal Incredulity.


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How does sex differentiation work in Paracerceis sculpta, the sexually tetramorphic isopod?
Paracerceis sculpta is a marine isopod species known for its unusual reproductive strategy:

female: medium-sized; lives in harems run by an α male
α male: large; keeps a harem of females
β male: medium; mimics a female in order to enter a harem and mate
γ male: small; mimics a juvenile in order to slip into a harem and mate

.
How does this 4-way sex differentiation occur? That is, what determines which of the morphs an individual develops into?

There's also the throat colors of the side-blotched lizard.

Shuster, SM & C Sassaman (1997)
  Genetic interaction between male mating strategy and sex ratio in a marine isopod. Nature 388: 373-377

As described in this paper, the chromosomal system of sex determination in Paracerceis sculpta is ZW=females, ZZ=males. Genetic evidence indicates that the morph of a ZZ male is determined by a second locus, Ams (alternative mating strategy) which exists in three allelic forms whose dominance relationship is Amsβ > Amsγ > Amsα. So for example, to be an α type male, an individual must be ZZ Amsα / Amsα.
That's the end of the answer, what follows is supplementary information.
The paper also describes an additional layer of complexity in the sex-determining system of P. sculpta involving sex changes in both directions. This is explained by a model in terms of two other factors: an autosomal locus Tfr (transformer) and a cytoplasmic factor ECF (extra-chromosomal factor) which interact as shown in the Table below (taken from the paper). However, this doesn't really add anything to the Ams story as far as male morphs are concerned, except that some of them start as females.

source: Stack Exchange

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

sort: votes


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How do members of cryptic species know who to mate with?
According to Wikipedia:

In biology, a cryptic species complex is a group of species which
  satisfy the biological definition of species—that is, they are
  reproductively isolated from each other—but whose morphology is very
  similar (in some cases virtually identical).

How do members of these species know who to mate with?  Or would they unknowingly mate with incompatible partners?

Do cryptic species not perform courtship rituals as other species do?

Olfaction (especially pheromones) has been very important for mating partner selection for millenia of evolution: this is often the mechanism that doesn't fail and disregards the morphology, size and other secondary properties of the partner :)

This is actually quite common in plants and is known as "pollen interference": essentially, the stigma is jammed up with pollen from incompatible partners, for instance other species. I suppose this could also be a factor in animals with broadcast spawning.

As both @Rory M and @Alexander Galkin suggest, there are various non-visual mating behaviors to allow these species to select mates and also allow taxonomists and researchers to identify these species. And they hit on the two major ones, courtship rituals (mating calls, throat bulging, dancing) and pheromones.
Let's have a look at some two examples:

The widespread amazonian frog Allobates femoralis is now being approached as a species complex, with mating differences between the biologically distinct species varying from mating call note differences to cephalic amplexus (head grabbing during mate selection) and other various behavioral differences.[1]
Some crickets mate preferentially based on their species-specific song. Though, there is probably some genetic mixing with those crickets.

I think it's important to note that the species are cryptic because we as humans have decided they're hard to tell apart. Now, that similar morphology is also potentially difficult for predators to tell apart, or may be used by one or both species to parasitize on the other, it may be kept similar by sexual selection, or it may just not have great selective pressures to change. But the important part is that "cryptic species" is a box that we've created to describe traits we see.
Cryptic species as a window on diversity and conservation is a decent overview paper. (it's avaliable here if you don't have journal access)

Thanks for that; I'm happy with that.  That survey paper, in particular, is quite interesting.

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


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How do porcupines keep from pricking each other while mating?
How do porcupines keep from pricking each other while mating? It seems like they would constantly be scratching each other.

The female stood with the tail held sharply to one side, and the quills on
  the back lying very flat.  The male stood on his hind legs, while the
  front legs grasped the sides of the female. There was no repetition  of the act.

The male's urethra is 115-120 mm long, and his penis is 75 mm, so the he doesn't need to be as close to the female as one might think.  The retractor muscles are attached to the lower portion of the pelvis, which is likely well below the level at which the male's quills end.
Apparently, a dozen or so porcupines will den up in close quarters for the winter, so one can probably guess they have a good sense of whether their spines are hurting another, but that's only conjecture.
I suppose the take-home message is, nature will find a way.
Struthers, P.H. (1928) Breeding Habits of the Canadian Porcupine (Erethizon dorsatum).  Journal of Mammalogy, 9(4), 300-308. http://www.jstor.org/pss/1374084
Mirand,E.A., Shadle,A.R.(1953).  Gross anatomy of the male reproductive system of the porcupine
Journal of Mammalogy, 34(2), 210-220. http://www.jstor.org/pss/1375622

I love the "There was no repetition of the act." The male learned his lesson the first time!

There are several other publications that describe the mating behavior of porcupines in detail.

@AndersonGreen Definitely add another answer, then.  This was by no means exhaustive! :)


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Species with reproduction barriers that can both reproduce with a third species
To start with, I do not have a sound knowledge in biology or any formal education in the area.
I was told that one of the definition of a species is a reproductive barrier, which means that if two animals can't reproduce, they are of different species. The barrier can be either the inability of the sperm to fertilize an egg, or a physical trait that inhibits reproduction, e.g. a cricket species that has a different mating song than another species or two species of flies, one that mates on yellow flowers, and the other on red flowers.
But what happens when, while two species can't reproduce, but there is a "chain" of "intermediate" sexual partners that can produce reproductive connection step by step. Like 6 degrees to Kavin Bacon, but with animal sex.
I'll try to explain with an example:
A Great Dane and a Miniature Pinscher dogs can't mate due to obvious size differences. But The Pincher can mate with a German Pincher (a slightly bigger breed of Pincher), which can mate with a Doberman Pincher. And the Doberman can mate with a German Shepard which can mate with a Great Dane.
I've also heard that such things happen with birds and crickets, where there is an original species, from which evolved several other, and while the original species (which still exists) can mate with all the new species. Some new species can't mate with some, or all of the other new species.
How are such species are defined, and at what point dogs stop being dogs anymore?

All dogs belong to the Canis lupus familiaris species (which is a subspecies of Canis lupus, that is gray wolf). Great Dane and Miniature Pinscher are not two separate species, but rather two different breeds. A better example would be horse and donkey, different species that can mate to give a mule.

How come they are not of different species if they can't reproduce, while crickets that develop a different mating song are different species?

Are you sure a Great Dane cannot reproduce with a Miniature Pinscher (e.g. through in vitro fertilization)? Anywat, crickets are not domesticated so they don't have breeds! Have a look at this: http://en.wikipedia.org/wiki/Species_Problem

What I was explained is that a physiological barrier that prevents mating only physically (such as a different mating song or different flowers upon which to mate), but still allows artificial insemination also counts as a reproductive barrier.

The stated problem reveals that the bar has been set rather low for macro-evolution: http://en.wikipedia.org/wiki/Macroevolution

There is also interesting phenomena of ring species - the boundaries of species are sometimes really hard to define.

As an aside, I'm fairly sure that a Miniature Pinscher can mate with a Great Dane and produce viable offspring. While I haven't seen that particular crossbreed myself, a friend of mine used to have a dog who was half Siberian Husky and half Papillon. (And before you ask, yes, the Husky was the mother. The moral of the story being either "love conquers all" or "make sure to keep female dogs in heat away from all males if you don't want puppies", depending on how you look at it.)

Ps. See also this question on Yahoo! Answers: Can you crossbreed a Chihuahua with a Great Dane?

As many have pointed out, Canis familiaris is one species.  A more interesting consideration might be wolf-dog hybrids, which are fertile, unlike mules: http://en.wikipedia.org/wiki/Canid_hybrid

You may want to have a look to Ring species and to this post.

How are such species are defined, and at what point dogs stop being
  dogs anymore?

This is a bit like the is-Pluto-a-planet-discussion. A group of scientists have to come together and hold a big conference.
You have a few principles that you want to adhere to and then it's big groups of people making decisions.

Please cite a source and/or big conference and name a few principles.

@JoeHobbit : If you want to pretend that decisions like this are purely made by following a few principles go ahead and write your own answer. I don't think that there's much peer reviewed sociology literature about biology taxonomy but if it exists I would doubt that the result would be that the biological taxonomists follow straightforward principles.

There are many definitions of a species, which may or may not include the concept of reproductive barrier. The Biological Species Concept (BSC) is quite popular and involves a reproductive barrier, but other concepts such as the Phylogenetic Species Concept do not include a reproductive barrier.

