text:
How much do urban pigeons move around cities?
Do they tend to live their lives in one area of the city or do they move around? For example, do pigeons born on London's Trafalgar Square live their whole lives centered around Trafalgar Square or can they move and become Marble Arch based pigeons?
What is the typical range of a city pigeon? Have Trafalgar Square pigeons ever made the trip to Buckingham palace just down the road from them, or do they hang out in the square all the time?
How different are these behaviors from their wild behaviors and how effected by humans actions in the city are they? For example, do pigeons learn that a particular city square will become busy with tourists in the summer and travel there at these times of the year seeking food?

Good question! You might want to restrict it to one species only though (such as pigeon for exmaple). There are interesting studies about crows for example and how they learned to predict consequences of human behaviours.

This will differ widely between different species, so you need to specify exactly what species you are asking for (e.g. pigeons).

Thanks for the feedback! I'll change the question to be just about pigeons.

I'm only aware of two studies that have looked at Rock Pigeon home range size. Note that this isolated research and may not be representative of Rock Pigeons everywhere nor of other pigeon species.
Rose and Nagel (2006) tracked 80 feral pigeons using GPS receivers and found 32% remained within 0.3 km of their roost location. Only 7.5% traveled over 2km from their roost location. Individuals of this species typically have 1-2 primary feeding locations within their home range which ranged from 3 - 151 ha in size (Rose et al. 2006).
Rose, E., D. Haag-Wackernagel, and P. Nagel. 2006. Practical use of GPS-localization of Feral Pigeons Columba livia in the urban environment. Ibis 148(2):231-239.
Rose, E. and P. Nagel. 2006. Spatio-temporal use of the urban habitat by Feral Pigeons (Columba livia) Behavioral Ecology and Sociobiology 60(2):242-254.


text:
Evolution & Celluar Chemistry
I'm new to this site but had a question on evolution, apologies if some of these questions seem basic but they are from a book i am reading challenging the role of chance in evolution.
Taking the example of Polar bears in the Arctic, how does evolution determine that it was white fur that was a beneficial trait rather than any other colour of fur? Is this a random change in cellular chemistry?
The book argues that there should be more evidence of polar bears of all shapes and sizes but with no evidence, asking "why should the creative factors provide only single options in the polar habitat and let natural selection sit idly by?"

Your question seems to be based on a profound misunderstanding of evolution, and from your quote you seem to be reading a creationist book that is deliberately misleading you; however, your actual question is unclear. Could you rephrase so we know what you're actually asking?

First and most important of all: Evolution neither knows nor determines anything. It happens. And if it is not negatively selected, it will occur.

@Chris I'd hold that last sentence, or clarify what "it" is.

Welcome to Biology.SE. You said The book argues. What book are you talking about?

The book is called "Revelation, Rationality, Knowledge & Truth", it is from a creationist point of view which is why i wanted to get some clarity on some issues. If my question is unclear i apologise and will attempt to ask again. It will probably help if i just quote the passage in question which i am having trouble understanding -

@ZainChawdry You won't learn much about evolution from a creationist. However, you might be interested in debunking creationist fake arguments. I would strongly recommend that you start by reading a science book and then when you know what evolution is you can get back to a creationist book if you want to see if what they say about evolution make any sense.

The reason you're having trouble understanding the passage is that the author is deliberately lying and trying to obfuscate his argument.  He's pretending that his description of evolution is related to the real understanding; it's not. It's as if someone said "Cars have square wheels, which is why they don't perform well on grass-covered interstate highways".  It's impossible to debunk the claim because it's not reality-based; there's nowhere to start.

You raise a good point, and are right to be confused by the book. "why should the creative factors provide only single options in the polar habitat and let natural selection sit idly by?" I literally don't know where to begin to answer this statement. A comparable question is If you squeeze play-doh through a square hole, why aren't there lots of different shapes and sizes of play-doh? Silly, idle physics.

The question is quite unclear but I'll try to say a few words that may help you.
You seem to be considering evolution as an individual that decides what is good and what is not. You seem to be considering the evolution as determing at any time point what will be good for a given species. That sounds very wrong.
Evolution is much more than Natural Selection (NS) but for the purpose of this answer I will talk only about NS. NS is a differential of fitness. Fitness is a function of both the expected reproductive success and expected survival of an individual. The environment is part of what determines the fitness of an individual.
So the question, you might be willing to ask is why is having white fur advantageous for a polar bear. The answer is on this post. In short, polar bear live in a very cold climate and their white fur is actually made of clear tubule which let the sun get through and reach their black skin. If it is unclear for you why dark matter warms up faster than lighter matter, you might want to follow a short physics lecture on light.
I would recommend that you have a look at a very introductory class to evolutionary biology such as Understanding Evolution by UC Berkeley for example. It is pretty short (much shorter than reading the book you're reading and you will learn so much more about evolution).
EDIT
I will not be able to explain you the basics of evolution theory entirely as it would not fit in a single post. So, I am reacting to your first comment but for the follow-up questions, please just have a look at an introductory source of information first and we will all gain lots of time. (No aggressivity here, I just want to avoid spending my day on this single post). Once you've finished an introductory course you are very welcome to ask further questions. Btw, evolutionary biology is a very big field. There are a large number of researchers (me and other users on this website included) who work during their whole to further our understanding of evolutionary processes.

Natural selection must wait for these painstakingly slow changes to provide a large variety of options for it to choose from

This is wrong for two reasons. 1) NS tends to be a relatively fast process for rising the frequency of beneficial mutations. 2) NS does not give options to chose from. It is even the opposite NS remove options to keep only some of them. Mutations create options. In more correct terms, mutation increase the genetic variance while NS (and genetic drift that I haven't talked about yet) remove variation.
A1 allele is a very simple software for students in evolutionary biology that help the to simulate the action of NS and genetic drift on an already polymorphic locus. You might not understand what is meant by "polymorphic locus" but this just mean you need to have a look at an introductory course to evolutionary biology.

if random changes in the cellular chemistry can suddenly alter the colour of hair from black to white, why cannot they change the colour of the hair from black to blue or red or crimson or violet or green, how did cellular chemistry know that what was needed in the arctic climate was only white?

Well, again the hairs aren't really white!
Mutation are random (although this statement can be misleading because there is variation in mutation rate). A mutation is just a "mistake" done during the replication of DNA. An organism does not make mutations to achieve a particular goal. It just make mutations. This is why the vast majority of mutations are deleterious (=decrease the fitness of the individual carrying it).
Now, some mutational effect (in terms of phenotype and not fitness) are more likely than others. For example, a polar bear may already produce a number of pigments that it could "easily" use for colouring its hairs. For example, a polar bear already produces dark pigments (such as melanin) and it is reltaively likely for that a single mutation could darken the fur of the polar bear. If having darker fur was beneficial then this mutation would increase in frequency in the population(assuming no genetic drift which is wrong but this is a story for another time). On the other hand, a polar bear does not produce violet pigments (to my knowledge). As a consequence, it would take a much larger number of mutation (each of which aren't necessarily beneficial) for a population of polar to have a light violet fur (and we would need to assume that having a light violet fur is beneficial).

Many thanks for your answer,what do you think of this passage in a creationist book I'm reading-"Natural selection must wait for these painstakingly slow changes to provide a large variety of options for it to choose from. For instance, if random changes in the cellular chemistry can suddenly alter the colour of hair from black to white, why cannot they change the colour of the hair from black to blue or red or crimson or violet or green, how did cellular chemistry know that what was needed in the arctic climate was only white?"

As said in the answer, its actually not white. And, as said by many others, evolution doesn't know anything; its just a matter of chance. Fur color would have also converted to blue/crimson/brown, but since white was more advantageous, so it flourished and took over other colors. Here by colors, I mean the species with that color.

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What is this animal?

Can someone tell me what is the name of this one? Then I can check a little more about it.

How big is it and where did you find it?

It is not a beast :P

@RHA The bug in that question looks pretty different from this one...

@Cactuswoman same family, different species.

It looks like a squash bug to me (Pyrrhocoris apterus). If not apterus, I'd say it is at least in the Pyrrhocoridae family. Note, they must not but confounded with Corizus hyoscyami. Here is a picture of Pyrrhocoris apterus:

Pyrrhocoris apterus have a very broad range covering a big part of Eurasia, from France to China. Is it where you found it?

This seems to be a species of the genus Pyrrhocoris, most probably the firebug Pyrrhocoris apterus. Its quite common in Europe, but according to the Global Biodiversity Information Facility there are also some occurrences in the US.

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Are immunosuppressors necessary after a bone marrow transplant for Bubble Boy Syndrome?
I know that under normal circumstances, immunosuppressors are needed to mitigate the host body's immune reaction to the graft. However, people suffering Bubble Boy Syndrome have pretty much no immune system to begin with. Graft versus host disease does occur in some cases, but not all. So, in these other cases, are immunosupressors required?
Thanks to all!


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Measuring, using and analyzing skin resistance in kohms
What are ballpark ranges of skin resistance in Kohms for average men and their significance (for example 500-1000s = stressed vs 1000+ = fairly relaxed)
What do various skin resistances in kohms say about a person's emotional or arousal state:
For example:
Is a skin resistance of less than 0 possible and what what does that say about the person

This fact depends on the moisture of the skin, for example. You could narrow your question further. Then, having emotional/arousal state is also dependent on the moisture. Your last question: possible in some conditions; last part of the question is subjective so I do not answer it. Your first question about classifications: subjective because too wide question; you need to narrow your topic.


