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Identifying three species of Datura
I have found a large, wild patch, some 200m long, of mainly Datura Stramonium, in our street. I have always been keenly interested and well read on the shamanic, and - very rare - medicinal uses of this species, but scattered amongst them, like family, are two other plants I don't know, but am convinced are also some kind of Datura. I would please like some help on identifying the other two based on the two photos I have of all three.

This is the well known - to me - Stramonium flower, the plant characterized by jagged leaves and the well known spiked seed pod of Jimson Weed seeds.

It looks like user29734's answer is correct, and the above is Morning Glory, but of course subject to confirmation. I now do recognize at least the purple flower as Morning Glory, but from some 30 odd years ago. And it now looks like what I confused with Datura Alba is really just another colour flower of the Morning Glory.
If anyone could please confirm my ID of the Stramonium, and confirm the identification of the second image as morning glory, and suggest what species.
These plants are all around my neighbourhood, with is the northern part of Randburg, South Africa. This city borders on the Northern side of Johannesburg. 1 It's a temperate climate, with very hot and rainy summers, and bitterly cold and dry winters. The soil is reddish and lacks much humus.
It is a semi-rural area, having been rapidly urbanised over the last ten or so years, when it was still just farms and small holdings. Farming is mainly vegetables or lucerne; and lots of maize further out from the city. We are a few km south of the Cradle of Humankind.
1 Strangely enough, there are two cities in the US with the same names, both in California, I believe. I know Johannesburg is.

Please [edit] your question and where you saw these plants. Location is often very relevant when attempting to identify species.

Could the second photo be a Convulvulus/Calystegia?

@RHA, no, the flowers are far less flat and cone like, but wide, not like the narrow Stramonium trumpet shape. I only have dried ones with me now, but I will find a very good example tomorrow and photograph it well, isolated from the foliage, with separate pics of the latter.

@terdon I have added as much detail as I could guess you wanted. I'm no biologist, so only have a rough idea of which factors count, so a tried a shotgun approach.

@AlwaysConfused Yet they are densely interspersed with the Datura, with zero gaps and much overlapping of branches, and I have not seen them elsewhere.

Yes, the second photo looks to me like a morning glory (Ipomoea).  Is it a vine?  The third appears identical to what I have growing as datura in my own garden.

@jamesqf Sorry for the OT, but how do you find growing Datura in you garden? I would imagine in requires quite frequent pruning. I wish to start doing the same.

@AlwaysConfused The leaves are definitely of the same plant, as I have picked flowers from the same stems as leaves.

@AlwaysConfused Because it turns out that is not a picture of the plant I was trying to identify, which is just a whitish type of ipomoea.

@ProfK: It does take a bit of space, but my garden is about an acre.  I do need to regularly prune the seed pods off before they're ripe (every few weeks during the summer/fall), or it will reseed quite enthusiastically.  They plants die back to the ground in winter here (USDA zone 6/7).  Very good nighttime fragrance.

The two left pictures look like garden morning glories, which are mostly hybrids of various species, some of which reseed quite well in my garden, and could have become naturalized.  The leaves on the right look something like Ipomoea leptophylla, but that's native to the US Great Plains area: https://plants.usda.gov/core/profile?symbol=IPLE and not common in commerce.  But there are a lot of Ipomoea species, and I'm no expert, just a gardener.

@AlwaysConfused It does, but the shape of the leaves in the image you linked to don't match the rounder leaves in my centre-bottom pic.

There is no third plant. All three bottom photos are flowers, leaf, and end of stem foliage from the same plant, and the other plant being the top picture, Stramonium.

Okay, so as far as the blue and white flower goes I'm pretty sure it's a cultivar of ipomoea called Flying Saucer which is a hybrid of heavenly blue (I. tricolor) and Pearly gates (also I. tricolor) meaning it's a hybrid and no seed output.
As far as the white flowers go it is most likely Datura since it is part of a short shrub and the petals are spiked. However you should determine if it blooms at night because its possible it could be moonflower. It may also be brugsmansia or pearly gates.
As far as 'alchemical use' datura contains scopolamine which is potentially lethal if consumed in indiscriminate amounts.

I am only too aware of the potentially fatal  and extreme effects of scopolamine, both from extensive study and several very interesting personal experiences. The best treatment for an unexpected or unwanted scopolamine experience is physostigmine and acetylcysteine, for the anticholinergic poisoning, and benzodiazepines for the extremely elevated heart rate. Physostigmine occurs naturally in the Calabar bean.

The second flower is, I'm guessing by the valentine shaped leaf and violet tubular flowers, a morning glory vine (ipomoea violacea or ipomea tricolor). These plants both are closely related cultivars of ololioqui and tlitlitzen which had a history of shamanic use in southern Mexico.

Aaha,, yes, I think I now do recognize that from them growing in a friend's yard when I was very young. So all the psycho-active plants stick together then, like mafiosi.

@ProfK yes, oddly. The morning glory species contains lysergamide and and it's analogues. However, there is a plant which is native from Carola all the way down to Micronesia called Argyria nervosa which contains the same active principle as the mesoamerican plants.

I have edited my question, and included much better images of the ipomoea flowers, of two colours, a leaf, and some other foliage at the top of a 700 - 1000 mm high stem where the thin vines with leaves and flowers start.

That said, as I am studying this plant as an alchemist, where would I locate seeds on the ipomoea?

The seeds on ipomoea form after the flower dies. It sort of dissolves because of its structure and a bulb begins to grow at the ovule. You can observe this as sepal will begin to bulge. You will begin to see a greenish looking pod emerge but you want to extract the seeds from it only when the pod dries and becomes brown. This is assuming that the plant is not a hybrid. If it has grape shaped leaves and heart shaped leaves it won't produce seeds at all. Fascinating, I suggest you read psychology and alchemy by Jung and gionardo bruno and the hermetic tradition by Frances Yates. Excellent books.