Disagreements and confusion also happen over just what the best
  criteria are for identifying new species. In 1942 the famous biologist
  Ernst Mayr wrote that because biologists have different ways of
  identifying species, they actually have different species
  concepts. Mayr proceeded to list five different species concepts, and
  since then many more have been added. The question of which species
  concept is best has occupied many printed pages and many hours of
  discussion.
Some debates are philosophical in nature. One common disagreement is
  over whether a species is defined by the characteristics that
  biologists use to identify the species, or whether a species is an
  evolving entity in nature. Every named species has been formally
  described as a type of organism with particular defining
  characteristics. These defining traits are used to identify which
  species organisms belong to. But for many species, all of the
  individuals that fit the defining criteria also make up a single
  evolving unit. These two different ways of thinking about species, as
  a category and as an evolving population, are quite different from
  each other. Wikipedia Species Problem

The Biological Species Concept does have it's problems:

It is also true that there are many cases where members of different
  species will hybridize and produce fertile offspring when they are
  under confined conditions, such as in zoos. One fairly extreme example
  is that lions and tigers will hybridize in captivity, and at least
  some of the offspring have been reported to be fertile. (see also
  Lions and Tigers)
Mayr's response to cases like these is that the reproductive barriers
  that are important for species are the ones that occur in the wild.
  But even so it is also the case that there are many cases of different
  species that are known to hybridize and produce fertile offspring in
  nature. Wikipedia Species Problem

The Phylogenetic Species Concept also has its problems:

it permits successive species to be defined even if they have evolved
  in an unbroken line of descent, with continuity of sexual fertility.
  However, because slight differences can be found among virtually any
  group of organisms, the concept tends to encourage extreme division of
  species into ever-smaller groups. Phylogenetic Species Concept

When does a dog stop being a dog? Technically all dogs are in the same species: See the definition of Dog, which is a subspecies of the species, Canis lupus, or Grey Wolf. The line between dog and wolf is poorly-defined as there may be hybrid wolf-dogs, since they are both from the same species. Up one level is the family Canidae, which includes wolves, foxes, jackals, and coyote species.

The Biological Species Concept is largely useful in looking at the process of evolution. Since speciation isn't typically (though this isn't always true either!) an instantaneous process, it is useful to observe it in action. The BSC is the best way of approaching this (at least for sexually reproducing organisms).
Back to your original question. It might be useful for you to search "ring species" as this is what you are talking about. The most famous example is the Ensantina salamander complex. They are essentially several species/one species depending on your perspective. It is more-or-less a spatial version of the hypothetical dog analogy, but it is also a natural phenomenon that occurs in many other species....


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List of all reported bacteria
I would like to know were to download a table file with all reported bacteria and its corresponding PHYLUM, CLASS, ORDER and FAMILY.
Basically, its the same table than this one from GOLD genomes but containing the non-sequenced bacteria too:
Thanks for you help, Bernardo

I am not sure if such a complete list exists. There are some lists available, which look pretty complete. Have a look at Labrat and Microbexpert. There is also a book available, which contains an approved list of bacterial names, see here. Otherwise you can of course search your way through PubMed and see, what comes out.

Thanks Chris, but I need the list in table format (tab or comma delimited file). I couldn't find this option in the websites you suggested.

Oh, I am not sure if this list exists at all. You could try to contact these websites and ask them if they can provide this data in a different format.


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What is an in-frame activating fusion?
In [1] it is written that:

Whole-genome and RNA sequencing identified recurrent in-frame activating FGFR3–TACC3 fusions

What is a recurrent in-frame activating fusion?
[1]   Cancer Genome Atlas Research Network, “Comprehensive molecular characterization of urothelial bladder carcinoma.,” Nature, vol. 507, no. 7492, pp. 315–322, Mar. 2014.

This is explained in the linked article.

We found several recurrent translocations of likely pathogenic significance, including an intra-chromosomal translocation on chromosome 4 involving FGFR3 and TACC3 (n=3). The breakpoints were in intron 16 (2 cases) or exon 17 (1 case) of FGFR3 and intron 10 of TACC3 (confirmed by DNA sequencing and RNA-seq). All three lead to fusion mRNA products whose predicted proteins include the N-terminal 758 amino acids of FGFR3 fused with the C-terminal 191 amino acids of TACC3 (Fig. 2a). Based on the structure of the FGFR3-TACC3 fusion protein, we predict that it can auto-dimerize, leading to constitutive activation of the kinase domain of FGFR3. FGFR3-TACC3 fusion, which was recently described in both glioblastoma21 and bladder cancer7,8, represents a promising therapeutic target.

FGFR3 is a member of the fibroblast growth factor receptor family. It is a transmembrane kinase that is normally activated upon ligand binding which triggers dimerisation. TACC3 is a protein that can dimerise through a coiled-coil domain.
The FGFR3-TACC3 gene fusion that is generated by the reported intra-chromosomal translocations thus generates a version of the receptor that is predicted to be constitutively active because it can dimerise in the absence of the growth factor.
Recurrent means occurring frequently.

Just one little comment: in-frame means inside introns or exons, but not within inter-genic regions?

in-frame means anything that  generates an open reading frame in the mRNA so that a fusion protein will be produced. Te endpoint in TACC3 was always in an intron, and in two cases the FGFR3 endpoint was also in an intron. This will generate a gene fusion with a hybrid intron. In the other case they say that the FGFR3 endpoint was in the next exon. Since all three fusion proteins have the same structure that means that the exon interrupted by the translocation must have become part of a hybrid intron. If you draw yourself a diagram it will become clear. But yes, not in intergenic regions.


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How does cold water help to overcome high fever?
Why cold water helps to overcome from high fever in body? As fever is inside the body and we're applying cold water over the body!

Fever is triggered when pyrogens cause release of prostaglandin that acts on hypothalamus (which is the center of thermoregulation).
Fever assists in the healing process by:

enhancing phagocytosis
decreasing negative effects of endotoxins
stimulates proliferation of lymphocytes

Although is a good reaction, when the temperature gets too high it could determine negative effects, like convulsions at children. Brain damage appears when the temperature rises as much as 42 degrees Celsius, and most febrile conditions go up to 40.6 degrees Celsius.
So fever must be kept under control, and cold water helps lowering body temperature. Lowering the temperature will prevent negative effects of fever. Cold water is a symptomatic treatment for fever. Most important is to determine cause of fever and do an ethiological treatment.
Source: Wikipedia contributors, "Fever," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Fever&oldid=614212619 (accessed June 27, 2014).

You missed the question a bit. The question not about why water is used; it is about how the water that is applied externally can regulate the internal temperature.

     As far as how the water cools the body it's simply a matter of physics. Water has a higher specific heat also called heat capacity than the air, clothes, or other matter that normally surrounds the body.       Specific heat refers to the amount of heat (keep in mind that heat is essentially the measure of the average movements of the molecules in a substance) per unit of mass it would take to raise it's temperature by 1 degree Celsius. Water is useful for temperature regulation because it takes so much energy for it to change temperatures. Metals tend to have low specific heats which is why we make frying pans out of metals like iron. They take less energy to become hot.      As systems naturally fall back to equilibrium, if the body is hotter than the water heat will be transferred from the body into the water until they are the same temperature which will be a lot closer to the temperature of the water (compared to the initial temp of the body) because changing the temperature of water 1 degree takes more heat energy than changing the same mass of human to change 1 degree in temperature.      While this primarily acts on the outer portions of the body, the process continues into the core of the body as now instead of having hot skin and cold water, you have hot muscles and cold skin, from there you have hot organs and cold muscles, and so on and so on.      I hope this is helpful! For more information on specific heat you can check out: http://hyperphysics.phy-astr.gsu.edu/hbase/thermo/spht.html


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Why is it that drinking caffeinated tea does not help one to stay awake?
I have never felt after drinking tea that I can have the power of being able to work late at night. Neither have I felt that it helps me to be awake while working or keeping eyes opened while I am not in mood for sleeping.
Drinking tea, then, does not helps me to stay awake.
Is it the nature of the tea itself, or does it have to do with how the body processes caffeine?

@jonsca, I would like if you edit it to make it more meaningful or more powerful.

I have given it a try, you can always modify it again if necessary.

Another idea I have come across is that caffeine absorption is much slower with tea, though my source is a Good Eats Episode.  The relevant information can be found at approximately 19 min.  Maybe it's true, maybe it's not, but regardless, it's a great episode to watch if you are into tea.

It could be tolerance if other caffeinated beverages are usually consumed, however it also depends on the type of tea itself, and other properties, such as how long the tea has steeped for.
For example, brewed black tea can have anywhere from 14-61 mg of caffeine, which is a large range and depends on which tea you are drinking specifically.  Whereas if you were drinking green tea that has not been steeped for long, it can have 24-40 mg of caffeine, which at the lower range will probably not help you stay awake.
From MayoClinic.Org:

The actual caffeine content of the same coffee drink can vary from day to day — even at the same coffee shop — because of various factors, such as roasting and grinding, as well as brewing time. The caffeine content of tea also is affected by how long it's brewed.