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Why are sponges sometimes not considered multicellular?
I read somewhere (I can't find where) that there is no scientific consensus whether sponges should be considered multicellular organisms.
It seems I don't understand where is the line between unicellular and multicellular life.
I am not able to find a more elaborate explanation of that doubt. What are the reasons for it?

Sponges are generally considered as colonial organisms because there is little cell specialization and little separation of function/role. All cells do pretty much the same thing; it looks more like a pile of individual cells than an actual multicellular organism. In reality it is a little bit in between.
In any case, what one wants to call multicellular or unicellular is a matter of definition and preferences. You cannot find the line between unicellular and multicellular because there is no such line that would not be very arbitrary and filled with special cases.
You can study a little more the physiology of sponges and then decide for yourself if it looks sufficiently like a multicellular organism or more like a colony of cells (a colonial organism).

A collection of cells can maintain their individuality, and  have almost nothing in common but their location. No doubt all multicellular organisms today are descended from such collections.
To start doing anything useful for survival, the cells of such a collection can begin to specialize: some for locomotion, some for digestion, some for protection, and so on. Specialized cells group into tissues, and then into organs.
Organisms with cells responsive to electrical stimuli, which occur only in the animalia, can develop specialized tissue for movement, leading to muscles. They can also develop sensory organs, because excitable tissue gives them a mechanism for transmitting signals, and acting in response to sensory inputs.
A collection of cells without any of these specializations may develop into a syncytium, a mass in which there are  many cells sharing a common cytoplasm, with many individual cell nuclei lying in it. This arrangement allows them to share nutrients without having any specialized tissues or organs for doing so. Although there are multiple nuclei, it can almost be said that they live in a single, very large cell. Not having specialized tissues, they don't display the characteristics of multicellular organisms, and not having excitable tissue, they don't develop nervous systems.
This is the strategy some sponges have adopted, and that's why such sponges are not regarded as multicellular organisms.
Not all sponges are quite as simple as this, and have some differentiation in cell function. Whether these form tissues or not is a matter of definition.
So some sponges are almost entirely syncytial, and can't be regarded as multicellular, although they are metazoan. Some are a little more complex. And that explains why sponges will sometimes be regarded as multicellular, sometimes not. I guess it depends on the sponge.


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Why does cold kill humans but not bacteria?
Bacteria can continue like nothing happened after being exposed to low temperatures why doesn't this happen to humans as well? Why can't our metabolic machinery continue as normal?

I think a better question would be something along the lines of "Do human cell lines tolerate cold temperatures?" The question as is is quite trivial - we are multicellular organs that rely on systemic functional integrity, whereas generally bacteria are single-cellular organisms. It's comparing apples and oranges at the minute. I think there is an interesting question in there, but major edits would be required.

@James Why would this be a homework question?

Let's look at what happens when a single cell within a cell wall freezes. We end up with a little drop of ice, within which are encased all the cellular structures. Thaw this ice, and all is well - provided neither freezing nor thawing happen too rapidly.
Now take what happens in a human being.
First, the blood in the extremities gets colder, and cools the interior somewhat. But we have mechanisms to conserve heat in the core, at least for a little while. This doesn't help the extremities much. If the blood freezes there, we get frostbite - the tissues die for lack of blood supply. Fingers and toes and the end of the nose, and other extremities, are compromised.
Now let the core temperature drop. Below a certain temperature, conduction in the heart slows and eventually stops. This is fatal.
There are many other effects, all of them related to the relative vulnerability of different tissues to cold. Freezing is generally bad for animal cells, which will rupture because of the mechanical effects of the expansion of water as it forms ice. Frozen body fluids can't do their jobs. Frozen nerves can't conduct impulses, so muscles won't contract once their temperature drops below the shivering point. And so on.

But why can't our cells resume normal activity after being frozen? Once that blood reaches the cells again why can't it function normally? What structures in our body or cells prohibits this from happening?

I edited to make clear that ice formation will rupture the cells. If the heart has stopped, the body dies. And when the formerly frozen body thaws, the cells do function normally by decaying, which is normal function for dead cells.


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Loooking for dataset of proteotypic and non-proteotypic peptide
I'm experimenting with peptide prediction using machine learning. I need some data for testing. I already have one dataset, but I need another one or two for verification.
I'm looking for data for a proteotypic peptide and a non-proteotypic peptide.


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Mendelian genetics - How can we infer the number of genes in play in this scenario?
So this is a practice question I got from school but I kinda lost here. So the question is:

In    Drosophila , four new recessive mutations have been found all
  of    which produce purple    eye colour.
Mutations 1, 2 and 3 are all found to be X-linked whereas mutation
  4 segregates with one of  the autosomes.
Crosses   between females heterozygous for either mutation 1 and
  mutation  2, OR mutation 1 and mutation 3, and wild-type males have
  been performed.
1st cross:    no  wild-type   males were  observed in 7500
  male  progeny.
2nd cross: two    wild-type males were recovered among 1510
  male  progeny.
What is   the minimum and maximum number  of  genes   identified  by  these four mutations    given   the above   data? Explain your reasoning.
How   would   you go  about   determining the actual  number  of  genes?

My best guess is either mutation 1 & 2 OR 1 & 3 must be allelic because we didn't observe any WT on the first cross. If it's not allelic, there should be complementation there and we will observe a WT phenotype.
I'm not sure what "OR" means.
I'm not sure why only 2 WT males were recovered among 1510 male progeny. I think it has something to do with recombination, but can't really find out what the gene configuration is to obtain that result.
And the way to determine the actual number of genes is by performing a complementation test, right?
Really appreciate if someone can help me / give me some hints here. I'm really lost!
Thanks in advance :)

I suppose that 2nd cross imply crossing offspring of both sexes with parents (of both sexes). Even then, I can't think of a scenario that would explain this pattern without some level of epistasis or environmental variance. Did you copie-pasted the exact question that has been asked?


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What does it mean for muscles origins and insertions to be the other way around in the right than left limb?
Herbert Srebnik writes in Concepts in Anatomy:

In the right limb, the muscle's origin is proximal to the joint and
  the insertion is distal to it. In the left limb, the muscle's origin
  is distal to the joint and the insertion is proximal to it.
  (The text appears next to an image of the biceps brachii)

What does that mean? What does it tell this paragraph tell me as someone new to human anatomy?

Muscles span joints, and their purpose is to affect movement of that joint. Typically a muscle's origin is the more fixed or stable point of attachment to bone, while the insertion is on the bone which moves when contraction or relaxation of that muscle occurs.
Usually with the muscles of the limbs we think of the more proximal end of the muscle as being the origin, and the distal end being the insertion, because muscle action tends to move bones more distal to the limb joints. For example, for movement of the elbow joint you can typically think of muscles originating on the humerus and inserting on the radius and ulna.
However the nomenclature is somewhat arbitrary, because one can in a sense reverse the origin and insertion by fixing the location of the more distal bone and moving the upper body. For example, by placing your forearm still on the table and moving your upper body, because of the nature of their action in this position you might consider the muscles of the elbow to originate on the radius/ulna and have their insertion on the humerus.
I suspect this is what is described in the book. The biceps brachii attaches to the scapula and radius. Depending on whether it is the forearm or the shoulder moving with respect to the elbow joint, the insertion and origin could be considered at either end of the muscle. It is not that the origin/insertion is always opposite for the right versus left limb.


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Thyroid hormone metabolism and excretion
My understanding is that hormones generated by the thyroid gland, including, for example, T4, are excreted and recirculated in the body through the digestive tract. The reason for thinking this is that bile acid sequestrants such as cholestyramine cause a lowering of serum T4. In fact, patients who have hypothyroidism are explicitly warned not to use sequestrants for this exact reason. Here is a statement from a clinical trial discussing the effect:

The enterohepatic circulation of thyroid hormones is increased in
  thyrotoxicosis.Bile-salt sequestrants (ionic exchange resins) bind
  thyroid hormones in the intestine and thereby increase their fecal
  excretion. Based on these observations, the use of cholestyramine has
  been tried. The present study evaluates the effect of low doses of
  cholestyramine as an adjunctive therapy in the management of
  hyperthyroidism. -- clinical trial NCT00677469

Therefore, there would appear to be a metabolic pathway in which T4 is being excreted into the digestive tract and then is later re-absorbed in the lower intestine somehow.
What is this metabolic pathway? How exactly does this mechanism work? Does it have a name?
For more information on thyroid hormone sequestration see:
https://clinicaltrials.gov/ct2/show/NCT00677469
http://www.ncbi.nlm.nih.gov/pubmed/8435884

can you name a primary article that demonstrates that bile acid sequestrates lower circulating T4? Also, I'm not following why you state that T4 is excreted into the digestive tract (?) - can you clarify? T4 is a plasma hormone that acts on nuclear receptors in a wide array of tissues/organs and I've never heard that T4 is secreted into the GI tract and then reabsorbed... bile acids on the other hand are secreted into the GI tract and actively reabsorbed in the distal small intestine

@VanceLAlbaugh I have updated my question with further details.

I have partially answered this question by discovering that the metabolic pathway is called enterohepatic circulation. In this interaction bile salts are absorbed and transported out of ileal mucosal cells by binding to albumin.
However, it is still unkown to me exactly how it is that thyroxine and other hormones are moderated in this process and how it works. Does the albumin collect thyroxine as well as bile salts? How is the process moderated? In other words, bile salts are allowed to be excreted according to some moderated control mechanism. What is this mechanism?