Thanks for advice and the great suggestions, especially Jung, who is fairly  unique amongst modern psychologists to not discard and instead value the ancient and evolved bodies of knowledge in magick and alchemy. I am myself a Hermeticist and in particular a Thelemite.

The top plant looks like it could easily be D. stramonium. Daturas can be a bit tricky. You should either provide an estimate of the scale or measure the flower, then compare with this simple key of invasive Daturas (in Australia): https://www.samorini.it/doc1/alt_aut/ek/haegi.pdf. It helps to note capsule size and shape. (It is NOT a Brugmansia sp.; those are trees with pendant flowers.) Also, the second flower photo seems to me is clearly a morning glory, possibly as IDed by user29734, and the center leaf seems from the same plant(s) or closely related.


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Do some genes follow Rock-Paper-Scissors model of dominance?
Assuming there are at least 3 alleles of the gene $G$ in total - $G_R$, $G_S$ and $G_P$ - is there any gene for which the following is true?

$G_R$ is more dominant than $G_S$.
$G_S$ is more dominant than $G_P$.
$G_P$ is more dominant than $G_R$.

Note that the "rock-paper-scissors pattern" is more formally known as a "non-transitive relation". You may be familiar with a transitive relation, where if A>B and B>C, then A>C. If instead A>B and B>C, but A<C (C>A), then it's known as a non-transitive relation, like the one you describe here.

A quick search gives this same question in this Reddit post.
Apparently, there is not yet an existing example of such dominance of three alleles on one another.
That said, if you're interested in rock-paper-scissor patterns in nature, then you will be interested in the side-blotched lizard. It has three genetically encoded male "sexes", that also determines their behaviour. At a population level, the three sexes follow a rock-paper-scissor pattern of successful sexual competition, in that orange-throated individuals can outcompete yellow-throated ones, which can outcompete blue-throated ones, which can outcome orange-throated ones. A simulation has been carried out to model the underlying genetics, but that model doesn't involve a rock-paper-scissors pattern of genetic dominance.

@ruakh You mean "outcompete", not "outcome".

@CJDennis: Yeah, I noticed that typo a few days after proposing the edit. (I also should have written something like "[...] but to be clear, that model [...]" instead of just "but that model".) But given that the edit took almost two weeks to get approved, it doesn't seem worth proposing a new edit just to fix such minor issues. :-/

@ruakh Too late now, but you can edit your edit before its approved.

@CJDennis: Oh! Oops. Good to know. :-P

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Incestual Reproduction in Animals
I'm quite curious on how animals view incestual pairings. Given there are enough mates around, i have quite observed that most females (subjects are dogs, cats, pigeons and chickens) would go choose another mate that is not a direct family member (parent, sibling, offspring). How does this work? Is it instinct to not favor family members or does it still revolve around who's the fittest mate?

Is your observation borne out in any studies? It's hard to explain how something works when one is unsure if that is true to begin with. For example, if I said, "I've observed that when I mix yellow and blue, I get orange. How does that work?" I had a farm, with lots of different animals and dogs and cats. If there was an animal in heat, the males of the species didn't seem to be hesitant in my experience. There is evidence that males like to cat around, but I don't know that this prevents him from going after a relative as well.

No it's not. Just a random observation on our domestic animals. True. Males would not mind relatives but most females choose those who are not directly related. Came here to read about specific studies about this and get enlightened.

Since inbreeding can lead to greater chances of genetic abnormalities, it seems reasonable that individuals who avoid it would be selected for in the long run but I don't know of any studies on this.

Interesting. Thought there would be tons about it. Found this one reference saying they actually rely on to avoid similar scent. But then read on few other sites saying this behavior greatly depends on the animal's social structure. http://www.thenakedscientists.com/HTML/questions/question/2908/

@anongoodnurse It's standard practice on farms to have a small number of bulls or boars or whatever breeding with all the females for several years, inbreeding is inevitable in this situation. Our own farm had 1 bull for about 10 years before we bought a second bull, but kept the first bull for another 5 years, so there was a lot of opportunity for inbreeding.

Anecdotally I have never observed a preference in lab mice, but we have never made a detailed study of it. Males do not seem to favor non-incestuous over incestuous breeding. Though inbreeding does tend to produce smaller litter sizes over generations and inbred strains of lab mice do tend to be less hearty. Though lab mice are a bit removed from the situation in the wild.

edited my question to be female focused. right, males would not hinder kin-breeding but observation seems that the females avoid it as much as possible.

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Why does A pair with T and G with C?
DNA is made up of pairs on AT and GC base pairs.
I know that A only pairs with T and G only with C. Does this apply just to humans, or are there animals where T will pair with G?
Also, surely there would be more possible combinations if A could pair with G or T or C, and DNA would have a better information density - less would be needed to hold the information?

There is no difference in base pairing between different kinds of organisms. Humans, animals and bacteria all share the same fundamental mechanisms as they all use DNA. Which bases can pair is determined by the chemistry of the individual bases.
The bases in DNA form the following hydrogen bonds when they are paired:

If you would try to combine other bases than the canonical Watson-Crick pairs, the hydrogen bond donors and acceptors wouldn't match. You need a donor/acceptor pair at each position.
There are different base pairs possible, but these situations don't really occur in DNA but in RNA. You can find G/U wobble base pairs and even base pairs that use different parts of the bases than the canonical base pairs, e.g. Hoogsteen base pairs.

My understanding is that even if there were more combos in DNA, this would not increase information density (the questioner suggests that).  Indeed, only one "side" of the DNA is read.  Worse, if there wasn't a one-to-one pairing, then one would get garbage when copying DNA, no?

Some pedantry: To be sure, they pair because it is energetically favorable for them to bind. It so happens that in this case, respectively two and three H-bonds are the most energetically favorable, but strictly speaking the bonds are not the cause of the pairing.