Caffeine beverage levels can be found here:
http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/caffeine/art-20049372

What is happening to you is 'tolerance'. It is a term used in pharmacology. It is a phenomenon by which a drug/medicine becomes less effective the body gets used to it. One explanation is less receptors for that drug are manufactured because of negative feedback.  You may have developed tolerance to tea.

He said that he has never felt that tea has been helpful. Couldn't another explanation simply be that there's less caffeine in tea than coffee?

@jarlemag, thanks but even coffee is not helpful to stay awake. So can I say that my body is not consuming Tea or Coffee as they should affect to my body? I am not saying I am unnatural but many people complains if they drink Tea or Coffee they could not sleep easily but for me drinking them never helps.


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Why does the hydrolysis of ATP increasing entropy increase the Phosphoryl-‐transfer Potential?
I am currently taking a biology class. I do not understand this concept. I understand that the electrostatic repulsion of the negative charges, resonance stabilization and hydration stabilization all contribute. However, I do not understand why an increase in entropy would help. Wouldn't it be more favorable to have less entropy in a system?

The phosphoryl transfer potential is one way to think about the free energy available to do useful work when ATP is hydrolysed.
As you can see from the free energy equation below, a positive change in entropy will help to decrease (i.e. make more negative) the free energy change.
This is why an endothermic reaction can still occur spontaneously if the entropy change is big enough to create an entropy term that outweighs the enthalpy term in the Gibbs free energy equation.

ΔG=ΔH - TΔS
where:
T= temperature
G = Gibbs free energy
H = enthalpy
S = entropy


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How can I save bacillus strains on filter paper without an -80 degree freezer?
I want to save my bacillus strains but I don't have access to a -80 degree freezer.  What are possible alternatives?

Use agar stubs: pour some Nutrient agar (or any suitable agar medium) in a test tube (~10% of the tube volume) and punch your inoculum halfway into it using a pipette tip or inoculation loop. Store it in 4⁰C.
Glycerol stocks can be made and stored in -20⁰C also.

How long can you store them in agar stubs? Also we use -70 to -80°C to store our glycerol stocks.

I had stored them for a couple of months but i think it can withstand one more month..


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What are some of the immediate challenges to break through before finding a cure for mad cow disease?
What are the immediate challenges to break through in seeking a cure for mad cow disease?
I know that mad cow disease has no treatment as of yet.

The main problem is that Mad Cow disease is not caused by a "normal" pathogen but by a prion, a protein.
Traditionally, disease causing agents can be classified into viruses, bacteria, fungi, and parasites. Bacteria, fungi and parasites are all living organisms, alive in the traditional sense. It is, therefore, possible to design drugs that kill them.
Viruses are trickier, while not really alive in the traditional sense, they still have to make copies of their genetic material (DNA, or RNA in the case of many viruses) in order to cause infection. Therefore, drugs like ganciclovir that stop the formation of viral DNA can be an effective treatment.
Prion based diseases such as Mad Cow disease, Creutzfeldt–Jakob disease and Kuru, are not caused by a classical infectious agent but by a simple protein, a prion. Prions are misfolded versions of proteins already present in the host's body. When a prion interacts with the host protein, it causes this protein to adopt the same, misfolded, state as the prion. Protein function depends directly on the protein's structure, the way it is folded in three dimensional space. Therefore, the misfolded protein can no longer carry out its physiological role and disease symptoms occur.
Now, since the prion is just a protein, one single molecule, there is no essential life process that we can disrupt. We have to attack them using chemical agents that target the prion while not affecting the healthy, correctly folded, host protein. This is very hard to do.
The blood-brain barrier mentioned by Larry_Parnell is another problem. Briefly, the BBB, is a kind of fence that only allows certain of the various items circulating in the blood stream to enter the organism's brain. This is a wonderful defensive feature but it makes it much harder to design drugs that can enter the brain and target pathogens found there.


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Transcription factor binding site located in intron
I have noticed that some TF binding sites are located in the introns of the genes.
I am puzzled about whether the TF only binds to DNA in the initiation stage of transcription and will detach during transcription. (I am thinking if the TF bind to the sense strand, it will block the PoLII for transcription, thus they should be removed.)
Many thanks in advance.

As Armatus said TF can remain bound without an effect.
There are some alternative explanations:

Promoters need not be always upstream to the Transcription Start Site (TSS). There are promoters called Downstream Promoter Elements that are actually downstream to TSS.
There can be alternate TSS within the introns
TF bound to intron may regulate elongation or splicing rather than initiation. [Elongation can also be regulated especially when a gene is poised for expression. RNApolymerase stalling is a well known phenomenon and is affected by epigenetic marks. Since splicing happens co-transcriptionally there can be DNA marks that affect the process. Although it has not been shown whether such a thing happens, but Intron-Exon boundaries are known to have a distinct nucleosomal pattern.{1, 2, 3}]

Hi, Thanks for pointing out the papers. I will read them carefully

Even in a quiescent state, DNA is bound to a lot of proteins. It is not a lone double-helix of DNA with an occasional protein attaching here or there. Rather, it is tightly wrapped around histones, which themselves have other proteins attaching and detaching constantly. Repair enzymes are always whizzing about and fixing the random damage that occurs in DNA naturally, and transcription factors may be sitting on the DNA for a while and then diffusing away again without doing anything. There are probably more proteins around that I've forgotten.
As you can see, the nucleus, DNA and in general the cell interior are extremely crowded spaces, and for transcription to happen it takes more than just removing some TFs attached to intronic sequences. Histones need to be modified to repel each other and make space. Ultimately, all proteins will need to detach for a short time when RNA polymerase comes through. If they don't, polymerase will stall until they move away, or it may simply fall off, producing an incomplete RNA fragment which will be degraded quickly. Another polymerase will come along soon enough and produce a new transcript if the promotor is still in a permissive state.

Hi,Armatus,Thanks for the detailed explanation! I didn't know nucleus is such a crowed place. I am wondering if the detach process of TF from DNA can be visualized under single molecular microscope.

Microscopy at such resolutions is possible using atomic force microscopy and transmission electron microscopy, but both of these are extremely complex procedures and require the sample to be fixed - i.e. dead.

I see, so it is not possible to observe in vivo. Thanks again~


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Why are males more likely than females to have autism spectrum disorder?
The male to female ratio in autism spectrum disorder is around 4:1. However it seems ASD is not a simple X-linked disorder.
Then how is it possible males are more susceptible than females, if the causal genes are located in autosomes?

Could you maybe add some background, e.g. references on the incidence of autism spectrum disorders?

Sure, I will do this later when I come to school

As the father of two sons with diagnoses of ASD, I think that it is best to think in terms of an extended spectrum which encompasses 'normal' people. We are all somewhere on this spectrum, but there is a threshold zone around where we cross from "normal" to "diagnosable as ASD". Now, if the distribution of spectral position for males is displaced towards the ASD end of the spectrum relative to females (because of some aspect underlying "normal' maleness, such as testosterone levels) then any genetic variation which pushes someone towards the ASD end of the spectrum by some fixed amount will tend to push more males over the threshold than females.

That is an interesting idea.  Do you know if there's a database of scores on an ASD questionnaire, for the general population so that we could verify it?  Simon Baron-Cohen's tests come to mind, but I'm not sure if they've looked at the distribution of scores.

Dear Alan, thanks for sharing the point. I hope the genetics study in the future can explain the mystery.

Nice thinking @alan-boyd, I wonder would it be nice to see a study correlating "manliness traits" with ASD test scores?

This spectrum that leads to autism on the far right tail is probably the empathising-systemizing trait, which shows half a standard deviation mean difference between man and women. This difference in mean pretty exactly results in the 4:1 ratio in a normal distribution, if you look at the right tail that corresponds to the autism incidence rate.

Males are more likely to develop ASD, but affected females tend to be more severely impaired. Why this occurs is an area of active research.
However, to address your question, there is a study suggesting that mutations on the X-chromosome account for about 1% of ASD and intellectual disability cases.  This clearly doesn't explain everything, but it's a start.  It might suggest that there are other X-linked loci involved. IIRC, ASD is one of those disorders that can be caused by many different combinations of (relatively rare) mutations, so it's hard to identify the genetic causes by GWAS.

hi, thanks a lot for the explanation. Another question came to my mind is that the one copy of X chromosome will be silenced (please correct me if I am wrong),so does the X chromosome which carry mutation always be deactivated?