Since you're answering your question, googling "Clearing of Metabolic Waste via Enterohepatic Recirculation" might help. Actually, googling enterohepatic recirculation and anything to do with thyroid hormone(s) will help.

This is an interesting question, but, unfortunately, there is little exact information available. In 1990, de Herder wrote a dissertation on the topic, which is available from http://repub.eur.nl/pub/50862/900411_HERDER-Wouter-Willem-de.pdf . A second mechanism, by which bile acids act on metabolism of thyroid hormones is an endocrine effect, i.e. stimulation of type 2 deiodinase via the TGR5 receptor, see http://dx.doi.org/10.1038/nature04330 for details.


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From an information perspective, are both strands of DNA necessary?
I am learning about the genetic code, replication, and transcription, and I have a question about whether or not both strands of DNA are really "necessary".
In replication, at a high level, we are taking 2 strands of DNA and creating 4 of them. Part of my question is: suppose hypothetically that the genome only consisted of a single strand (instead of the double helix), couldn't replication just as well occur by turning 1 strand into 2 (instead of 2 into 4)? I suppose this could be done by taking advantage of complementary base pairing as usual, and then splitting the two strands?
In transcription, I believe only one strand of a gene is read by RNA polymerase, so I don't think think the second strand is "necessary" here.
Can someone shed some light on this for me? I realize this is pretty speculative, and DNA is what it is, and does what it does. but I think this sort of question will allow me to see deeper into tits finer workings.

From a replication perspective, having two strands is definitely necessary, as that is how a lot of errors get repaired, such as pyrimidine dimers which can be repaired by nucleotide excision of the damaged bases, with new bases added by reading the opposite strand.

Having 2 strands with informative part in the core ensures safety of DNA from enzymes and also ensures that you have 2 copies of same info, one for use and another for back-up. You might want to read this

Don't forget that the DNA is "read" only in 1 direction (i.e. from the 5'-end to the 3'-end). For example, some genes are expressed from one strand while others are expressed from the complementary strand. In other words, you would, strictly speaking, lose information by only having 1 strand.

GGGCTCGATCGATTCA ... So a strand of DNA will match up like this: A goes to U. C goes to G; Example: DNA= ACGTAG the mrNA=UGCAUC ...

It's easy to forget that many DNA-binding proteins, which are important in determining what gets transcribed—by silencing, enhancing or chromatin remodeling—recognize a binding site made up by both strands.

From a strictly information theoretical perspective, no, a second strand does not provide any additional information that cannot be inferred from the complementary strand. But as many comments have pointed out, there are many practical reasons for DNA's double strandedness.

DNA is biochemically more stable in a double stranded state.
The redundancy of two strands allows for maintenance and repair mechanisms to ensure the integrity of the genome.
Proteins that bind to DNA can only recognize the sequence of that strand, so even though the complementary strand can always be reconstructed from the primary strand, DNA binding proteins cannot target that complementary strand unless it physically exists. In some cases, a DNA binding site encompasses both strands simultaneously.
Proteins (such as polymerases) traverse DNA in the 5' to 3' direction, so if information from the complementary strand was required it would have to be read "backwards".

Can another point be that the sense DNA strand of one gene may be the antisense DNA strand for another gene? So having both is necessary.

@SanjuktaGhosh — I would say not. This "can" happen, but it is not necessary. Indeed, although the points listed, although of possible interest to the poster, are not strictly relevant. However, "No" is too short for an answer.

@David Certainly the exception and not the rule, but there are certainly cases in which genes occasionally overlap. It's more frequent in smaller, compact genomes with less intergenic space, and it's more common that non-coding untranslated sequence is involved than coding overlapping with coding, but it certainly can happen. And then when you consider regulatory sequences and other features, I'd say it's not extremely uncommon for different pieces of important information to be encoded on  complementary strands of the same stretch of DNA.

@DanielStandage — I know as more than most about that sort of thing, but my point is that it's useful rather than necessary.

@David Ok, fair point! :-)

Although the title refers only to an “information perspective”, the question itself brings in the processes of replication and transcription. It is not entirely clear whether the poster envisages ‘piggybacking’ on existing DNA- and RNA polymerases which operate on double-stranded DNA (dsDNA) or whether he is envisaging completely different enzymes. I shall consider how the existence of single-stranded DNA and RNA viruses make it possible to argue that, both scenarios are possible in theory.
My answer to the question, therefore, like that of @DanielStandage, is no.
Single-stranded genomes relying on a double-stranded replicative form
Many viruses exist in which the genome packaged in the virion is single-stranded DNA (ssDNA). Replication occurs using either virally-encoded or host-coded DNA polymerases, often going through a double-stranded replicative intermediate (but see next section). Transcription normally occurs using the nuclear host DNA-dependent RNA polymerase, acting on the dsDNA.
In order to have all the information for transcription and translation on a single strand in a non-cryptic form, the individual genes would all have to have the same orientation so that the codons of all the transcribed single-stranded mRNA made sense. There seems no reason why this should not be so, although in practice most DNA genomes of which I am aware have genes in both orientations. However the banana buchy top virus has a genome composed of six individual ssDNAs, each apparently with a single gene.
Single-stranded genomes without a double-stranded replicative form
The rolling circle mechanism of DNA replication involves generation of a single stranded form without a double-stranded replicative intermediate, and, although the most well characterized examples are dsDNA viruses, the ssDNA banana buchy top virus replicates by the same mechanism.  If we think of what might be possible in linear ssDNA genomes by extrapolating from what exists in linear ssRNA viruses, it is not hard to  envisage replication mechanisms involving the production of many copies of a ssDNA of opposite sense to a single copy of a ssDNA template. Replication is therefore not a problem with ssDNA-dependent ssDNA polymerases analogous to extant viral RNA-dependent RNA polymerases. For transcription it would seem more logical to make a further step of a ssDNA-dependent ssRNA polymerase, rather than ‘mutating’ extant dsDNA-dependent RNA polymerases.
Why bother?
As things don’t operate this way it may seem to be a waste of time discussing them. However:

The poster is reassured that his reasoning is — in principle — correct.
The poster and reader is made aware of the varieties of viral genomes and replication strategies of which he might previously have been ignorant.
The answer provides food for thought in relation to the idea that a world in which cellular organisms had RNA genomes preceded the current one in which they have DNA genomes.

A final word about information
The way in which the question is posed relates to information as a linear sequences of nucleotides in DNA, specifically codons. This can be extended to other signals such as transcriptional start sites, splicing sites, polyadenylation/cleavage sites etc. However it is also possible to conceive of three-dimensional information. Although three-dimensional structures are possible with ssDNA, some. e.g. cruciform DNA do require  dsDNA.


text:
Why do mutations in Drosophila dsx (double sex) affect both males and females?
Reason: Loss-of-function mutation of dsx gene in female embryo leads to production of a nonfunctional protein that fails to repress male specific gene expression. So somatic characters of both the sexs persist forming an intersex.
...This is all that I have figured out.
But what is the reason of appearance of intersex characters in male drosophila? Is it due to gain-of-funnction mutation.

Alternate splicing  of the dsx gene leads to sexual differentiation.

My answer may be too late for your homework deadline, but I'd appreciate your seeing whether you understand it and whether it answers your question.

Expression of the double-sex gene is rather unusual, so it is not surprising that you are having difficulty understand mutations in it. The simplified diagram below (adapted from Gilbert’s Developmental Biolgy — available on-line) should help clarify the matter.

The key concept is that although the double-sex gene (dsx) is expressed in both male and female flies, the gene products (DsxF add DsxM) are different in the two cases. This is achieved by alternative splicing of the RNA transcript, controlled ultimately by X and Y chromosome dosage.
The second important concept (the details of which, I admit, I am less familiar with) is that sex is determined by both activating genes specific for the particular sex and inactivating genes for the opposite sex. Thus, the diagram shows that DsxF both activates expression of genes for female sex differentiation and represses expresses of genes for male sex differentiation. Likewise DsxM activates expression of genes for male sex differentiation and represses expresses of genes for female sex differentiation.
Thus, according to this schema, if dsx is completely knocked out there will be consequences in both male and female. In the female, in the absence of DsxF, the genes for female sex differentiation will not be activated, but those for male sex differentiation will not be repressed. This presumably results in the intersex phenotype. Likewise, in the male, the absence of DsxM prevents the expression of the genes for male sex differentiation, but does not repress those for female sex differentiation. Again, I presume this results in the intersex phenotype.

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text:
How does an octopus eye react in free fall?
according to Wikipedia:

Attached to the brain are two special organs, called statocysts, that allow the octopus to sense the orientation of its body relative to horizontal. An autonomic response keeps the octopus's eyes oriented so the pupil slit is always horizontal.

so how would an octopus' eye react on the ISS (assuming the octopus has an aquarium or something it can live in)? In which direction would the eye be parallel to?

Statocysts are composed of a spherical structure with smaller granule statoliths inside; the orientation of these granules is recepted by cilia receptor cells. So in a situation like the ISS, statoliths would be randomly floating around, being recepted by cila receptor cells. At some times, the distribution of statoliths may be concentrated on one side, triggering random changes in the direction of the eye. So in this situation, the direction of the eye may be constantly changing.

did you make this account just to answer this question?

No, when I was deciding the title for the account, I looked at the window and saw my neighbor's ham radio.

late follow up question, would this cause harm, pain, or confusion to the octopus?