@OP The reason GT pairs don't exist in DNA because it can distort the structure. See the bonding patterns for details

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Could someone entirely absorb smells by smelling?
When smelling, your nose detects the smells by absorbing them.
Does this mean that, if you were in an enclosed space, you could smell so much all the smell goes, and there is none of that molecule left to smell?
Would it take so long it would never happen in reality, or does it happen?

It seems unlikely purely in terms of the amount of air which comes into contact with the nasal epithelium - the tissue which contains olfactory receptors.

Nose doesn't really absorb it. THe odorant molecules bind to olfactory recpetors that transduce that signal as action potentials. Even if some amount of odorant actually is irreversibly absorbed that would hardly affect its concentration in the air.

Besides, the odor rapidly diffuses across the entire available space - in your case this would be the room - so it is not possible to get rid of the odor until the source is removed and all the air recycled

On the contrary, your olfactory epithelium - the bit that does the smelling up at the top of your nasal cavity - doesn't absorb smells. The olfactory receptors bind small molecules reversibly.
However, the olfactory epithelium has a coating of mucus, and so small molecules dissolve in the mucus in order to meet the receptors. Molecules will also evaporate off this mucus, but some vanishingly small fraction of the odorant in a room may stay in the mucus of the nose and the upper respiratory tract long enough to be moved by cilia to the stomach.
I think that for water-soluble molecules, the surface area of mucus lining the airways that odorant can reach is a more relevant factor than the number of a particular receptor (which is very low); but depleting a room of an odorant (which is concentrated enough for you to sense in the first place) by breathing would surely take an extremely long time; as the concentration dropped the remaining molecules would become 'harder to catch', and you'd suffocate first in this enclosed space.
Interestingly, hydrophobic molecules that do not readily dissolve in mucus may be bound by soluble 'shuttle'-like proteins which bridge the gap to the receptors: http://www.ncbi.nlm.nih.gov/pubmed/12044155
These odorant-binding-proteins probably contribute to the diversity of molecules we can smell, and presumably also bind odorants reversibly and may release them back in to the nasal cavity.


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Is this a carpenter ant?
I stumbled upon a few hundred of these swarming around two different places in my living room today. They kind of look like a carpenter ant to me, but I'm not sure.
Also, I'd love to know how you identified the ant.
// EDIT, per a helpful suggestion, I'm in Los Angeles, CA, US. We just had rain come through within the last 4-5 days and it has since dried up.

Welcome to biology stack exchange. With insect identifcation it often helps to know a little about your geographic location.

No, this is not a carpenter ant...it's possibly a Pavement Ant (Tetramorium
caespitum) - only it's a male & hence winged....for identification...follow these guidelines-

Pavement ant workers are small, l/8-inch to 3/16-inch
  long, and blackish brown with light-colored legs and two spines at the
  end of the thorax. A distinguishing character, visible with a hand
  lens or microscope, is the series of fine parallel groves on the head
  and thorax

This is completely wrong. It cannot be a Tetramorium because there is no post-petiole between the thorax and the abdomen, and it is not a male but a queen as you can deduce by the absence of external reproductive organs at the end of the abdomen and by the fact the the head is fully developed with eyes relatively small compared to the head and mandibles entirely developed. The concave thorax indicates that this ant is from the genus Camponotus, also known as carpenter ants.

Hymenoptera, Formicidae, Formicinae, Camponotus sp (queen). "Carpenter ant"
The unique segment between the thorax and the abdomen indicate this ant is in the subfamily Formicinae; the color pattern, the shiny cuticle and the concave thorax indicate this ant is from the genus Camponotus. It has wings so it is either a queen or a male, and you can exclude that this a male by the absence of external reproductive organs at the end of the abdomen and by the fact the the head is fully developed with eyes relatively small compared to the head and mandibles entirely developed.


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What species is this blue and white bird?
I want to know what kind of species this bird is

Please add your location, where you got the birds, and an approximate size of the birds. A better photo would also be helpful

The bird in the photo appears to be a white faced "variety" of Lovebird - Genus Agapornis - mainly identified by beak and nares not being visible (cere skin and nostrils not visible). The exact species is uncertain due to ease of hybridization between species and the availability of many color varieties.  The links below may be of further help.
https://en.wikipedia.org/wiki/Lovebird#Species
https://www.agapornidenclub.be/eng/?page_id=2

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Can anyone ID this flower plant by the photo?
Can someone identify this plant? It has big red flowers when it flowers! Not sure if it is native, but it is in my grandmothers garden in Vancouver, British Columbia, Canada.

It seems like it's either a Paeonia brownii or Paeonia californicus.  According to Wikipedia, these are the only peony trees native to North America, but there aren't any that are native to Canada specifically.  I guess these are the closest you can get.  I added some images to hopefully help you out a bit.
https://en.wikipedia.org/wiki/Paeonia_brownii
https://en.wikipedia.org/wiki/Paeonia_californica

That'd be a peony tree. I'd say they're a pretty common occurrence!
https://en.wikipedia.org/wiki/Peony
I'm afraid I'm unfamiliar with identifying the individual species, however, if anyone is more knowledgeable here than me.


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Species-ID: What kind of bug is this?

What kind of bug is this?
Size: About the size of a pencil tip
When was it found: spring time
Where was it found: In northeastern USA, inside the bathroom of our house

Anyone trying to answer will need more information: size, location, time of year.

About the size of a pencil tip, spring time, in the northeast, inside the bathroom of our house

The northeast of what? The stereotype is that Americans typically assume it is obvious to anyone that the coordinates are relative to the USA (no offense), so I edited your post to add these info assuming you meant northeast USA. Please correct it if this is not what you meant

Yes, Northeast USA

It could be a cockroach nimph. Distinctive characteristics:The overall shape and size, the long antenae, the segmented abdomen and the visible rear cerci.