I'm not expert on the topic, but whenever males more predominately have a condition than females, it might point to a sex-linked (recessive) trait. Males have one X chromosome, while females have two. This means that a male only needs one copy of a gene to have a condition (inherited from their mother), while females need two X chromosomes to be inherited to have the condition (mother and father).

Being a Special Education Trainer at ACCEL Centre, I have done some research regarding this topic, but haven’t found a shred of full-proof evidence to support this theory.
Well, first of all, autism is a sensory integration disorder showing visible signs of speech delays and communication difficulty with others.
The main reason that causes autism spectrum is still not known and various researches are still in progress, together with erratic proof that men/women ratio ranges between 2:1 and 16:1.
One probable factor is a diagnostic bias, suggesting that females obtain autism diagnoses later in life as compared to males, indicating that it is harder to spot.
Signs of autism spectrum also look different in females. They have fewer restricted interests and repetitive behaviors and may have socially acceptable interests.
References:

https://www.autism.org.uk/about/what-is/gender.aspx
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4164392/
https://www.spectrumnews.org/news/autisms-sex-ratio-explained/

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


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What are some atypical examples of positive transcriptional cooperativity?
Cooperativity in gene expression is an important feature of many regulatory networks. Described using the Hill function, the most common example is a transcription factor (TF) that when bound to its target regulatory site, increases the rate of binding of other transcription factors (usually through TF-TF dimerization).
There are numerous example of TF dimerization-based cooperativity in the literature. However, I am trying to find examples of positive transcriptional cooperativity that involve mechanisms other than TF dimerization. In the dimer model, an unbound TF binds to its cognate promoter (containing multiple enhancers) with a certain affinity. With the first TF bound, another identical TF now has increased affinity for its target - binding to the enhancer and binding (dimerization) to the first TF. The expression profile is sigmoidal (near binary) and represents sharp on/off switching in activity.
Although peer-reviewed articles experimentally or theoretically characterizing alternative mechanisms are preferred, I'm also interested in user hypotheses and discussions that are more speculative. Specifically, I'm interested in positive cooperativity that occurs without feedback from the regulated genes.
One potential mechanism could involve a DNA-binding TF consisting of a transcriptional activator domain and a chromatin remodeling or DNA methylation domain. When the TF binds it not only activates transcription but remodels local chromatin. If the remodeling increases affinity for the next TF, they act cooperatively (and positively). Perhaps something similar to this has already been described.

What proteins do you think about? Transcription enhancers which are not involved directly in transcription but enhance it?

Yes, transcription enhancers, not the core machinery.

A similar mechanism to the one I proposed in the last paragraph above, but without the chromatin remodeling domain, does appear to result in cooperativity. http://www.pnas.org/content/107/52/22534.full

Positive co-operativity without feedback from the downstream genes:
I guess Polycomb/Trithorax complexes will fit this criterion nicely.
Polycomb group (PcG) represses Hox and other differentiation related genes (such as neurogenin) while Trithorax (TrxG) group promotes their expression. They are not like usual transcription factors that bind to promoters and recruit/exclude RNA-polymerase; they bind at regions called Polycomb Response Elements/Trithorax Response Elements and mediate epigenetic regulation of nearby genes by histone modifications (primarily methylation).
PcG froms two main complexes PRC1 (Polycomb Repressive Complex-1) and PRC2. Different components of the complex have different molecular functions. For e.g SuZ has a Zinc finger domain and can bind to DNA/RNA, Ezh has histone methyltransferase activity etc.
This is an old review but is still quite informative.

Can you explain or propose (or reference to) the underlying mechanism for polycomb/trithorax cooperativity? Thanks.

@nbogard Edited the answer..

The Polycomb/Trithorax system looks like it does exhibit cooperative activity. Thanks for the reference. I found this one also: http://www.nature.com/nrm/journal/v15/n5/full/nrm3789.html
Specifically, the last section and fig. 7 where the authors propose that Polycomb/Trithorax Response Elements, found in target enhancers, promote bistability in target expression. Thanks!

Interesting question. I think I have two examples for you which might be interesting.
The first is the co-regulation of the microphthalmia-associated transcription factor (MITF) in pigmentation by SOX10 and PGC1a/b. See this paper:

PGC-1 coactivators regulate MITF and the tanning response.

The second is about the regulation of brown fat tissue by PGC1a and IRF4 which seem to interact in these cells. See this paper:

IRF4 Is a Key Thermogenic Transcriptional Partner of PGC-1α.

In both cases a transcription factor (SOX10 or IRF4) interacts with the co-activator PGC1 proteins to regulate gene expression. If the co-activator is missing, the expression is at least downregulated. These activations are not so atypical or rare but are occurring quite often. If you have problems in getting these articles, let me know.

Thanks, @Chris but I could not find an example of measured cooperativity in either of the two studies. I've edited my question to better define what I mean by 'cooperativity'.

In the first paper SOX10 interacts with the PGCs. The knockdown of the PGCs leads to reduced pigmentation. The same is true for the knockdown of the PGCs in the pigment cell of the mice, which leads to much lighter pigmentation. In the second paper the interaction happens between IRF4 and PGC1a. If one of the partners is not present, the regulation in the fat tissue is not working. They also present data on from co-ips on the interaction of both proteins.

I do see that the activity described in these papers requires binding between the different factors, but I do not see where they measured cooperativity. I think there is some confusion about what cooperativity means. I'm specifically referring to cooperativity of biochemical binding that results in a non-linear response. http://en.wikipedia.org/wiki/Cooperative_binding#Examples_of_cooperative_binding


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How much energy does a cell expend maintaining its contents?
In software engineering, an analogy is sometimes made using biological cells. I would like to know whether it has basis in fact.
People say (Alan Kay was first) that "objects" in software should be like cells: separate from one another, communicating by passing messages. This separateness has been argued by saying that a cell spends much of its metabolic energy keeping its insides in and its outsides out. The implication is that programmers should likewise spend significant effort maintaining boundaries between parts of a system.
Is this actually true? What percentage of its energy does a cell generally spend maintaining its contents?
(My guess is that the answer varies wildly depending on the cell and its environment, but some ballpark example numbers would be nice.)

This could be a difficult question to answer, because where do you draw the line? Just the energy required to maintain the phospholipid bilayer? Or would the estimate also include the energy required to maintain the cytoskeleton? As you say, these components vary drastically between cell-types so an accurate estimate will be hard to come by. Arguably the majority of the cells energy is spent on maintaining the integrity of the cell - which includes all the component parts, without which the cell would not fully function and may not be as effective at maintaining its 'boundary'.

@Luke - unfortunately, I lack the knowledge to frame the question more precisely. Given the ambiguity of my question, an answer like "depending on the definition and the cell, a minimum of about %X and a maximum of about %Y" would be perfectly fine.

There's "more to it" than just that. Does the energy needed for transcription of the proteins that diffuse out of the cell count?

@NathanLong my apologies for not being very helpful, but the answer could surely be anywhere between ~5% and ~95% (extremes obviously), because it depends where the line is drawn. I will be interested to see what others put as answers though!

@LanceLafontaine - sorry, as I said, I don't know enough to answer that; please assume whatever seems most reasonable to you.

I'm going to take a stab at this.  Its a difficult question to get right, just to put is in the right mood here.
Lets leave energy out of this as the proper term is structure.  The cell is designed to compartmentalize itself to differentiate its own living tissue from other cells.
In this regard Alan Kay's analogy is pretty good.  In multicellular organisms, individual cells (mostly) each maintain their own DNA and energy storage, though they get their nutrients and energy from outside.  They create the organism as a whole by differentiation; each cell changes to take on a specialized role and depends on other cells to support it. E.g. in animals some cells/organs digest the food and distribute nutrients to the rest, others form the lung and help distribute oxygen and others scrub the blood of waste.
This is somewhat like good code design where functions are partitioned out into specialized parts of the software for the sake of maintainability and organization.
Somewhere after this point I think the analogy breaks down since after all the point of good coding practice is to organize the code for understanding within reasonable human conceptual limits.  The cells and how they organize themselves are still plenty mysterious to us as they have their own definition of roles and function much of which is still being discovered today.  For instance the many kinds of neurons in the brain and the sorts of structures they form are extremely diverse.  We have few organizing principles for predicting how many cell types would exist in a system and these only create partial answers.
After all its just an analogy...
getting close to an answer?