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How to estimate heritability from breeding data
I have a lot of plant-breeding data (tens of thousands of results) that are composed of phenotypes of parents and offspring. The plants however went trough years of selection and it is not balanced. Moreover, I have a lot of inbreeding data. What is the best way to estimate heritability from this type of data, having the exact pedigree relations and the phenotypes (But no accurate environmental data).
Moreover, how would you estimate heritability from nominal traits (like color or resistance)?

The (biometric) heritability of a trait is the slope of the regression line of the mean phenotype of offspring on their mid-parent. When you have multiple traits, you need to use a general linear model rather than a simple linear regression. The GLM accounts for underlying genetic correlations among traits. Nominal data poses no problem, you simply assign numeric values to each category. For example, red = 1, blue = 0. For the relevant theory, I would consult Falconer & Mackay (1996) "Introduction to quantitative genetics". Also look up the 'multivariate breeder's equation'.

http://www.d.umn.edu/~jetterso/Ecological%20Genetics/documents/Anecologistsguidetotheanimalmodel.pdf

Thank you very much, it was very helpful. I went on trying with the REML/MCMC methods, and will check how it goes.


text:
What is this wood-infesting insect?
I have these insects in a very old wooden floor. I would like to know whether they are possibly termites, and if not, what they are.

They are about 4 mm in length (and I've had difficulty taking a picture with a standard camera, I may be able to get a better one in a couple of days). This one is dead and may have been crushed a little. Another sign of their presence is little heaps of wood dust appearing with a periodicity of 24-48 hrs, which are about 1 cm in diameter.
Following the indications of @usr137, I think it's rather an ant, indeed it has a slender mid-portion of the body, corresponding to detail (4) in this termite/ant comparative:

But they are much smaller than the ranges I find for carpenter ants (6—19 mm).

sounds like termites to me - it would be best to get an exterminator to come and take a look.

I'm asking because pictures of wood-infesting termites I've found around the internet don't look like this, but there seems to be a large variety. We have definitely planned to have someone come and tell us what to do.

That picture looks more like an ant. Carpenter ant maybe?

@user137: the abdomen is very long and thin, not really like the ants I'm used to around here (S-E France). And I don't know that ants will dig hard dry wood at that rate?

@user137: actually, reading about carpenter ants you may very well be right! The abnomen I see is longer than what is documented, and they are smaller too, though. I'll investigate this further, thanks.

Note that the Wolfram image identifier got it right even with this rather poor photo! Quite amazing -- unless it used bio.SE to acquire its knowledge of carpenter ant and is simply repeating what we came to here...?

To close this, we're now reasonnably sure that they were carpenter ants or a close relative. One more clue is that they infested the wood close to a window receiving sunshine and were much more active when it was warm there. Thanks to @user137.


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How do chromosome pairs get "paired up" for protein synthesis?
If my understanding is correct, during interphase a normal human cell will have 46 chromosomes scattered about in the cell nucleus. These chromosomes can be thought of as pairs: there are two copies of "chromosome 1", one from mom and one from dad. Same goes for chromosome 2, chromosome 3, ... chromosome 22. Although we think of these as coming in pairs, are they actually attached or paired up in some way?
At some point, protein synthesis will take place via transcription. What I'm having trouble understanding is how and when the above pairing takes place. Does transcription occur independently for each of the 46 chromosomes? I don't think this is the case, because in my head I imagine that we will only get one set of proteins from the pair of each chromosome. Also, I'm unclear as to how dominant/recessive genes can come into play unless protein synthesis occurs as a function of both pairs of chromosomes.
I hope this is clear enough. Thanks.

This is actually a quite complex question. No, they are not paired up in the nucleus but rather just scattered around. The exact 3D location of each chromosome in the nucleus is not fully understood yet and is believed to be a dynamic process. Transcription does not occur, strictly speaking, independently because similar genes will use similar transcription factors. Now another factor impacting gene expression is the chromatin state at the location of the gene which is not guaranteed to be the same between chromosome copies (i.e. could be independent).

For dominant/recessive genes, the effect is not necessarily linked to gene expression but rather to the function of the protein. A recessive mutation disrupting the protein simply means enough functional proteins are made to conserve the biological function and vice-versa, if the same mutation was dominant then having a decreased level of the functional protein leads to a complete disruption of the overall biological function.

Although we think of these as coming in pairs, are they actually attached or paired up in some way?

Chromosomes only pair up during metaphase I of meiosis. And meiosis only occurs during the production of gametes (sperm and oocytes). Say Chr1 from mom pairs up with Chr1 from dad. http://media.web.britannica.com/eb-media/76/94976-004-7D0416E7.gif
Mitosis is what happens when somatic cells (say in your toes) replicate.  Chromosome (inherited from your mom and dad) do not pair up in mitosis. Instead each chromosome is replicated
You are probably confusing chromosomes pairs (one copy from mom and another from dad) sitting side by side... undergoing chromatid crossover... with sister chromatids (ie the same chromosome which has been duplicated, so each daughter cell can have its own copy.) This forms the X shape that you think off when imagining a chromosome.
Transcription occurs on all 46 chromosomes. Aside from situations where the gene is controlled by parental epigenetics... both the paternal and maternal copy of the gene is active.
As for  recessive/dominant allele... it has more to do with the function of the protein. If the protein is produced by one allele in sufficient to give a normal phenotype, then the allele is dominant. A dominant negative tends to occur when the mutant allele codes for a mutant protein that can interfere with the normal function of the protein that is encoded. A common example is that the protein works as a pair. And is one member of that pair is mutated, the entire complex is non-functional.

About the chromosomes.
The chromosomes are not paired physically in the cell but yes, there is 23 chromosones, that have two copies of each, one from the dad, one from the mom. The homologous chromosomes are physically paired during meiosis, where cross-over of DNA will happen but only for a littel time.
About protein synthesis.
These are two cases in a recessive/dominant allele combination.

Both synthesize the protein, but the protein from the dominant gene will have the effect and the other just won't be able to.
The recessive gene transcription is blocked. The dominant can be the reason by synthesizing an inhibiting protein, or it could be a physical change to it's DNA etc.

This is only a small example since there is a large numbers of regulations that exists from the DNA, methylation of DNA, mRNA, transcription inhibition etc.
Conclusion.
There is a lot more cases and exceptions since this is an extremely complicated subject. To learn all of them you would need a genetic book or a complete review on this subject.
Sources:
Genetics (Book)
Random monoallelic expression of autosomal genes: stochastic transcription and allele-level regulation
Chromatin regulation at the frontier of synthetic biology
RNA-mediated epigenetic regulation of gene expression


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Is Einstein's mass energy equivalence ($E=mc^2$) relevant to biological systems?
I'm more than 100% sure that the kilograms I eat don't get directly converted to feces and urine.
I'm sure some of it goes to regenerating tissue that is constantly being disposed as well, and maybe some of it is  also being exhaled.
But I have a feeling that $E=mc^2$ might have something to do with the disposal of ingested kilograms.
We are constantly radiating electromagnetic waves in the nonvisible spectrum, we generate heat, we generate chemical bonds, all of these processes can convert mass to energy.
So I was wondering if $E=mc^2$ is relevant to biology?
Thanks.

Short answer
Any law of physics will of course be applicable to living beings. However, in the absence of mass gain and mass loss, the input = output equation for matter holds true and does not require any spontaneous creation and destruction of matter to equate. In other words, the effects of Einstein's discovery has no measurable/practical consequence on biological system (it is here but it is negligible) and the law of conservation of mass applies nicely.
Input and outputs of matter
There are two main sources of matter input:

Eating and drinking
inhaling (gas through the trachea and the lungs)

There are three main sources of matter output

excretion (urine and feces)
exhaling
sweating

The importance of inhaling and exhaling
Just to get an intuition about the importance of inhaling and exhaling matter in this input = output balance, note that when one make sport to lose weight, she/he principally lose weight through exhaling (see this popular video from SciHow). Similarly, trees mass mainly comes from  what they inhale (see this popular video form Veritasium)
Possible duplicate on Physics.SE
You might also want to read the How does mass leave the body when you lose weight? on Physics.SE.

No, the mass-energy convertibility has no practical relevance to biology.  The amount of mass produced or lost in the chemical reactions in biological systems is so small as to be immeasurable and is ignored for biological purposes (other than the conversions which happen as consumed radioactive elements decay).  One needs a nuclear reactor, atom bomb, or star to convert significant quantities of mass to energy.  Chemical bonding does convert between mass and energy, but the mass change is infinitesimal, as described in this question: "Do chemical bonds have mass?"

No, it is not. There are no nuclear fission or fusion reactions being performed in a biological context, for reasons that should be immediately obvious. Mass is not being converted to energy, or vice versa, when we generate heat or create or break chemical bonds.
Biological systems are covered by the laws of the conservation of mass and energy, so kgin $=$ kgout and Ein $=$ Eout. The inputs are food, beverages, and inhaled $O_2$, and the outputs are urine, feces, and exhaled $CO_2$. The making and breaking of various types of chemical bonds converts energy from one form to another, including heat.
I'm not sure what you mean by "electromagnetic waves in the nonvisible spectrum" aside from infrared light (heat).

Fission/fusion is not the only way you use $E=mc^2$. E.G. a water molecule weighs less than its constituent parts.

Are you sure that fusion and fission and energy to matter (and vice-versa) transformation does not occur in our body? It is obviously not an influential parameter in the input=output balance but it still occurs, doesn't it? I might be wrong, my knowledge in physics are a little shaky!

@DavidV and how does that happen?

@Remi.b yes, technically there is some radioactive decay of isotopes in our body. However, I said "in a biological context", meaning it has no impact on our biology - it just happens.