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Please help identify insect found indoor in Malaysia, south east Asia

Found this insect in my home. About half an inch long. Would appreciate it if any of you could help me identify it. Thanks.

that's a cricket

In the USA we call these insects crickets. Because they make a noise that sounds like the pronunciation of their name. This one looks like a male with two cerci.


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Can anyone ID this ant queen species?

It was found in Hong Kong! Below are a few basic information:
Place: Hong Kong
Habitat: Forest. I live very close to a mountain with lots of forestation.
Where Collected: Found it in my window slit of my apartment.
Coloration: Major body parts are black, but legs are light brown.
Distinguishing characteristics: Appears to have one spine in the mid-body (not sure); Huge mandibles
Length: 14mm to 15mm
Width: 3mm
Anything else distinctive: It could move incredibly fast (like a cockroach). Also, it appears to be quite aggressive. When I put in an ant (male ant with wings) of a different species to its tube, it attacked the introduced ant with its mandibles immediately. During its attack, it shook its abdomen periodically.


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Need help with insect identification
Saw this bug in my hallway tonight, crawling alongside the baseboard, it didn't seem like it could crawl up the wall despite trying to countless times. Google wasn't much help, although I saw a weevil that looks sort of similar to it.
Location: Augusta, Georgia, US

It would help if you could edit the question and add the location where you took this photo. City/state and country is usually sufficient.

@Chris It's updated now.

I don't know about weevil, those usually have a long snout looking thing. https://en.wikipedia.org/wiki/Weevil#Gallery Almost looks like a type of ground beetle, but that's because ground beetles are typically black and boring looking. Plus, it's shaped a lot like this north carolina ground beetle: https://en.wikipedia.org/wiki/Brachinus#/media/File:Brachinus_spPCCA20060328-2821B.jpg

That is definitely a ground beetle. Family Carabidae. These are running predators. They are rarely found in homes, and are not pests. It must have gotten in by accident.

@Karl Kjer agreed, and I believe that the out-of-focus photo will not let anyone go deeper than you have (had the palps--the short antenna-like appendages at the front of the head--been in focus we might have eliminated tribe Bembidiini [where the last segment is abruptly narrowed and shortened], but that isn't possible with the evidence at hand).


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Can anyone help to identify this fruit?

It stays the same color when ripe. It's about the same size as a pear. Grows in sub tropical climate of Meghalaya, India.

It seems like cutting it open and showing the inside would give us more insights

Will cut it open and check if it is indeed Solanum Muricatum as suggested.

I think this looks a lot like a pale variety of Solanum Muricatum or Pepino dulce/melon/pear.

It's native to South America, but I think that it would be able to be cultivated in India as well.

Thank you so much. This very much looks like the plant I have as well.

@JamesSyngai Did you know already that you can mark an answer as accepted, if it answers your question? You just need to click the check mark symbol next to the up and down arrows of that answer.

It looks like Tinda (Praecitrullus fistulosus), also known as round melon, Indian round gourd, Indian baby pumpkin, apple gourd, or Indian squash.

Source: https://www.bigbasket.com/pd/10000372/fresho-tinda-250-gm/

Source:  http://fruitspecies.blogspot.com/2008/10/tinda-indian-round-gourd.html

I am not fully sure but in my opinion the leaves look more like chili pepper leaves and it resembles a tomato or eggplant in the fruit, with a similar stem. It's likely a member in the nightshade family (also known as Solanaceae) https://en.wikipedia.org/wiki/Solanaceae .
For reference, a green eggplant:

However, I am unsure what the specific species might be as the leaves don't match the typical eggplant pattern.


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What are "+" and "Ar" in consensus binding sequence of amino acids?
So I was reading this paper and found a figure as below:

I understand that [LEAM] means any of LEAM residues, pS is phosphoserine and X means any amino acid residue.
What is [+] here ? Is both R and Ar arginine itself?

Ar means aromatic and + means positively charged residues. However, this is not a standard code (as of now).
From the same paper:

Sequences closely matching these optimal binding motifs, R-X-[Ar/S]-[+]-pS-[LEAM]-P and R-[S/Ar]-[+]-pS-[LEAM]-P, denoted as mode 1 and mode 2 consensus sequences, were found to be present in many known 14-3-3 ligands ( Yaffe et al. 1997), where Ar denotes aromatic residues and + denotes basic residues.

From the mention of “aromatic residues” in the figure legend (in a different context) I assume Ar stands for aromatic residues. Ar is certainly not an abbreviation for arginine.
I would guess that [H/+] means either histidine or any positively-charged residue.
I think that the authors of the paper should have pointed this out in the figure legend, and that the referees should have insisted on it.


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Omics integration questions
Let's say that I have a population of Mus musculus in the lab. I divide it in a control group and a test group. The test group is constantly subjected to a stress (example: elevated UV radiation). Both groups are allowed to reproduce for 20 generations.
I want to fully characterize and compare what changed in each offspring (control vs test group) by using omics. The objective is then to integrate all these information in a new database with the pathways that change and by what magnitude.

Should I use genomics or/and exomics or/and epigenomics?
If I do one of the above and proteomics, why could I need the transcriptomics for?
Would the metabolomics, which are mainly punctual measures, add any valuable information?

This is a purely didatic exercise.

Should I use genomics or/and exomics or/and epigenomics?

Depends on what you want to look at. Whole genome sequencing will give you all the mutations. If you are interested only in the coding part of the genome then you can go for exome sequencing. Though, exome sequencing will save your time and resources considerably, you may lose out a lot of relevant information from the non-coding and regulatory part of the genome.
Epigenomics is a very broad term. There are several aspects to it. You can go for the DNA methylome, Nucleosome positioning, or ChIP-Seq for Histone modification/variants.
I would suggest that if you can afford it then go for whole genome sequencing. Next choice would be exome sequencing. Once you have these data it might be relevant to add the third layer of DNA methylome.