This is an old question by now, but thought I'd give it a shot anyway. I am guessing the "insides in and outsides out" refers to maintaining intracellular concentrations of nutrients and other important molecules.
The cell does spend a lot of energy to maintain high concentrations of amino acids and other key metabolites in the cytoplasm. The cell membrane is permeable to these molecules to allow uptake from the surroundings, but this also creates the problem that molecules are as likely to diffuse out as diffuse in. To maintain a concentration of any molecule higher than that of its surrondings, the cell must actively "pump" molecules inwards, which obviously costs energy. This goes on all the time; it's a constant fight against thermodynamics.
A number of active pumps exist in cells, and it's experimentally difficult to measure the energy consumption of all of them. One very important pump though is the Na/K-ATPase, which uses ATP (energy) to maintain sodium and potassium gradients across the cell membrane, which are in turn used to drive transport of other molecules. The energy requirement of the Na/K-ATPase is readily measurable; this review article estimates 19--28% of total energy consumption. This should be viewed as a lower bound.


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Can an organism obtaining a part of its genome via horizontal gene transfer be called a "hybrid"?
Wikipedia definition of "hybrid" offers many competing definitions. But most seem to be centered on sexual-reproduction gene transfer.
Is there an official (in a textbook or widely accepted peer reviewed work) definition of a "hybrid"/"hybridization" that would clearly include ANY genetic mixing, most specifically obtaining genes via horizontal gene transfer?
If not, is it specifically because "hybrid" requires sexual reproduction, or merely because it requires a certain minimal amount of inherited genetic material from both sides, and horisontal genetic transfer in practice involves significantly less genetic material being inherited?

Full transparency: the question originated on SFF StackExchange, pertaining to whether Alien chestburster can legitimately be called a "hybrid" from a biology point of view, on the basis of it obtaining a variety of phenotypal features of the host body via horizontal-gene-transfer. It's mostly a definition issue.

As you point out, there isn't a singularly accepted biological defnition of 'hybrid.' The most basic would be a single organism that exhibits traits of two individual organisms, but that will find perfectly acceptable disagreement depending on who you talk to. You, for instance, are human - but a hybrid of your parents' genomes.
So I would personally say that horizontal gene transfer is equivalent to gene inheritance, and that as long as the organism exhibited traits of both 'parent' individuals - then yes, it is a hybrid. Some might include that even if it didn't exhibit traits and merely contained the genes in any inherited genomic data that the hybrid label would be appropriate.

I'm looking for definitions that could be considered "legit". Textbooks, or barring that, widely respected/cited paper; that explicitly defines "hybrid" as inclusive of H.G.T. (or rather not exclusive of it). E.g. where the end result (gene mix) is relevant as opposed to mechanism of mixing.


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Why do cockroaches flip over when they die?
This question has always mystified me since young. For beetles, I can reason that they flip over because they have a higher centre of gravity causing them to be in unstable equilibrium when they tuck in their legs when they are about to die. For cockroaches with a lower profile, I would expect them to stay upright. But why do they flip over? Is it more comfortable for them to die this way or is there a scientific explanation for this?

Edit:
As noted in some of the comments below, this is a general observation based on cockroaches being killed by insecticide. I haven't got the chance to observe (or notice) cockroaches that die in other ways and therefore do not want to limit the scope of my question to just insecticide poisoning.

Do they flip over? I’ve always considered that to be just a comic representation. Maybe it’s just easier to spot dead cockroaches which have flipped over, since the others aren’t easily distinguishable from live ones? …

@KonradRudolph, image for your reference.

That's a picture of some cockroaches on their backs. There's no way for the viewer to know whether they died that way, or (as it seems) were arranged that way.

@RichardSmith: I am pretty positive that when you put some roach poison you will then find them on their back.

I agree, I was just pointing out the the picture doesn't demonstrate anything. The reason, if I remember rightly, is that most cockroach control agents are neurotoxins which cause the legs to spasm, so they get flipped onto their backs.

Yesterday I found ~200 dead chinese stink bugs on my hallway carpet(I assume they crowded the light and someone sprayed them with insecticide) and spent some time cleaning that up, having an opportunity to observe A LOT of dead bugs. A lot of them were indeed on their backs, which puzzled me. It might be of interest to clarify your question with the cause of death. Is it natural death of "old age" or due to poison bait /insecticides?

@AlexStone, please refer to my clarification under "Edit". I am not fortunate enough to observe cockroaches dying a natural death. If someone has made that observation to prove or disprove, feel free to answer below :)

Flying insects land on their back when they fall since it's heavier. Stands to reason whether that applies to cockroaches.

It is a result from the insecticide you are using.  From this excerpt from the 10th Edition of the Mallis Handbook on Pest Control:

Neurotoxic insecticides cause tremors and muscle spasms, flipping the cockroach on its back. A healthy cockroach can easily right itself, but without muscle coordination, the cockroach dies on its back. Cockroaches exposed to slow-acting insecticides that target respiration (energy production) also can die “face-down,” as they run out of energy without experiencing muscle spasms.

Here's also a website from UMass describing it in more detail:

Most of these insecticides are organophosphate nerve poisons.  The nerve poison often inhibits cholinesterase, an enzyme that breaks down acetyl choline (ACh), a neurotransmitter.  With extra ACh in the nervous system, the cockroach has muscular spasms which often result in the cockroach flipping on its back.  Without muscular coordination the cockroach cannot right itself and eventually dies in its upside down-position.

And an entomology professor even answered this for Maxim:

Most insecticides are poisons that target a bug’s nervous system. When you spray a roach, those neurotoxins cause tremors and muscle spasms, which flip
  it onto its back, and without muscle coordination, that’s the position it dies in

Thanks. This answer is really useful. I guess the rapid leg kicking caused by muscular spasms is powerful enough to lift the cockroach on one side and flip it over.


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Mass change in deamidation from Glutamine to Glutamate
To detect the deamidation from Glutamine to Glutamate in a protein, normal practise seems to be a mass spec, where it is claimed there is a change of 1 dalton.
EG It is claimed that:

Deamidation of an Asn to Asp/IsoAsp results in an increase in mass of a single dalton.

But when I look at their table, they are using Glutamic Acid as being 1 Dalton heavier than Glutamate, but at pH 7 the Glutamic Acid will be deprotonated to Glutamate. Do they  put the sample in pH 4 to protonate the Glutamate first? But then you are risking catalysing the hydrolysis of Glutamine anyway, rendering your results useless!
There should be a charge difference though, as you are going from neutral to a negative charge, so that would show up in a change in mass/charge on the mass spec, rather than a mass change.
Any help would be appreciated.

This might be better on chemistry SE.

Its more relevant to Biology as its to do with Proteins I think.

I am not an expert in this area but this is what I understand. Usually ESI based protein mass spec imparts a positive charge on the proteins by protonation. Formic acid is usually added to help in protonation. In deamidation -NH2 is replaced by -OH thereby increasing the mass by 1 dalton (14+2 -> 16+1). I think that glutamine may be also acquire multiple charge (by NH2 protonation). You can see this article, which talks about dealing with deamidation artifacts resulting from sample preparation techniques.

Ah, so the samples are put in acidic conditions to protonate the glutamate which can result in false positives, interesting.

Biochemistry is still chemistry :)

Are you performing native or non-native MS?

@harpalss I'm currently reading papers/data from other sources and was trying to work out how they were doing it. The details seem to be glossed over rather a lot!

I do alot of ESI mass spec, so i might be able to help. Alot of my work is on native MS. Are you looking at the whole protein in the mass spec or a peptide fragment?


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Systems Biology of triacylglycerol (TAG) synthesis in Jatropha
I need the genetic regulatory network of TAG synthesis (Kennedy pathway) of Jatropha plant??
Or is there any way to convert metabolic pathway into genetic regulatory network?

Please look up some literature. Look for transcription factor binding sites in the promoters of the genes involved in the pathway. If jatropha genome is not sequenced then look for homologs in the nearest species. it is not possible to obtain a gene regulatory network from a metabolic network.