Ok it makes sense +1. I was pretty worried about this possible misunderstanding when I wrote my answer that I wanted to highlight it in yours.

@MattDmo the difference between the mass of the bound system and the unbound system gives you the binding energy. In a fission reaction this would give a tremendous amount of radiation, in the case of the creation of water it will give you a minuscule amount.


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How can plants be grown in hydroponics, and yet not handle too much water in soil?
It's pretty much common knowledge that plants planted in pots or soil that doesn't have good drainage can't be watered too much, or they'll "drown". Regardless of what actually happens, experience seems to show that it's true that plants planted in soil can't handle too much water in the soil.
Yet on the other hand, in hydroponics, plants can grow and grow very well indeed with their roots entirely submerged in water. Clearly, it's not about "drowning".
So what's the deal? Why do soil-planted plants die when they're watered too heavily?
(I wasn't sure if this is a Biology.SE or Gardening.SE question, but I figured it was biology since I'm looking for a more theoretical answer about what happens to the roots, rather than practical advice.)

I would actually recommend deleting this post and asking on Gardening. I'm sure users there have a much greater understanding of the mechanics of hydroponics than biologists might.

In hydroponic methods which submerge the roots, the liquid medium is oxygenated with an air pump (as in an aquarium) to provide the roots with oxygen, without which they stop functioning.


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What is the substrate for glycogenesis?
In glycogenesis (i.e. the synthesis of glycogen), are sugar phosphates the direct substrates for glycogen polymerization? I would certainly think so since glucose is phosphorylated and then stuck onto a glycogen chain, but my textbook seems to think no.

What exactly makes you say that your "textbook seems to think no?" What is the textbook? Sugar phosphates are, by definition, substrates of glycogenesis.

It must be a typo then...it's a true or false questions and that is the literal question "In glycogenesis, are sugar phosphates are substrates for polymerization?" and the answer is F

@user2879934 phosphorylated glucose is not the direct substrates for polymerization... for glycogen synthesis UDP-conjugated glucose molecules are used, not glucose-phosphate (maybe this is the distinction that your book is trying to make) UDP-glucose is different than glucose-phosphate (in my opinion a nit-picky question... but these are the sorts of questions found in textbooks all the time - the book is trying to be tricky)

@VanceLAlbaugh so basically phospohrylated glucose + uracil, so it's false because no uracil?

The books wants to say "what is the substrate for glycogen synthase?" You often end up with really vague questions in the more elementary texts, however, so they (the publisher) thinks you know what they mean by "what's the substrate for glycogenesis?" Really, and a quick fact check via Google or what have you would confirm, glycogen synthase is more formally a UDP-glucose-glycogen glucosyltransferase. The substrate for the enzyme is therefore UDP-glucose, and the function is that of a glycosyltransferase, just very specifically utilizing an activated glucose moiety.

@user2879934 I would not consider UDP-glucose a "phosphorylated glucose" - it's a glucose with a UDP moiety on it

A pathway doesn’t have substrates, only a reaction does. And therefore there’s no such thing as a direct or indirect substrate. You can perhaps ask what the precursors are for glycogen (but do you mean immediate or distal), or what the substrates are for the first reaction in the pathway (but only if it is quite clear what the first reaction i).
That’s the trouble with trick questions. They are generally badly worded and tend to lend nothing to biology education.


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Material recommendation: molecular biology for mathematicians and computer scientists
I am wondering if there are some introductory learning resources on molecular biology designed specifically for scientists with heavily math-oriented curricula (math/physics/computer science).
They should be capable of conveying the main ideas in a concise way; if they could represent some concepts in a mathematical language, that would be a big plus.
Additional details
As it was pointed out in the comment, molecular biology is a very broad field so I should be more specific - although it is difficult for me. Personally, I would like to acquire some basic knowledge to interpret NGS data and go in the direction of system biology.

If it's a concise overview you're after, I'd recommend anything from the instant notes series.

from wiki, quantitative research is the systematic empirical investigation of observable phenomena via statistical, mathematical or computational techniques.This definition applies to any empirical science (which excludes math). So I am not quite sure what you mean by "quantitative scientists"

Molecular biology is a big field. Are you sure you don't want to narrow it down to any subfield of molecular biology? If you are rather interested in system biology, in molecular biophysics, in molecular genetics, in biochemistry or in molecular population genetics for examples you might want to specify.

@Remi.b ok, I have just edited to be more specific

@Remi.b So I guess molecular genetics and cell biology are the most relevant ones for NGS data analysis and system biology, but I am very ignorant so your feedback would be appreciated.

I have also come from purely non-Bio background (I am a Software/Electrical engineer who didn't study Bio even in his high-school).
As others have pointed out in comments above that Molecular Biology is a vast field. But if you want resources covering all the basics of Genetics/Molecular Genetics, then I can easily recommend the following to anyone (which are both easy to understand and very authentic ones):

Nature Scitable
Genetics by PS Verma, Agarwal, S Chand.

There are other books like this one but they all are on bioinformatics/advanced and expect some knowledge of Molecular Biology. My recommendation (proved one) are above two. Best of luck!!

I haven't started it yet, but practical computing for biologists by Haddock and Dunn might be a good place to start. Its what I will use for my Bioinformatics class. This course looks at large sets of genomic data and seeks to use analytical programs to parse out the data into codons, genes, single nucleotide polymorphisms, and mutations. If you can write a code to identify it you can sequence the genome of whatever your interested in an let the program do its thing. You just have to know the language and get comfortable with some beefy programs.

I like this book and strongly recommend it. However,  not for the OP. The book is for biologists needing to learn programming whereas the OP is a computer scientists needing to learn biology.


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What is this white stuff inside apples?
I live at Vancouver, BC, Canada and I often find this kind of white stuff inside the apples I buy

I used to live in Europe (Switzerland) and never saw that before. It very much look like a fungus. Is it? What species is it? What is the geographical range of this species?
When I cut my apples open, I just remove it and assume it did not lay too many mycotoxins in the rest of the apple but when I directly bite into the apple, it has happened to me to eat some of this white stuff. What are the health consequences of it?

I see it in Europe as well. I also suspect it is a fungus.

I am pretty sure that it is a moldy core rot which would be caused by a fungus that infects the apple during the flowering stage. The fungi is also referred to as "apple fuzz".

From SF Gate

fungus sometimes does enter apples at the blossom end and damage the core, especially if weather is wet, a condition called "moldy core,"

From PennStateExtension

Moldy core is caused by several different fungal pathogens. Many cultivars of apples are affected, including Delicious, which is very susceptible. Moldy core may develop into dry core rot if the pathogen penetrates into the core flesh, but the fungus is generally restricted to the core or carpel region.

The Disease cycle

The moldy core fungi colonize the flower parts as soon as the blossoms open. The fungi then enter the developing fruit through an opening in the calyx. Moldy core is primarily a problem during years with light fruit set or when dry weather in early summer is followed by heavy rains in late summer. In addition, wet weather during bloom may cause conditions favorable for the fungi to produce spores.

What kind of fungi is it?
Mycelium

Geographical range
The fungi is mostly found in the apple sorts “Delicious” and “Idared”. Idared's origin is from Idaho, and delicious is originally from Iowa, USA.

Is it dangerous to my health?
Not more dangerous than usual mold would be to your health. You can find more information here. On some forums online I read about people consuming the white fuzz, and did mostly not complain about any problems. However, I read about one case where the fungi evoked an allergic reaction.

Picture

Further reading

Principles of Forest Pathology page 558

The information from your first source is opposite to your conclusion: Dave Wilson fruit experts to whom he showed your photos agreed that the appearance of the cores is normal for Fuji apples, so the entire apple should be fine for jelly production. He said that fungus sometimes does enter apples at the blossom end and damage the core, especially if weather is wet, a condition called "moldy core," but your apples are free of fungus.

I don't have enough rep to post an opposing answer, so here's a comment explaining why I disagree with your conclusion. The picture that the OP posted is very similar to normal white fuzzy tufts present in some apple cores. From PennState Extension: "I’ve received some pictures of apples where the core has white fuzzy tufts (see pictures below). We’ve determined in the lab these “white fuzzy tufts” in the core are not fungal, but part of the apple tissue. Consequently, these apples are perfectly fine and disease-free."


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where can I find a full list of examples of data types in biology?
I have no background in biology and I would like to build a collection of the data types in biology. I start searching and reading bout that and found there are 7 data types:
1-Sequences: DNA, RNA, Protein
2-Structures of biological molecules
3-Gene expression profiles
4-Biochemical pathways
5-Chromosomal mapping
6-Phylogenetic data source
7-Single Nucleotide Polymorphisms (SNPs)
and I search for a schema that defines these types and found EDAM ontology http://edamontology.org/pag but it does not help me.
Do you have any idea where I can find a complete list of examples of the data types mentioned? or at least for one of those data types? Any reference will help me.
Thank you

How are you defining "data types"?

From your examples, it looks like you are interested in data in molecular biology, not biology as a whole. You need to be more specific, and "data types in biology" is way too broad.

Please [edit] your question and clarify what you mean. A "data type" in biology could be anything from an ASCII text file, through a blood or tissue sample, to a beetle.