If I do one of the above and proteomics, why could I need the transcriptomics for?

Transcriptomics is easier and better standardized than proteomics. There are also many good analysis tools.
There are several ncRNA, which has been shown to play important role in cellular homeostasis and gene regulation. You will miss out those.
You will save money. The reagents used for the transcriptomics experiments are the same as the ones used for the genomics experiments. Proteomics is a different domain altogether. You might need to look for collaborators.

Would the metabolomics, which are mainly punctual measures, add any valuable information?

Sure, they do add information. Whether of great value or not depends on the study that you are carrying out. For e.g if you are studying the role of stress in diabetes then doing a metabolomics study may be of great value.

Small note.. Do exome if you don't have money/resources for WGS.. else do WGS.


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What is the scientific name of this plant that is possibly called ogre ears?
I already did a reverse image search and came up with "ogre ears" as a name for this plant. However, this name is associated with other plants: Crassula argentea and Crassula ovata. What is the scientific name of this plant?
Thanks

plant identification I believe falls under gardening.

This (lovely) succulent is Crassula ovata variety "Gollum", known also as "gollum jade" or "finger jade".  Search for the name and you'll find lots of commercial sources.  One informative source is here.

Okay thanks. Looks like Wikipedia has pictures of other varieties mixed in with this one.

You are welcome.  Any plant of horticultural interest can be tough to track down if there are lots of varieties.

That plant is crassula ovata; crassula argentea is a synonym of crassula ovata. Specifically, it appears to be the cultivar Gollum.

You exactly (more or less) repeated the earlier answer. This does not add any new information. Additionally: Please add some references to your answer.

@chris I added that crassula argentea is a synonym of crassula ovata


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Do chicks in eggs excrete?
I want to know if, as a baby chick grows inside the egg, does it excrete waste?
If it does excrete waste, does the waste just sit inside the egg with the chick, until the chick cracks open the egg and gets out?

Yes they excrete uric acid which is stored in the allantois of the embryo; which acts as a reservoir of nitrogenous waste.
Uric acid is not very soluble in water, so it stays as a small solid mass.

@setek Welcome :) Keep on asking good questions!


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Degenerate primer design for DIG in situ hybridization
New to molecular and have learned to design primers from google/youtube so any info would help
Would someone be willing to share their protocol for degenerate primer design?
Breakdown:
Trying to design degenerate primers to amplify/clone specific GPCR genes from an unsequenced genome of a particular fish.
I'm using Ensembl and Genbank for sequences of closely related fish but the complete gene has only been sequenced in 2 other fish species.
I use ClustalOmega for alignment. Is it okay to just use 2 other species for generating degenerates?
1) are there any other good databases for gene sequences?

If the gene is supposed to be well conserved then you can use the sequence from the related species.
For protein coding genes target the ISH probe to the coding region which is more likely to be conserved.
What you can also do subsequently is to:

amplify the CDS
do 3' and 5' RACE
Clone in a plasmid (do a blunt end or TA cloning)
Sequence the insert
Design exact primers

are there any other good databases for gene sequences?

EMBL and DDBJ


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How long can Cholera bacteria survive in a dead host?
How long can cholera bacterium survive inside a dead host? Can they remain dormant in such conditions?
BACKGROUND
On a hill not far from where I live, there was a hospital operating since 16th until 19th century, for cholera patients, and a cemetery for those, who didn't make it. It was closed in 1st half of 19th century and until 20th century not even ruins of the hospital remained; the gravestones got lost under a layer of soil.
Currently, the area is being built over. Large amounts of soil are being excavated for foundations and basements of new houses. Rainwater falling on the piles of excavated soil floats down through driveways, backyards and gardens of houses down the hill, including my own.
Should I worry?

What is the climate of the region that you are talking about? Is the soil generally moist?

Moderate climate, central-eastern Europe, the soil is common clay loam (I may be wrong on this); the hill top area made persistent groundwater non-issue, but the weather is rather on rainy side and the soil is poorly transpiring water and retains it, remaining moist most of the time.

Do you, or your community, readily use ground water for drinking, cooking, or cleaning of food preparation sites?  I'm inclined to think the "Should I worry" part of the question is off topic for medical advise, but the general cholera question is a good one.

@AtlLED: We have gardens with fruits and vegetables. Our pets run free in the gardens. Sometimes we wear sandals, exposing any tiny injuries on feet to the moisture in the grass. I can easily imagine children picking up food that fell on moist ground and eating it, disregarding hygiene. Also, during rain we inhale droplets of water aroused from the ground by rainfall.

None of what you mentioned is likely to have a infectious dose of v. cholerae.  It's more a problem of directly using the water in your day to day life.

This is relevant again now that James Polk might be dug up.

No, I don't think so.
Mostly estuaries (brackish water) and marine biofilms on submerged surfaces are a reservoir for Vibrio cholerae. Vibrio cholerae is isolated from rivers, creeks, washes, irrigation ditches, hulls of ships, etc. (Indeed, cholera spread rapidly throughout the world after the 1817 epidemic, largely due to the inadvertent transport of contaminated bilge water, mainly from British ships.)

Transmission is by the fecal–oral route. Infections are particularly common after ingesting contaminated water or food. Cases are occasionally seen in people who have eaten raw or undercooked shellfish, particularly oysters, from contaminated waters. V. cholerae is excreted in the feces and vomitus. Viable organisms can be found in feces for up to 50 days, on glass for up to a month, on coins for a week, in soil or dust for up to 16 days and on fingertips for 1 to 2 hours. Bacteria survive well in water and may remain viable in shellfish, algae or plankton in coastal regions.