Triacylglycerol synthesis in plants is probably highly conserved.  The metabolic pathway is here.
The Jatropha genome sequence is also available.
Given this some effort has been made to figure out how these genes are regulated.  This is a microarray study of Jatropha focusing on fatty acid and TAG biosynthesis.   This gives some idea of how TAG genes respond to one another, but of course will not find the promoter sequences or the transcription factors themselves.
Having spent a summer going over fatty acid synthesis, I can only say that there has been a lot of wet lab work done on these pathways which would probably be conserved in the Jatropha plant.  The literature would be quite extensive.  Integrating all of that is more like a paper for publication than an answer on stackexchange.  This sort of outlines the procedure... do you have a more focused question?
I'll outline one way of approaching this - there are an uncountable number of variants if you tweak it.  There are other ways to get this, most notably looking for defective mutants, the method which is still used in plants quite a bit.
Anyway here is a genome based approach:
1) Identify genes in the pathway of interest. choose 10 or so genes that you think constitute your network.  This is an editorial decision. Ultimately if you start looking at genes regulated by the same transcription factors as being included in your network, you will eventually take in the entire genome and the work will be impossible to accomplish.
2) find candidate promotor binding sites. look at the upstream promotor regions for all these genes.  you can look at how these are conserved between similar plants by examining the same gene promotor regions aligned against each other.  This doesn't work very well.
2b) Another way of finding these is to do a pull down experiment where transcription factors are bound to DNA and a DNAse digestion is done and remaining fragments identify the binding sites.  All this somewhat assumes that you kind of know which transcription factors are responsible for each gene. That is probably not the case here.
3) find the transcription factors important for the plant pathway.  this is not easy - one way is to try knock outs of the TF genes.  I imagine this plant has 4000 + of these genes.  around 1-2% may be involved.
So far these methods have been use for the ENCODE project as well as some bacterial genomes.  a plant is a new scenario which will have issues of its own.

Yes..I need the details of how to get the gentic regulatory network of TAG synthesis Pathway?? A step wise protocol please. How to get The regulatory gene network from geneome of Jatropha curcas.

do you mean transcription factor binding sites or also the mechanims of regulation? still sounds like you are looking for a few hundred pages or a review article.

I dont have much knowledge about systems biology and gene regulatory network. I have do the pathway modelling in two forms...frst for metabolic pathway and then for gene regultory network. I dnt know how to do it with gene regultory network?


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fibrinogens and fibrins - are they the same molecule?
Some proteins are "activated", like fibrinogens; they are turned into fibrins by thrombins, and then the fibrins can aid in blood clotting.
Are fibrinogens and fibrins the same molecule, just in different states? If so, are all "-ogen" ending proteins and their activated forms the same as well?
If they are different molecules, why do us even bother to convert a protein into anotherto work, instead of simply activating a protein?

You could say they are the same molecule, but a molecule whose function is to change its state and properties very quickly when activated by thrombin.
Fibrinogen is a soluble protein - a complex of six protein chains.
Thrombin is an enzyme called a protease which very specifically cuts the ends off of two of those protein chains.
Once those bits are removed from Fibrinogen, the resulting molecule creates fibers very quickly to form clots.
You could also say that fibrin is a different molecule than fibrin because it really consists of many fibrinogen fragments.


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What is the current consensus, if any, about why long term potentiation is not clearly correlated with learning?
I was watching a video where a professor said that according to some experiments, Long Term Potentiation (LTP) is correlated with better learning, while in yet other experiments, LTP is correlated with poorer learning.
Are there any models that explain this phenomenon? What's the current theory on this?

Can you clarify what you mean by "LTP is correlated with learning"? Learning is a complex process and synaptic plasticity is certainly a necessary biological process.

I meant the strengthening of synapses. Some studies show that when synapses strengthen the learning is better, while others show that when they weaken, it is better. (There was no more detail given, but the professor just mentioned that it is an area that is controversial).

the idea that LTP is correlated with learning goes back decades. it would help if you could detail his statements if he had any further info. what is "poorer learning"? iirc LTP incidence is known to be higher in the hippocampus which is correlated with long term memory formation. (re famous patient HM in psychology). also lets remember that the "learning" that is measured in psychology experiments may not be the same as LTP or that maybe humans are still learning stuff that is not measured by the learning tests vs whats expected (ie there is the problem of "false negatives" here).

@Joebevo learning may require strengthening, weakening, or both of synapses. It will depend on many things including the learning task, context, which synapses, and so on.

I'm going to answer your general inexact question with a general inexact answer. The consensus is that LTP is correlated with learning.
To clarify in more detail, studies have shown that when an animal performs a learning task that involves the hippocampus(which is important for memory), and the animal effectively learns, less LTP is seen in-vitro in brain slices from these same animals. LTP is said to be occluded or blocked since potentiation of those synapses have already maximized through the in-vivo mechanisms. This can be interpreted as learning affecting LTP or at least both acting on the same basic mechanisms of the synapse(strengthening and weakening).
See for ex.
Learning induces long-term potentiation in the hippocampus.", Jonathan R Whitlock, Science (New York, N.Y.), 2006;313(5790):1093-7

I think this needs to be expanded upon to be a useful answer

I expanded on this; still not sufficient?


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level of organisation of proteins

Is there any disulphide bond in a quaternary structured protein?
If yes, please provide examples.
In tertiary structured proteins, what is(are) the most important characteristic(s)  of tertiary structured proteins?
a) globular in shape
b) have both alpha helix and beta sheet
or, is there any characteristic that I do not mention?

Aha, this is not a homework question, just that I feel like I do not understand protein quite thoroughly. Anyone can help?

Interesting protein structure trivia question!
Disulfide bonds form more or less spontaneously when two sulfhydryl groups from cysteines are close enough to each other in the proper orientation in a reducing environment.  So given this, its possible for them to exist, even though in most cases the distance between the cysteines in a disufide bridge is small and intra-domain.
Inter-domain disulfide bonds are rare.  The most common example is that some immunoglobulin domains in antibodies have an intrachain disulfide bridge.  I also found reference to one in a starch synthetase from rice.
In tertiary structure, the overall shape is an important one.  Globular shapes are the most common, but elongated protein folds, triangular folds,  rings, disk-like structures made out of wedges are popular examples of how protein structures can do amazing things when selection requires them to.

Surely immunoglobulin molecules are excellent examples of the involvement of disulphides in the quaternary strucure of proteins?

sorry i didnt use the same term, but i did mention this.

Apologies Shigeta, I just didn't see it, possibly because I was still puzzled by the term 'intra-domain". I know what that means, but it doesn't map on to quaternary in my opinion.

i didn't bother to explain.  I felt that a disulfide between two cysteines in different domains on the same chain would be a result of similar forces as a quaternary disulfide.  I didn't really have to go there in the reply though


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Species identification, tree from Ecuador
This tree is recently photographed in Quito, Ecuador. It grows everywhere. I'm new to South American flora, so I'd like to know what the species it is?

Your plant appears to be Chionanthus pubescens, the pink fringe tree, which is native to Ecuador and Peru. The genus has a number of species. It belongs to the family Oleaceae, which includes well known plants like jasmine, forsythia, ash trees and olives. I could not find much biological information on the pink fringe tree but plantlist.org contains a number of links to various databases that may be helpful if you want to dig deeper.


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Why do I see so many handicapped dorbeetles?
Living in southern Germany, I often visit nearby forests and pastures.
From early spring to autumn, I frequently see lots of dorbeetles on my wanderings. An estimated amount of 50% of those bugs seem to be somewhat handicapped or crippled. All of them share the same symptoms:

They stretch their legs away from their body, moving them in a
swimming-like manner, which causes them to be unable to get over the
smallest rocks or plants. It looks very clumsy, almost drunk. Often they draw back one of their rear-end legs, getting caught in parts of plants.
Many of them are lying on their backs, struggling to get back on
their feet. When I turn them around, they will start walking in the
fashion I described above, falling over again almost instantly

Like already pointed out, not all of the dorbeetles behave like this. I see lots of bugs that seem to be perfectly fine, too.
What can possibly cause this?

My first guess would be senescence (i.e. old age after reproduction), since most adult insects are rather short lived (often less than a couple of months). The same type of apparence can be seen in e.g. bumble bees in late summer, when the bumble bee colonies start to break down, and you can se lazy and uncoordinated males and workers barely hanging on to the flowers they visit. However, I do not have any specifics for dor beetles (Geotrupes), and there might be other reasons for this particular taxa. Disease/parasites would seem like another obvious reason.