I am also a little confused about what exactly do you mean by "data type". As far as I know in programming "data type" is something you use to obstruct 0s and 1s e.g string, int and array is the way you'd reference your own data and something that language interpreter/compiler can understand and allocate right memory for. Whereas type of data you can get in biology (bioinformatics), I think is what you are asking. The type of data you get is flat text file i.e ASCII or binary and there are few different binary formats in bioinformatics.
In genomics, which is DNA/RNA type of data you mainly dealing with ASCII files. These are the files that I know of:

FASTQ hold raw - sequenced data. The main two types of sequencing you can do is DNA sequencing (DNA-seq) and RNA sequencing (RNA-seq). Usually FASTQ files always gzip ed and file extension is fq.gz or fastq.gz I wrote this tutorial explaining FASTQ
FASTA can hold different type of sequence data, which is different to raw-sequence held in FASTQ. You can actually convert FASTQ to FASTA, but you'd loose quality information. The two broad classes of sequences you can have in FASTA file are nucleotides sequence i.e DNA/RNA sequence or  amino acid sequence i.e protein/peptides sequence. FASTA is also almost always gziped, file extension varies a bit, most common once are fa.gz or fasta.gz, but you will see fna.gz or fna or faa which tries to indicate FASTA with nucleotides or amino acids. FASTA usually used for reference files e.g reference genome. Here is a link to Ensembl repository for mouse genome
GFF and GTF files these are annotation files, used together with reference genome FASTA files. Here is another one of mine tutorials
SAM and BAM okay here is an example of binary type of data. Sequence Alignment Map, file extension .sam depending on the organism, can be very big. For mouse RNAseq data for example SAM file can be between 1 Gb - 40 Gb, makes sense to compress it. BAM is binary SAM. you need samtools to work with BAM files. Here is pure python BAM parser if you are interested.

This should cover first two of your points. Although proteomics has few more type of data, again mainly text. Mass Spectroscopy is the tool proteomics people use to get they "raw-data" and there is some finny file format(s) that I'm not aware of and there will be a few downstream file formats I'm sure.
As for gene expression, that's mainly tabular data, csv or tsv again flat text file.
One other format that I should mention that covers your point 7 is VCF which is variant calling format here is specifications for it again flat text format.
One thing that I should say; it is somewhat common and preferred, at least in the past to be able to parse biological files with Unix tools such as grep, awk and cut and therefore most of the files are tab separated text files.. I think now bioinformatician coming around and using more structured and compressed data formats.
This isn't exhaustive list of file format by any means, but I think this should give you enough to google for.
One last link to Kegg pathway which is your biochemical pathways, they might explain there the type of data they use


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Glucose Oxidase, Condition to be Active?
I most recently was reading/watching information on honeys antibatical and antimicrobial properties.  The enzyme Glucose Oxidase came up often as a main antimicrobial, yet it is inactive in honey.  How much would honey need to be diluted to make this enyzme active? I may potentially use honey in a dilute for as a backpacking emergency antibiotic/antimicrobial and/or something to irrigate wounds if severe.
I do have an basic (High School) understanding of chemistry if that helps

An interesting point about honey for sure. But why would you prioritise honey over medical supplies whilst back-packing?

This is a common "alternative medicine" claim. But: Where do you see honey being used as an effective medicine? Don't rely on something which will most likely not work (how would you get effective concentrations throughout your body for example) and use real medicine.


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Ant trail behaviour
I observed an ant trail through a house for some years. I wonder why the ants established that trail.
The ants are small ants of common type for middle europe, found almost everywhere in this region.
The very small trail (about one ant per second) enters the house through gaps near the front door, travel the entire house almost hidden except some short parts where they need to cross nacked floor and exit the house through gaps on the other side. They pass the kitchen, but do not enter it, missing the easy chance of picking food there.  Before and after the house, the place is sealed (eg. asphalt or stone plates).
Ants are passing the trail in both directions.
The trail is almost impossible to fight. If cleaned up (using alcohol to remove the traces) it reestablishes in about one day. If holes are blocked, new ones are made (even through silicone or soft concrete) in some days. If hidden gaps are sealed, they tend to use visible trails for some days, but work hard to repoen the hidden gaps.
If all ants on the trail are killed or collected over some time, it doesn't seem to have a long term effect at all.
I've never seen any of the ants visibly carrying anything, if the carry something it must be in their stomach.
So why are the ants so eagerly establishing this trail?

Interesting question. BTW: do you know the species? Lasius niger?

Most likely it's Lasius Niger. But I am no expert in this.


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Estimating RNA concentration from Specific Activity of Labeled RNA
The question reads, Using T7 RNA polymerase to transcribe in vitro a 100-nt RNA off a DNA template. This RNA contains 19 Adenosines. In your 100 uL transcription reaction you added 1.00 µL of α32P•[ATP] that had a specific activity on its reference date (May 6th) of 10.0 µCi/µL. The concentration of "cold" (non-radioactive) ATP in  your transcription reaction was .500 mM. At the end of a 2.00-hour transcription reaction, you run a calibration curve using autoradiography on standards of radioactive ATP plus 2 µL of your reaction to obtain the following data:
Sample-------------------------------------------------------------Pixels
1:1000 dilution of α32P•[ATP] Stock (10.0µL)-------------3.211x10^7
1:10,000 dilution of α32P•[ATP] Stock (10.0µL)-----------2,483,565
1:100,000 dilution of α32P•[ATP] Stock (10.0µL)---------299,215
1:1,000,000 dilution of α32P•[ATP] Stock (10.0µL)-------31,444
Your transcription reaction (2.00 µL)-------------------------102,784
-
Estimate the concentration of RNA (in pmol/uL) that exists in your remaining 98 uL of the reaction.
I am using the equation: S.A = (Chn*(.5)^d/14.3 *Vhn * N * cf)/
                                        Vt*Ccn
where Chn = concentration of the S.A. of the α32P•[ATP] in µCi/µL =10 µCi/µL
Vhn = volume of α32P•[ATP] used in the labeling reaction =1.00 µL
N = the number of A nucleotides in the NA= 19
cf = calibration factor from the standard curve (“pixels”/µCi)= 10278.4 pixels/uCi
Vt = volume of the reaction=  100µL
d = number of days past your isotope’s “reference date” = 7 (May 6th to May 13th given in problem)
Ccn = concentration of cold ATP in the labeling reaction (pmol/µL) =.500 mM =500pmol
After I calculate the S.A. how do use that to estimate the concentration of RNA that exists in my remaining 98 uL of the reaction. I am beyond confused, any help would be greatly appreciated.


text:
What negative effects does cannabalism have in other species (like prion diseases) and how are they mitigated?
It is well known that human cannibals are likely to suffer from a variety of ailments, particularly prion diseases.
However a great many other species, from insect to ape practice cannibalism at much higher rates.
Do they suffer from similar diseases as a result of their cannibalism? If not why not? and do they have evolved mechanisms for dealing with these negative effects?

First, to be clear, the very act of cannibalism does not cause the development of prions, but the consumption of an animal infected with a compatible form of them, particularly when eating nervous or digestive tissue (i.e. the brain, spine, stomach, or intestines).
To directly answer your question, yes, there are other animals that are susceptible to prions diseases when they consume infected members of their own species, or members of compatible carrier species. In the late 80s and 90s, there was a moderate epidemic of Bovine Spongiform Encephalopathy (Mad Cow Disease) that was concluded to have been caused by including bovine parts in cow feeding stock.
A common defense that I know of against infection from the consumption of infected animals is to simply not consume them at all. I know it's not really the answer you were expecting, but indeed, many animals have an active aversion to corpses, notably perceiving the smell of Cadaverine and Putrescine as repulsive. Evidently, a great defense against disease is to just not eat dead or dying things.
I've never heard of insects or arthropods having neurodegenerative prions, and wasn't able to find anything alluding to them having them, but I wouldn't be too surprised if they had other prion diseases that were infectious between them.
Sources:

Matravers et al. FST (2001);17,1-19

Also available at The National Archives

Cadaverine on Wikipedia
Putrescine on Wikipedia
Sacculina on Wikipedia

My guess is that a large part of why animals don't seem to get prion diseases is age. They take a long time to develop, even after eating a lot of prions. Humans live a long time compared to most animals, so they have more opportunity to develop the disease.

Yeast has prions - I'd actually be moderately surprised if arthropods don't, even though we haven't found any yet.

Some of the processes working against cannibalism:

conspecifics (especially similar-aged conspecifics) are likely to be able to fight back effectively, increasing the risk of injury to the would-be cannibal
for organisms with limited dispersal, nearby conspecifics are likely to be closely related; killing them will decrease inclusive fitness
possible spread of disease

However, a theoretical argument by Rudolf and Antonovics (2007) shows that

... group cannibalism, i.e. shared consumption of victims, is a necessary condition for disease spread by cannibalism in the absence of alternative transmission modes. Thus, endemic diseases transmitted predominantly by cannibalism are likely to be rare, except in social organisms that share conspecific prey. These results are consistent with a review of the literature showing that diseases transmitted by cannibalism are infrequent in animals, even though both cannibalism and trophic transmission are very common.

That is, kuru and bovine spongiform encephalopathy ("mad cow disease") are anomalies; they spread effectively because tissue from diseased individuals was eaten by many other individuals - in contrast to the more common ecological situation where a single cannibal eats a single diseased conspecific.


text:
Why wrap a dolphin in wet towels?
In this video, a dolphin jumps into a vessel.  Even though the guides know they will be quickly helping the dolphin back into the water, they first make sure they wrap the mammal with wet towels.
Why did they rush so quickly to wrap the dolphin with wet towels?  Is there something about the biology of dolphins that made that action essential?