In 1855, a wave of cholera hit London. Thousands became ill and died before John Snow identified the Broad Street water pump as the single point source of that outbreak. Today, patrons of the John Snow Pub (built on the site) can enjoy local ale, and more importantly, a glass of crystal clear, pathogen-free water.

V. cholerae [is] an autochthonous aquatic bacterium rather than a human pathogen that is a transient resident of the aquatic environment. V. cholerae has over 200 serogroups, with O1 and O139 being the causative agents of cholera, due to their carriage of the genes encoding cholera toxin (CT) and the toxin co-regulated pilus. ...[A]ssociations with the human host is only one small aspect of the V. cholerae life cycle and is not necessary for environmental persistence. ...[T]his bacterium is a cosmopolitan aquatic species that is capable of causing illness in humans.

Vibrio cholerae attachment is mediated by pili, which promote surface attachment and subsequent biofilm formation. It is rather difficult to believe that an aquatic biofilm was preserved on the hill for all those years, even in a dormant stage.

...they could transform into a unique dormant stage that was able to survive for months in the sediment of the estuary. ...These exciting new data enabled investigators to now integrate information regarding the seasonal nature of events surrounding an outbreak in populations living near estuaries.

I have found nowhere that the dormant stage can occur outside of water.
Environmental reservoirs and mechanisms of persistence of Vibrio cholerae
Medical Ecology Main Page
Cholera
 Something goofy going on with these, sorry.


text:
What is this frog I found
What type of frog or toad is this? I found him in my backyard in southern Alabama and he is clearly very small. I’m not sure what species it is, it’s mostly brown but has small spots on the top of his mouth and under his eyes and he is completely white on his belly. Anyone have any idea what this little guy is?


text:
Can anybody identify this plant?
I'm from Brazil. And I have this plant at home.
Can anybody identify this plant?

Strongly related: https://biology.stackexchange.com/questions/36542/what-is-the-name-of-this-flower

It's an Epiphyllum Oxypetalum. Epi is greek for around (epi-center) and phyto is plant, epiphytes are plants that live on other plants, for example rainforest plants that grow on the canopy of tall trees.
There are lots of hybrids and lots of colors.

It is a water loving cactus from Central America, I have some but I do not know the latin name. I asked a similar question.


text:
Could someone help me identify this insect from Malaysia?
Could someone help me identify this insect? My grandfather went on holiday to Malaysia and found this interesting beetle it looks like and has been trying to find out what it is, he placed it in resin to preserve it and I was hoping someone might have the answer to what it could be. The beetle itself is about two inches long and is mostly a vibrant yellow. and sorry the picture is so blurry

I don't know the species, but it's from the superfamily Pentatomoidea, probably family Pentatomidae.

I agree. Not a beetle, but a true bug.

That is Catacanthus incarnatus (Pentatomidae). http://cyy4993.blogspot.com/2012/11/stink-bug-pentatomidae-catacanthus_17.html
http://eol.org/pages/3685880/overview

aka Man-faced Stink Bug


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Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
To be specific: Assume chromosomes A and B are homologous. They've both replicated into A1, A2 and B1, B2 and have formed a tetrad at the equator (synapsis). Most textbooks show either A1 and B1 OR A2 and B2 exchanging genetic material, but I've never seen an experiment/paper proving that this is actually the case, and now I've come across this figure showing both A1, B1 and A2, B2 crossing over https://web.archive.org/web/20160314020121/http://www.uic.edu/classes/bios/bios100/lecturesf04am/lect16.htm
see ("crossing over" under meiosis)

So which version is correct, or do we simply not know for sure? Thanks in advance.

Welcome to Biology.SE. You might want to correct. It is sister chromatids and homologous chromosomes (not homologous chromatids).

In the case of meiosis genetic material is not being exchanged between sister chromatids, and to simply say that crossing over happens between homologous chromosomes doesn't really denote which of the two cases listed in the question is happening. I dunno what else to call this :/

Yes, it is perfectly possible for both pairs of non-sister chromatids to cross over in a single tetrad. The "standard textbook" depiction is a simplification, true tetrads can sometimes be very complicated and the nested crossing-over would be difficult for entry-level textbooks to cover.

This microscope image clearly shows two chiasmata occurring on two sets of chromatids, with both of the "blue" chromosome's chromatids undergoing crossing over.
In fact, even more complicated chiasmata complexes can form during meiosis. For example, this slide depicts many chiasmata occurring in a single tetrad. More examples can easily be found by searches.

One or both pairs of homologous chromosomes could exchange genetic material during the process of crossing over.  The number of cross-over events depends on the number of chiasmata. There are also ways for meiosis to occur with no exchange of genetic material between homologous chromosomes.
The image you reference at uic.edu is incorrect.  The purple arms and red arms would not be "swapped" like that until anaphase of first division. The sister chromatids are bound together prior to anaphase of first division.  Many textbook and internet depictions of this are incorrectly drawn.
At diplonema of first division, sister chromatids A and A (and B and B) have axial cores holding them from separating.  There are chiasmata holding the bivalent (all four chromatids) together that end up being cross-over sites. For each chiasma (singular) two of four strands are affected.  There can be multiple chiasmata per bivalent.  Humans average two chiasmata per tetrad (four chromatids).  Without at least one chiasma, fertility would suffer.

Can you provide references for your claims?


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Whats this bug?

My friend found this bug today and we are trying to find out what it is. Long black (about an inch and a half).

Please edit the question and add the location (city/state/country) where you took this image.

Meloid beetle (blister beetle).  Wikipedia images suggest genus Berberomeloe.  This one below, from Spain, is identified on the Wiki page as Berberomeloe majalis. There is at least one other species described from the genus (insignis).


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What is this beautiful bush?

Found this gorgeous bush at Port Orleans resort in Walt Disney World, but none of the employees knew what it was. Can anyone identify it for me?