I do not know for certain but one possibility is an internal parasite.
A number of parasites have been documented to alter the behavior of the hosts to suit the life cycle needs of the parasite.  For example, Toxoplasma is a parasite use rats and cats as hosts. Toxoplasma alters the behavior of the rats so that they no longer respond to the smell of a cat. That makes the rats much more likely to be captured by the cats, which transfers the parasite to the cat from the rat (Berdoy et al. 2000).
This YouTube video shows how a fungal parasite of ants alters the ant behavior to help the fungus reproduce.
My favorite example, which I use in my introductory biology course, is Euhaplorchis californiensis, a parasitic fluke. The parasite lives in marshy habitats, such as Carpinteria Marsh in California, USA. This parasite uses wading birds (herons and egrets), a snail and a fish as it's host.  The adult lives in the gut of the wading birds. Eggs from the adults pass out with the bird feces. Horn snails consume the fecal material and the eggs.  The eggs hatch inside the snail. The larvae actually castrate the snails so that the snails cannot reproduce. Instead, the snails only feed, which provides nutrients for the parasite larvae. The larvae then leave the snail and swim into the marsh, where they are consumed by the California killifish (Fundulus parvipinnis). The parasite works its way from the gut of the fish to the brain, where it releases chemicals that alter the behavior of the killifish. Normally, if a killifish sees a wading bird, it would dive deep. Instead, the parasitized fishes no longer dive. They remain near the surface and swim eratically. This behavior makes it much easier for the wading bird to see and catch the killifish. The parasite is transfered back to the wading bird, and its life cycle begins again. Details of this fascinating life cycle can be found in (Shaw et al. 2010).
Therefore, it is possible that the behavior of the dorbeetles is being influenced by an internal parasite. These dung beetles may consume a parasite when they ingest dung from a certain species. The parasite could alter the behavior of the beetle making them more vulnerable to a particular predator, thereby continuing the next step of the parasite's life cycle.
Your description of the beetle behavior would fit this hypothesis but I stress that I do not know this. I raise the idea as one possibility among many.
A good not technical book on parasites is Parasite Rex by Carl Zimmer. It covers the biology of parasites, the many ways that parasites can affect their hosts, and the creative scientific minds that uncover the complex life histories of many parasites. (I have no connection to the author or the book.)  The book covers the above examples and more in some detail.

Thanks for your thoughts. I am truly amazed by Euhaplorchis californiensis


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Why don't birds in flocks fly into each other?
I've seen videos of hundreds of birds flying in the same general direction but creating incredible patterns in the sky seemingly instantaneously! How do they all know in what direction to turn at the same time? Is there a "Lead" bird dictating this somehow?

Not an answer because I've totally forgotten where to find the papers involved, but this is an active area of research in fields ranging from biology to machine learning to mathematics.

Is there somewhere you can point me where I may be able to gather a little more info on this research?

Searching scholar.google.com for swarm, swarm behaviour and the like should yield some results.

I'm sorry I can't be more help, but remembering references from a talk I heard 3 years ago is hard! You might have to experiment a bit to get the right search terms. If you have access to ISI Web of Knowledge, you may be able to search better there (narrow things down by field, etc).

The guy who gave the talk has probably published at least one paper on swarm behaviour, so this should give you a starting point if you can find the relevant paper. If you can get hold of the paper (or email him for a copy), the citations list is probably a good place to start. http://scholar.google.co.in/scholar?q=author%3A%22Shan+He%22&btnG=&hl=en&as_sdt=0%2C5

You might be interested in artificial life programm called "Boids".

Ive recently stared designing a similar program for some collision detection practice, it is in fact what led me to this question. Boids will not collide because of the code written but i'm 99% sure there's is no collision detection code written for birds:-)

This might be a good starting point....http://www.npr.org/2013/06/13/191348007/what-flocks-of-geese-and-fish-can-teach-us-about-the-future

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution.
The birds, in the aforementioned example Starlings, 'know' which direction to fly and where to be by obeying simple local rules concerning the distance and spacing of other members of the flock in their immediate vicinity, without any global knowledge of the size or shape of the flock in its entirety.
The key to this behavior is that there is no choreographer and no leader.  Order, organization and structure all emerge as by-products of rules obeyed locally, many times over.
Dawkins equates this to 'bottom-up' design or 'self-assembly'.  This is also how embryology works.  Beautifully 'designed' bodies emerge as a result of single cells obeying local rules.  The idea of a blueprint is a misconception.
Dawkins mentions a man in the book named Craig Reynolds who wrote a program in 1986 called 'Boids' which models the flocking behavior of thousands of birds - http://en.wikipedia.org/wiki/Boids


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What advantage would the initial 'donor' in horizontal gene transfer by conjugation have received?
I am struggling to think why horizontal gene transfer between bacteria would have persisted during the course of evolution as surely it puts the 'donor' at a disadvantage?
For example, consider a hypothetical situation where only one species of bacteria has a gene to resist a new (almost) omnipotent antibiotic.  When growing on this medium, this species of bacteria has nil inter-specific competition for the resources it needs.  Yet if it passes on the plasmid containing the resistance gene via conjugation to individuals of a different bacterial species, they then too are able to grow on the medium and potentially out-compete the first species - thus the conjugation could possibly be extremely detrimental to the survival of the original population.
I'm obviously missing something as the feature has persisted, so what is the advantage to the donor species of conjugation?

The donor bacterium, viewed as a unit, may well gain no advantage from sharing its genes.  The genes that are shared, however, may gain a very substantial reproductive advantage from being able to spread to other strains.  If some of the genes that are capable of being shared also promote sharing, they may be selected for by evolution.
This is a good example of the basic principle of the gene-centered view of evolution, famously popularized by Richard Dawkins is his book The Selfish Gene: evolution selects for genes that are good at spreading themselves.  This may, but need not always, imply helping the organism containing the gene to survive and reproduce.

Excellent point. I'm working with a collaborator that specializes in social insects. One of the things I remember her discussing is that when the level of cooperation in a colony reaches a certain level, evolutionary forces begin acting on the colony rather than (or in addition to?) the individuals within the colony. So although we often think of evolution in terms of populations of organisms, there are cases when it makes sense to look at it in terms of populations of genes or populations of colonies, etc.

This is also a good example why the “selfish gene” view does provide new insight, contrary what is often claimed by detractors. Without such an explanatory framework, LGT would indeed be much harder to explain (parasitism might work, but would probably result in some sort of evolutionary arms race which we would expect to observe).


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In which order did the cells of the immune system evolve?
Thinking about how complex the interactions between different types of immune system cells (T-helpers, T-Killers, Phagocytes, B-Cells etc.) are, it's fascinating how they all combine to get the desired effect.
However, I assume that they didn't all evolve simultaneously!  Is there any way to tell which immune cell developed first or any theories to that effect?  Perhaps that question is too specific, in which case was it humoral or cell mediated immunity that developed first?
You may find this paper helpful - unfortunately I'm still months off a campus so can't access it.

As I'm lucky enough to have access to that article, I'm going to extract whatever I can find to answer your question.
To begin with, innate immunity must have evolved first - we can see it at almost all stages of evolution. According to Cooper & Herrin, ever since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms.
They state that around 500 million years ago, the first adaptive immune systems evolved in vertebrates, but do not explain how although they attempt to. Instead, they explain why we are not able to discern at the moment how this evolution came about. The main reason given is that it is unknown when some key cells evolved (namely natural killer cells and dendritic cells) Additionally, mice and humans evolved two different kinds of natural killer cell receptors relatively recently while sharing a common ancestor only quite a long time ago.
Apparently jawed and jawless vertebrates have also evolved two different kinds of adaptive immune systems. They both seem to rely on the same mechanisms but on a different molecular and genetic basis. Cooper & Herrin conclude that at the current level of research, we are not able to determine the evolution of our immune system.
Source: How did our complex immune system evolve?
Personally, if I'm allowed to give in to the temptation of speculation a bit, I would go by a similar strategy as the evolution of Krebs cycle - look which bits make sense even without the rest. There is of course the major obstacle that the cells of the immune system require an entirely new branch in haemopoiesis: all innate immune cells (aside from natural killer, NK cells) derive from the common myeloid progenitor, whereas all adaptive immune cells (and NK cells) derive from the common lymphoid progenitor.
I think this may even be a first hint: NK cells are innate immune cells but they derive from a different lineage at the highest level - they may have evolved as the first lymphoid cells after the myeloid innate immune cells. The next closest related cell is the cytotoxic T cell (CD8+, aka Tc), which utilises the exact same killing mechanisms (perforin+granzymes and Fas ligand) and attaches to other cells in almost the same way as the NK cell (immune synapse). It is also independent and can kill on its own, as long as it recognises its specific antigen. This is the main difference and also a very large step - the generation of the specific T cell receptor. Once the specific T cells receptor is developed, the step to helper T cells (CD4+, Th) is not far, although these perform a relatively bystander-like role in the immune response, steering the other immune cells from behind the scenes and not directly effecting any killing of the pathogen. Therefore I would guess that before helper T cells, B cells evolved, which are capable of producing antibodies. Antibodies themselves are very similar to the T cell receptor (not in gross structure but in the underlying genetic domains and their processing), so a 'detachable' antigen-specific T cell receptor may have evolved and ultimately caused the development of a new cell type. Once all these components are present, it is necessary (or beneficial) to control which cell types are the most active and in which way they act at the site of infection. This is exactly what helper T cells do, by steering the local immune response either into a Th1 (cytotoxic) or a Th2 ('humoral', anti-parasitic) response direction.