I don't have any scientific sources for this, which is why this is a comment instead of an answer, but it's my understanding that their skin can dry out very quickly, killing the skin cells and reducing its flexibility. Dolphins don't have sebaceous glands or other forms of lubricating and moisturizing their skin, so drying could potentially be rather harmful, not to mention painful.

@MattDMo Thanks.  Before posting, I asked a friend, and she said something very similar.  She said "it hurts them to go dry", but she didn't know why.


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Proteins in water vs proteins in crystal
I am not very familiar with the experimental procedure of x-ray crystallography except that it involves the very delicate matter of producing crystal that contain proteins and then diffracting rays through it to get a pattern that tells us about the shape of the protein.
I am curious though when you crystallize a protein that usually stays in the cellular fluid, does it go through any conformational or size changes. For instance isn't there some pressure applied by the water that would potentially result in protein being smaller then what it might be under less pressure. Or what about hydrophobic\philic effects that play an important role in protein folding. Of course once the protein is folded it is bonded through interactions stronger than hydrophobicity so it is not that delicate. But still a complete change of surrounding environment should count as a big change, should it not? So are there any theoretical or experimental explanations as to whether the protein changes size and\or shape during crystallization? References to both experimental and theoretical work are very welcome. Although I guess experimental evidence would make more sense in this matter since usually potentials are optimized to account for the crystal structure to be the minimum of the energy so it I can't see how theoretical works could potentially help to understand this issue. I guess one way would be to take a native protein structure determined by X-ray and run it through AB initio  molecular mechanics where potentials do not depend on parameters obtained from the native states of proteins on PDB database. I don`t know how theoretically sound that would be though.

a similar question was asked recently on chemistry.SE: http://chemistry.stackexchange.com/questions/48788/

so its expected that the volume of the protein stays the same, that it does not shrink or expand after crystallization but only side chains might be fixed in one of many confirmation?

The assumption is that it stays (at least somewhat) the same, otherwise the structure would not be biologically relevant. This assumption is not always true, there can be changes as a result of crystal formation/buffer/pH/etc. This is why crystal structures are often verified by targeted mutagenesis or another method like NMR.

This is a very good question that's not talked about enough. I often find it hard to believe that structures from incredibly extreme solutions could possibly reflect the native protein state. In some cases, at the very least we one could argue that a structure would have very different surface protein dynamics and particularly flexible regions would be forced into non-native conformations.

I would totally agree with this comment. I am also interested in the packing density and whether if crystallization has any effect on packing density. I guess at this point one could do an AB initio molecular mechanics to see if there is any length difference for the bonds. I would assume it must have been done already thousands of times and we would have known if there were significant differences?

Protein crystals are not like crystals of more commonly found substances like salt [NaCl] or diamond [carbon only.]  These materials do not include other atoms in their crystal structures.  For instance, a crystal of NaCl will contain sodium ions and chloride ions.  X-ray crystallography of that material will, after mathematical processing, show electron density peaks of two varieties, each easily distinguished by intensity as either a sodium ion or chloride ion.  Any other electron density peaks will be few and far between, as well as clearly identifiable as an interloper.
Because most proteins have hydrophilic regions on the exterior surface of the structure, crystals of proteins actually contain a considerable fraction of water molecules within the crystal itself.  These water molecules are part of the crystal because they are interacting with those hydrophilic residues on the tertiary surface of the protein, both by hydrogen bonding, in some cases, and less specific polar interactions in other cases.   This is at least one of the reasons why obtaining a crystal of any random protein is not at all a routine endeavor.  The large proportion of water in these crystals make them very fragile once they do form, as well as not necessarily likely to form in the first place.
If you go into the technical literature to look at the electron density maps that the more commonly diagrammed structure maps are derived from, you'll be able to actually trace water molecules surrounding the individual protein molecules.
In fact, in the days of development of protein crystallography, assigning correct specific atoms to the various electron density peaks was a decidedly non-trivial task.
Effectively, despite being a crystal, the microenvironment experienced by the protein within the crystal is very much like that in an aqueous environment.  The hydrophobic interactions & hydrophilic interactions will not be very different from those in solution.
That is, the crystalline state achieved is not, in fact, "a complete change of surrounding environment" to use the phrase that you've used in your post.

I think your answer generally explains well why protein crystallisation can be used for structure determination in the first place. However, in order to address the main point of the question it might good to include some caveats of the method (e.g. problems with highly unstructurerd regions & the inability to capture confirmations that are less stable than others or only occur under specific conditions).


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Banana cultivar identification
I found a cultivar of banana that I haven't seen before (and that was significantly different from the standard Cavendish cultivar) in a market in Hong Kong today, due to the language barrier (Mandarin Chinese vs Cantonese), I was unable to ask the store owner about the name of the banana.
This is a picture of the banana, pictured next to a pack of standard AA batteries, as well as the peeled banana and a transverse section of the banana.
Can anyone identify the specific cultivar of this banana?

I found the same cultivar of banana being sold in a market while on a recent trip to Sulawesi, Indonesia. I was told by the owner that this cultivar is locally known as the pisang kepok, or alternatively the Saba banana. This cultivar is thought to originate from the Philippines.


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Genetics - Ancestry DNA relationships
If my uncle and I both got our DNA tested and compared ancestry results, should we have 50% or 25% similarity? I get normally it would be 25% but since the mitochondrial DNA and Y chromosome are (mainly) used to figure this out using the test we did, shouldn't we share the same exact maternal DNA since it's my mom's brother and that doesn't recombine or anything and they got it from their mother? I just want to know if this is a different genetics problem than normal. Thanks!

This question would probably be better asked on Genealogy & Family HIstory SE.

The coefficient of relationship between you and your uncle is 25% (see wiki > coefficient of relationship for more info).
However, the percentage of similarity depends on the genetic diversity in the population of interest. If you were studying a population of fully homozygous clones (no genetic diversity), then no matter what the coefficient of relationship is between any two individuals, they would still be clones and therefore perfectly similar.

Usually relatedness is described via the coefficient of relationship because it is natural, relatively simple to calculate, and corresponds well to the actual amount of DNA likely to be inherited.  In this system, you are 50% related to your mother, and your mother is 50% related to her full brother (your uncle), so you are 50% $\times$ 50% $=$ 25% related to your uncle.
This measure is an expected value, the average amount of DNA inherited across a large number of instances.  A particular instance can vary from the measure due to randomness in the biological process.  Although the percentage from parent to child is always the same, more distant relationships are affected by genetic recombination resulting in a bell-curve distribution around the expected value.
The coefficient of relationship matches the biological behavior of the autosomes (nuclear chromosomes other than the sex chromosomes, X and Y), which contain the vast majority of the cell's DNA.  The behavior of the X and Y chromosomes and the mitochondrial chromosome differ, however, so this measure does not provide an exactly accurate expected value for all inherited DNA.

"... got our DNA tested and compared ancestry results ... since the mitochondrial DNA and Y chromosome are (mainly) used to
  figure this out using the test we did ..."

The above pieces of the question suggest a misunderstanding of DNA testing.  There are three main kinds of consumer DNA tests: one tests only a few characteristics of the Y chromosome, one a few characteristics of the mitochondrial chromosome, and one tests many characteristics of all the autosomes (and optionally the other chromosomes).  The first two are older and not used so much today.  The last is what is usually done today to indicate ancestry, and it provides results consistent with the coefficient of relationship measure.

Just a note regarding your last paragraph – Y-DNA testing is still a very popular test in genetic genealogy, especially surname studies.


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Can anyone identify this bug/insect?
!Saw this bug/insect/spider? on a ranch in Santa Ynez, CA. Pretty fast moving-this was the only photo I could get. The creature is the thing in the photo that looks like two puff balls on a very black body. (The smaller puff is the front of the body.) Maybe a bumble bee? Did not appear to have wings.

Welcome to Biology.SE. Can you please indicate the approximate size and speed (as well as mode) of displacement. It might be hard to say anything with this picture.

You might want to edit the post to improve the grammar, start sentences with a capitalize letter and don't end sentences with things like ...!]

Perhaps it was a species of velvet ant (a type of wasp from the genus Dasymutilla). The females lack wings, and it appears like what you describe and vaguely see in your image.
Here are some photos:

Photo 1 Source
Photo 2/Information Source


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What model of epistasis best fit the reality?
In theoretical population genetics, it is very common to have to assume a model of epistatic interaction. The two most common models are the additive model and the multiplicative model.
Additive model
Under the additive model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is
$$w=1-\sum_{i=1}^n s_i$$
, which becomes $w=1-sn$, for the special case when $s=s_i \forall i \in [1,n] $
Multiplicative model
Under the multiplicative model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is
$$w=\prod_{i=1}^n (1-s_i)$$
, which becomes $w=(1-s)^n$, for the special case when $s=s_i \forall i \in [1,n]  $
Old observation
In Population genetics: a concise guide, Gillespie reused data from Mukai (1968) to plot the following graph

, where the additive $\left(w=1-sn\right)$ and multiplicative  $\left(w=(1-s)^n \right)$ models correspond to the two lines that poorly fit the data. The line that best fit the data is a quadratic model of synergistic epistasis
$$w=1-sn-an^2$$
In all cases, $s$ and $a$ where estimated from these data. We probably have better data and better studies today.
Question
What model of epistatic interaction would you recommend?

Here are some clarifications if needed
Consider $n$ mutations. The fitness of an individual carrying only the first mutation is $1-s_1$. The fitness of an individual carrying only the second mutation is $1-s_2$, etc... the fitness of an individual carrying the $n^{th}$ mutation is $1-s_n$. What is the fitness of the individual carrying all $n$ mutations? Of course, there is no single answer to this question and it will depend on the epistatic interactions between these loci. However, there is probably a general trend that a theoretician would like to consider in its assumptions.