It's a Queen's Wreath Vine, aka:  Purple Wreath, Bluebird Vine, Sandpiper Vine

This native Central American flower, which blooms in the dry season, is striking in its unusual blue violet color.  Gracefully arched sprays of delicate flowers contrast with the crisp, sandpaper-like leaves.  The flowers are five deep purple petals about 2 cm across in the middle of five slender, blue or lavender sepals that create a distinctive star shape.  Although the flowers last only a few days, the star-like sepals in the cascading clusters persist for many days, gradually becoming lighter.  They are very attractive to butterflies.

I guessed them to be sepals from the picture op provided. Thanks for confirming my suspicions.


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What is this mushroom that only grows next to my tomato seedlings?
So far something like ten out of fifty seedlings (20%) have had this mushroom grow right next to a tomato seedling and nowhere else in the planters.
The black gooey caps are between a peppercorn and a small pea in size. They only seem to grow at night and collapse within a couple of hours after
I have removed the glass jar cover in the morning. The jars are used to keep out the slugs at night. What type of mushroom is this and is this a symbiotic relationship?

(Answering my own question from three FB remarks a friend of mine received):                                                                                ...this is a pin mold fruiting body...
...deliquesced Coprinoid...
...genus Coprinopsis...


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Can ant colonies have two "branches"?
Could an ant colony have 2 or more "branches" located far from each other (i.e. physically separated but interconnected nests) ? If so, how far is the limit?

Yes, sub- or satellite colonies are common in many species (see e.g. Hölldobler & Wilson, 1990; Debout et al. 2007), and these are then labelled as polydomous species. Subcolonies can either contain extra queens, but sometimes only contain foraging workers. The purpose can be both to expand foraging grounds or as a pre-stage for colony budding. The distance between colonies can differ dramatically between species, but there are cases of supercolonies (especially in the Argentine ant) streching over hundreds of square kilometers (Moffett 2012).
Satellite colonies are also common in e.g. Carpenter ants (Camponotus) and wood ants (e.g. Formica rufa), and when colonies are found inside a house there is often a primary colony somewhere outside the building (see e.g. Ants in the home).


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Historical recovery from mass extinction events
Is there a way to generally characterize how species "regrew" after the various mass extinction events happening periodically from 450 Ma to 65 Ma.  Would the surviving species just start back where they had left off and evolve willy-nilly as if the destroyed 50% or 70% of biodiverse species had never existed?  Or would the biome in some way have the capacity to regrow something resembling the former order based just on the remaining species.  This is probably a whopper of a dumb question, my apologies in advance.

I think the concept of adaptive radiation is what you may be thinking about, since adaptive radiations have been observed following historic mass extinctions.
When organisms are placed in environments with low diversity (either due to mass extinction or the recent creation of the environment) they can undergo adaptive radiation.  This generally occurs when there are lots of unoccupied niches in the environment - essentially there are lots of potential ways to make a living that are not being exploited by an existing organism.
In this situation, any organism with a heritable trait that was able to utilize a niche better than other organisms would have a selective advantage and would increase in frequency.  Over time this process can result in new species of organisms.
There is nothing really different about adaptive radiation and the normal process of evolution and speciation except that in an environment with lots of unoccupied niches, the probability of having a trait that gives you a selective advantage is greater so speciation occurs at a faster rate.
It is the normal processes of evolution and speciation that give the biome the capacity to increase diversity based on the remaining species.


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How well supported is the hypothesis that aging is mainly caused by the number of mutations in tissues?
I heard the hypothesis, that the (main) reason of aging is the increasing number of mutations in body tissues. The higher the number of mutations is, the older tissue is.
Is this true? And how well supported is the idea?
Have somebody measured the numbers of mutations in different tissues at different ages, and if so, where I can get these numbers?

I think telomere shortening largely accounts for the replicative cell aging.
http://www.ncbi.nlm.nih.gov/pubmed/22901253
The increase in no. of mutations with age surely does affect the tissue/organism survival too. There's a recent study that I'd like to share here. It is quite interesting and informative.
http://www.iflscience.com/health-and-medicine/mutations-found-115-year-old-womans-blood-could-help-unlock-secrets-aging

The article says telomeres are shortening in stem cells too (par. 5 end). Is this true? I read stem cells have telomerase working, which is preventing telomere shortening?


text:
Are There Rules for How Proteins Are Formed?
Proteins are formed by stringing together different amino acids.  Different amino acids have different properties (such as being attracted to or repelled by water, positively or negatively charged, large, small, etc.).
What I would like to know is if there are any rules or principles which determine how amino acids are strung together to form proteins?  If so, what are those rules and can anyone recommend any resources where I can learn more about this subject?
Thanks.
MORE DETAILS
Let me try and explain what I am trying to ask.  I understand that there are rules of grammar that I need to follow in order to put together a well formed English sentence.  I am wondering if there is something akin to that for stringing together amino acids in order to create a 'well-formed' protein. (I am NOT referring to how DNA codes for amino acids).
For instance, imagine that I wanted to create a new protein and I had a pile of amino acids at my disposal.  It seems to me that if I understood the principles and rules by which amino acid chains work then I could know which amino acids to string together and the order in which to string them together in order to create the particular type of protein that I wish to create.
This is similar to how I can string together letters and words to form well formed sentences or how I can string together well-formed sentences to create logical arguments.  There's a logic to how to form a sentence and a different logic for how to form an argument -- and it is possible to discern that logic by studying syntax and reasonable arguments.
I assume the same is true for proteins.  There must be some sort of logic or system for how amino acids are strung together -- some sort of connection between the 3-dimension, functional protein and the nature of the properties of the individual amino acids and how they are organized together.  What I am wondering is whether or not we have any idea what that system of logic is.

You mean besides their sequence in the DNA code? Basically how they get the form they have?