I talked about this to one of our professors; he mentioned that this sort of information is hard to find because funding is hard to find for these sorts of projects because they have little chance of being applicable to medicine :)

i dunno, I think it's a very interesting question... I'm in medical school and I find evolution to be a useful tool to help me understand a lot of concepts (anatomy, obviously, but other stuff too)... I guess big picture is frowned upon, since it doesn't follow some linear thought, even though nature may not use the same line of thinking we do...

To add to this, "To begin with, innate immunity must have evolved first ... since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms."
I remember reading somewhere that the first TLR receptor began in Sponges...

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0051657

Information being interesting or useful for medical students doesn't necessarily make it applicable to medicine ;)


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What is the current molecular explanation of Mendel's pea cross?
With reference to the simplest Punnet square for Mendel's pea plant experiments it occurred to me that I could not connect the little I know about genetics to the little I know about molecules.
The mathematical model assumes that there are two factors (alleles) involved. With respect to Mendel's pea flower colors, to what do those alleles correspond at the molecular level? Genes--minimally it might be two codons, each with binary states so that a protein involved in the manufacture of color molecules changes at two specific amino acids.
Of course it is not so simple. But it must be true that there are two physical objects which in the aggregate have two binary states for this particular case. Do we know what they are, exactly, for Mendel's peas?
Thanks for any insight.

I think the following goes a long way. The language is confusing in on respect--the authors speak of the 'A gene' and a bit later of a G to A transition, and I assume the latter refers to bases.  http://www.ncbi.nlm.nih.gov/pubmed/20949001/

The article you have linked to does explain everything thoroughly, though in a somewhat complex way. I did not know how much genetics you actually know, so I tried to answer very thoroughly.
So the article states that the gene Mendel studied and that was responsible for the white color of the pea flower is ANTHOCYANIN1 (in the article it is also called - bHLH, that is the name of the protein family that ANTHOCYANIN1 belongs to). So, ANTHOCYANIN1 is a transcription factor - a molecule that activates the transcription (making of mRNA) of other genes, basically it activates other genes.
The white flowered peas have a mutation (Guanine to Adenine transition) in the sixed intron of the gene ANTHOCYANIN1. Introns are sequences of non-coding DNA, that does not encode amino acids, and is removed from the RNA transcript by a process called splicing. The mutation occurs at a binding site for the Spliceosome (a protein and RNA molecule) that splices the RNA, because of this the RNA transcript is not spliced correctly. The faulty RNA transcript for the gene ANTHOCYANIN1 contains 8 extra nucleotides and because the genetic code is a triplet, a frame shift occurs. When a frame shift occurs all of the codons bellow the frame shift sight get changed. In this case, this leads to a premature stop codon. The translation of the ANTHOCYANIN1 RNA get stopped before a full protein can get synthesized and a non-functional protein is made.
If ANTHOCYANIN1 does not function, no genes are activated and no pigment is synthesized.
To summarize - the white pea flower color is a consequence of a nucleotide mutation (Guanine to Adenine) in a intron sequence of the gene ANTHOCYANIN1, this leads to incorrect splicing of the ANTHOCYANIN1 RNA (a frame shift) and to the production of a shorter protein that is non-functional.

Regarding the mathematical model can we say, in short, that what Mendel knew simply as a/A involve mutant and non-mutant versions of the transcription factor? Thanks. +1

Yes Daniel you are correct, what he studied in truth was the mutant and non-mutant versions of the transcription factor, he just did not know it, nor understand it that deeply.

My apologies, I misread you original comment.

@canadianer: no problem, thanks. i deleted my responses.


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How is a stem-cell induced to assimilate a knock-in DNA construct?
While looking at (daylight) color perception I came across a paper by Jeremy Nathans (et al., Proc. Nat. Acad. Sci., vol. 100 no. 20, 2003, full text here) in which he describes the creation of a mouse with genetically modified vision.
My threshold question is just about the mechanics of the process, which he characterizes as "site-directed mutagenesis." My understanding (a guess, really) is that embryonic stem cells are induced to assimilate homologous human DNA sequences and these cells are injected into mouse blastocysts.
In outline I understand the idea of the DNA construct but wonder physically how the stem cell initially acquires the knock-in construct.
Thanks for any enlightenment.
Edit: I see that there are several ways to do this and that the paper's "Materials and Methods" section focuses on the molecular genetic details. Maybe we can't get the information from the four corners of the document? If so I'd still be interested in whatever process seems likely given the sort of mouse they made. Thanks.

So, essentially your question is just "How is a transgenic mouse created?", is that correct?

@MattDMo: If I am correct about the injection into blast cells, my question is about what happens before that.

OK, I understand. Can you post a PubMed link to the paper so I can see what kind of mouse they made?

What is the title of the paper - "Genetically engineered mice with an additional class of cone photoreceptors: Implications for the evolution of color vision"?

@MattDMo: That's the one, yes.

The bounty is for an accessible explanation of the physical process of getting the human gene into the mouse. Thanks.


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Is there an antagonistic association between Penicillium and Aspergillus?
Some Aspergillus species appear to like walnuts. My question concerns the association of Penicillium and Aspergillus. No sooner does Aspergillus colonize a walnut (or some other challenging carbon source) than Penicillium seems to move in, eventually killing the Aspergillus colony.
A totally unscientific guess is that Aspergillus is a good colonizer and Penicillium a good opportunist and that this is a common pattern with these two species. Is there any science in this direction? I do recall a sort of well-known picture from an old text in which Penicillium is shown more or less strangling a species of Aspergillus. I didn't think about it much at the time.
The image attached is not very incriminating but the theme is the same. Penicillium are the green hand-like structures strewn about the clover-like Aspergillus. Foot-cell of the latter cropped.
This seems like a simple question but a quick search doesn't reveal a lot, I think in part because this would generally come up as a contamination issue.

It is hard to find any articles on the association between Penicillium and Aspergillus species, although they are both considered two of the most common mold species found indoors.

In this study, the most prevalent spore types detected in both the indoor and outdoor air samples were generally from the Penicillium/Aspergillus group [...] these ﬁndings are qualitatively similar to those observed in other geographical locations, conﬁrming the ubiquitous nature of these fungi.

Although these genera seem to be found commonly, it also has to do with environmental factors, and the relative humidity of the area as well.

Geographical location, climate, and short-term meteorological
  conditions are responsible for outdoor types and levels of fungal
  spores.

As for the association and apparently colonization/opportunistic behaviour of the genera, it seems like there are not any associations between the two, unless perhaps environmental conditions are subject to changing, and different mold species have different moisture/temperature thresholds, although again these mold groups tend to be generalists and do well at a wider range of environmental conditions than other fungi.

A laboratory procedure was developed in which viable peanut seeds were wounded and inoculated with field soil containing natural populations of fungi, then incubated under different conditions of seed water activity and temperature. [...] A. parasiticus colonized peanut seeds at lower temperatures than A. flavus, and cool soil temperatures relative to temperatures of aerial crop fruits might explain why A. parasiticus is found mostly in peanuts.
Other fungi, dominated by the genera Penicillium, Fusarium and Clonostachys, colonized seeds primarily at water activities and temperatures suboptimal for section Flavi species and A. niger.
Eupenicillium ochrosalmoneum frequently sporulated on the conidial heads of section Flavi species and showed specificity for these fungi. The inoculation of wounded viable peanut seeds with soil containing natural populations of fungi provides a model system for studying the infection process, the interactions among fungi and those factors important in aflatoxin formation.

Any associations with different fungi species and their different structures, including, for example, with the conidial heads of Aspergillus seem to be currently under study:

The genus Penicillium comprises species that mostly colonize plant matter. However early reports suggest that several species are capable of parasitizing Aspergillus and sporulating on the conidial heads of the host. More recently Eupenicillium ochrosalmoneum and E. cinnamopurpureum, [...] have been observed sporulating on the heads of Aspergillus species belonging to section Flavi during the colonization of peanut seeds.

Little is known about the host specificity underlying these Aspergillus-Penicillium associations. [...] all species spread across Aspergillus colonies by means of aerial hyphae that grew from head to head. Additional studies are required to clarify whether Eupenicillium and Penicillium species are parasitic or simply epibiotic on their hosts.

+1 This is informative, especially the last. Will wait a while before accepting because it is always risky to assert a negative--the articles you cite appear to support your position.

A year after the fact I found a short passage in Thom and Raper's 1945 text, Manual of the Aspergilli. At page 59 the authors relate that Aspergillus niger colonies are commonly overrun with Penicillium rugulosum which "winds its hyphae within and about the conidiophores, and fruits in a radiating series of short-stalked penicilli surrounding the heads and upper halves of the conidiophores." There is a photo illustrating this on p. 60.

authors: Мирослава Бодь