All models are wrong but some are useful :P

I think that if the genes are actually interacting then they are not independent. If they are not independent, their effects cannot be additive. I have not really studied or worked with the models that you mention above but this is a general sort of rule that additive effects are usually because of independence.

If you're fitting real data, try both; if you're doing a purely theoretical model, use whichever is more mathematically convenient. Note that you haven't defined what you mean by "fitness" here; additive effects on growth rate are multiplicative effects on offspring number.

I don't understand what is unclear about my definition of fitness. Fitness is the expected number of offspring of an individual. The statistic I use here $w$ is the fitness of an individual relative to a hypothetical individual that bear absolutely no deleterious mutations (and I ignore the existence of beneficial mutations). I do not talk about the growth rate of a population and would be happy to assume that the carrying capacity is not influenced by the population mean fitness. Thanks


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Do blind birds bob their head when they walk?
Birds try to keep their heads still for short periods of time between steps to improve their ability to see. You can find amusing videos of chickens used as small video camera stabilizers. But does this happen to blind birds? Is it something all birds do regardless of their ability to see?

I did not know that birds (mainly pigeon and a few other species) are moving their head the way they do when walking in order to improve their vision. Do you have a reference for that?

@Remi.b I wouldn't be surprised if it was influenced by this question.

Oh indeed thank you. @user1306322 you should relate (and link) to this post (if it is indeed your reference) and make sure to not over interpret what is being said (it does not talk about walking).

My question was inspired mostly by Mumbles, a chicken born without eyes and prior knowledge about the reason why birds bob their heads. No SE questions were used as inspiration for this post. I'd appreciate if users did not assume unnecessary things for everyone's sake here.

The forward thrusting movement so peculiar of pigeons and other fowl (Fig. 1) while walking is thought to be related to shifting the visual field. The less visible backward motion of the head is thought to be related to fixating the field of view (Dunlap & Mowler (1931).
According to the meticulous observational study by Dunlap & Mowler (1931), blindfolded pigeons stop making head movements altogether while walking. They stop their forward thrusting motion, the backward motion as well as more random scanning head movements. Hence, the authors conclude that the forward and backward jerking movements are related to vision, and not to hold their balance or whatsoever.

Fig. 1. Snapshots of a pigeon walking. The head thrusts forward in the middle frame. source: Dunlap & Mowler (1931)
Reference
- Dunlap & Mowler, J Comparative Psychol (1931); 11(1): 99-113

Is there any other, more recent study on the subject? 1931 was long ago, and it would be strange if no one had investigated this ever again.

@RichardHardy not that I know of, no.

That was fast! Thanks! Does it not seem a bit weird that there are no newer studies? I assume we just might not know of them, but I am not a biologist (nowhere near).

@RichardHardy, yes there might be newer studies.  I must say it took me quite some time to find even one study addressing this. And unfortunately,  it's pretty dated indeed. But nonetheless, it was a well controlled study as far as I can see and it addressed the question here quite directly. And in fact,  I seriously doubt there is any newer study on this,  but I can't be sure.

@AliceD by any chance do you know how one could instigate researchers to organize such a study these days? Perhaps by sending some emails to parties interested in making viral study videos (the credible kind)?

Here is a related YouTube video bearing essentially the same message.


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Which biological kingdom comprises the greatest biomass on Earth?
Which of the five biological kingdoms - animalia, protista, plantera, monera, or fungi - has the largest biomass?
To clarify, if the biomass of every species in each of these kingdoms was added up, which kingdom would have the greatest sum?

A really clear, well defined question with great biological significance. In a silly way, this number can help us quantify which is "winning"! Welcome to Bio.SE!

Please note that the 5 kingdoms you list are NOT monophyletic groups.

Probably Eukaryotes. Specifically, plants.
This is a very fundamental question of life that is often overlooked. It goes without saying that plants and animals are the strongest contenders. However bacteria may also rival them. Be aware though that this is a contentious claim given more thorough estimations that take into account fluctuations in bacterial presence. This EMBO Reports science and society article claims that plants account for 99% of Eukaryotic biomass.
For further reading the Wikipedia page on biomass doesn't seem too shabby for more details on tonnage and methods of calculation.

The most numerous organisms could possibly be viruses or bacteriophages depending on if you count viruses as "living".


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How does the muscle return to its resting state after muscle contraction?
I know that when ADP binds to the myosin head, it moves along and as it does so, it releases the ADP. The ATP attaches to the myosin head and releases the myosin head from the actin filament. Then the enzyme ATPase hydrolises the ATP to ADP, causing the myosin head to move to the original position.
My question is:

How does the actin filament (troponin) move to its original
position? Does it use a mechanism similar to a spring?
Is there a limit to how much the myosin head can pull the actin filament?

Christiaan has answered your first question, it is external constraints that restore the muscle `rest' shape — this is also the case for nonskeletal muscle as the bladder.
On question 2, I will give a little more details, broadly based on Huxley 1957: imagine the muscle is trying to contract against something infinitely resistive. Full contraction cannot be achieved. Myosin heads still bind to actin, but actin cannot slide wrt myosin filament, and only a local deformation is possible under this tension increment. But myosin heads don't stay bound for ever, and when one detaches, this tension increment is lost locally (there'll be heat produced, dissipating this energy), thus the global muscle tension doesn't increase further. This is a built-in limitation rather than a question of how much energy is available.

ad 1. : In skeletal muscle, contraction of the antagonist stretches the agonist to its original position (Fig. 1).
ad 2. : Yes, ATP generates a fixed amount of energy that limits the force generated.

Fig. 1. Agonist/antagonist pairs in the skeletal musculature have opposing actions. source: wikipedia

Does the (maximum attainable) force saturate when available ATP is above a certain threshold? If so, what would be the new limiting factor?

@fs137 - At the protein scale, each power stroke uses 1 ATP per cycle, so ATP concentration is not the limiting factor

Thanks. So the time scale for each power stroke (and number of 'units') limits the amount of force that can be generated?

@fs137 - afaik, yes


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How does epigenetics affect the birth conditions via alcohol?
Recent study has shown that epigenetics can play role in male-caused infertility and it cites for example studies which showed an enhancing of silent genes when drinking alcohol. Since the study argues this as a reason to the negative newborns' conditions, it has to act negatively on the organism somehow.
I would call an epigenetic influence on the fetuses an influence that is meant to prepare the fetus on the change in the conditions. Does the evolution of the enhanced genes any relate to the alcohol consumption, or is it just a negative coincidence?

You need to rephrase your question. The "study" you mention is a review. Like pretty much it reviews, it proves nothing. In general we have very limited abilities to change the epigenome in controlled, experimental conditions - a requirement in order to prove anything. Also, I searched with Ctrl+F, in the paper you mentioned, "enhance", "silent", "infertility", and did not find any mention. Can you give an example of gene that you are thinking of?

I mean the conclusions from the chapter: Effects of environmental exposure on parental epigenetics: alcohol             Sorry I can't get to the original study.


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How can birds disperse seeds when they are able to digest them?
I've just read in a book that birds' guts can digest almost all the consumed seeds with the exception of mistletoe and loranthus (which stays stuck on the branches). On the other hand, I know that the co-evolution with birds caused the enlarging of the fruits - for the fruit trees as an advantage in fast spreading.
But how do exactly birds spread the seeds they consume if they're digested in their guts?

Birds may indeed digest seeds under conditions of rest. It has been postulated that almost all current knowledge on mechanisms of internal seed dispersal has been obtained from experiments with resting animals.
A study with the mallard Anas platyrhynchos (common wild duck), claimed to be quantitatively one of the most important seed dispersing animals in aquatic habitats in the Northern Hemisphere, has shown that physical activity affects gut passage survival and retention time of ingested plant seeds. The authors fed seeds of nine common wetland plants to mallards trained to subsequently swim for six hours. They compared gut passage survival of seeds against a control treatment with resting mallards.
Intact gut passage of seeds increased significantly with mallard activity (up to 80% in the fastest swimming treatment compared to the control), and hence revealing reduced digestive efficiency due to increased metabolic rates. This enhances the dispersal potential of ingested seeds.
An extensive work-out after a meal generally slows down metabolism, as blood is redistributed to the musculature and away from the digestive tract.
These findings imply that seed dispersal potential by mallards calculated from other experiments with resting birds may be underestimated.
Reference
- Kleyheeg et al., Oikos (2015); 124(7): 899–907

Reduced digestive efficiency due to increased metabolic rates?  That seems a bit counter-intuitive, no?  You would think that higher demands on the system would translate to a higher need for efficient energy and nutrient extraction!

@MasonWheeler - An extensive work-out after a meal slows down metabolism, as blood is funneled to the muscles away from the digestive tract.. Good point, and added to answer.

So, are they saying that motility increases with exercise, leaving the seeds less time to be digested, and "pushed out" more quickly, or that the energy demands of the muscles reduce the amount of energy devoted to digestion, and motility remains constant?

@noncom I'm asking what the study concluded, if anything.

The fact that birds are able to digest seeds doesn't mean all seeds get digested. That may depend on activity as in the article cited by @Christiaan. There will probably be other factors like size and shape of the seed and protective coats around the seed.
Humans, whose digestive system is longer than that of birds can digest seeds as well. However, seeds of stratiotes aloides can pass through a human and germinate afterwards.