Your question is a bit unclear. What do you mean by how? Are you trying to ask if there are any rules for which amino acid follows which amino acid? Or are you trying to ask about how proteins fold?

@tel Yes, this is unclear.. However, I am pretty sure he means how proteins are folded

There certainly are a number of rules, and many (but not all) of them are known to science. You can learn about these rules from any introductory biochemistry text, given that folding now comprises a whole subfield of investigation. What exactly are you asking?

this could be worded as a request for some pointers to protein folding, the poster should be forgiven for not using exactly the right words.

Without the OP weighing in to clarify exactly what is being asked, this question should remain on hold. I have rolled back the previous edit, as it makes assumptions that cannot be verified. As I read it, the author is clearly asking about the template that describes the order in which amino acids are added. Editing the question invalidates the answers already given. @Moshe, please clarify your question - are you asking about the order in which amino acids are added, or are you interested in how the linear chain of amino acids forms a 3D structure?

Sorry about not being clear enough.  Here's another try (also please see my edit to the original question):  DNA dictates which amino acids are used and in which order, but it doesn't tell us anything about the logic or system which determines which amino acids to use and which order to use them in.  I am wondering if we know anything about the logic or rules of the system which determines the connection between the order of amino acids and the 3-dimension protein that results.

Related topics: http://biology.stackexchange.com/questions/23246/how-does-protein-denaturation-work http://biology.stackexchange.com/questions/23763/is-there-a-difference-between-polarity-and-hydrophobicity/23777#23777 http://biology.stackexchange.com/questions/23586/why-is-cysteine-and-tyrosine-used-to-calculate-a-sequence-isoelectric-point/23597#23597

http://fold.it/portal/

It sounds like your question is "what are the rules to protein folding?"
That's not the only way to read your question.
Protein Folding is a unique problem - a 1D sequence maps to a 3D object.  Since proteins mediate nearly all biochemical transformations and therefore mediate life's processes, protein folding one of the great unsolved problems in science today.
You can see in the example folded structure above there are helices and flat sheets of connected strands.  You can see below in the schematic alpha beta barrel motif of triose phosphate isomerase (TIM) how elegant these structures can be.

Although the combinations and overall organization of the beta sheets and the alpha helices are boundless, there are some unifying motifs in these structures.
Long ago, a couple of researchers tabulated the amino acids probability of being in alpha helices or beta strands.  The Chou-Fasman model is important in that it has approximately ~70% chance of detecting alpha helices and beta strands.  Its not a great accuracy but what's really amazing about these algorithms is that they show that local forces - the interaction of amino acids near each other in the sequence have something to do with the formation of at least alpha-helices and beta strands.
There have been pounds worth of papers written since then.  In general, statistical surveys of protein sequences have been able to identify folds or motifs by a long list of string and machine learning algorithms.  Hidden Markov Models and Bayesian profiles are popular. Of course all these are similar to Chou-Fasman in that they work on the sequence in short segments more or less.
For a while it was thought that molecular dynamics and other discrete simulations might help to solve protein folding by allowing long distance interactions to be involved.  Just simulating the entire protein molecule in a computer program as it moves into a folded conformation, but this has not proven to be possible for a couple of reasons: (1) it takes a long time for a protein to fold relative to the length of a tractable simulation (2) the forces involved in protein folding and molecular size scales are not really easy to simulate - they do not precisely simulate the forces and behavior experienced by molecules and they involve many more solvent molecules than most computations can involve - even today's server farms would get clogged up with respectable protein folding simulation.
Since 1994 the Critical Assessment of Structure Prediction (CASP) have provided an open competition every 2 years where 3D structures that have been determined experimentally is held from publication.  While its well attended a new class of algorithms showed up around 2000.  These algorithms work on the assumption that local forces are important to protein folding, but often incorporating molecular dynamics.  Using MD or statistics based on protein structures (see the RCSB for the repository), segments of the protein sequence are tested for structural tendencies.  chaining these predictions together, initial protein folds are put together.  Once put together long term interactions can assemble a protein structure.
BTW that is not to say that Protein folding is solved - the solutions that come out often produce a structure that is really similar to the final structure, but often there are substantial differences.
Just looking at the individual sequence there are no simple rules to decide how the protein fold - ultimately molecular physics of the individual sequence determines where the fold will go.
This is incredibly terse, but it could get you started.  Study of protein without any helices or beta strands is a topic in itself - they can be treated the same way as above.  Then there are also proteins who do not have a single fold, but are dynamic and flop around all the time, or only have a shape when in contact with a surface of some kind.  So there's even more.

Thanks for this answer (very helpful).  You wrote:  "ultimately molecular physics of the individual sequence determines where the fold will go".  Might not the rules that I am inquiring about "simply" be the 'knowledge' of how to implement the principles of molecular physics based on the properties of each amino acid?
What leads me to think that something like this might be true is the fact that all proteins (in their vast variety of shapes and functions) are formed from just 20 different amino acids.

Yes - it really depends on what you call rules. If you call Newton's laws 'rules about how objects move' you could just call them rules. we could say "vanderWaals forces, Maxwell's equations, Hooke potentials and Newton's Laws" are the rules of protein folding, but its not much of a guideline.  Oh nuts i also forgot to mention that protein folding is not really solved.  I will put that in..

Disclaimer: This is an interesting question if I have understood what you are trying to ask. But unfortunately the case is that there are so many different cases its impossible to cover them here. Other answers talk about folding and modification, but these are still heavily dependant on the "2d" DNA sequence and aren't useful if all one has is a final protein, so I'll discuss the 'rules' of a final structure. This started as a comment and got too long!
In summary, no, there are not many examples in the grand scheme of things where rules at a protein level exist in any sort of grammatical way. Its all about 3D chemistry.
Protein Structure in relation to Function.
Functional areas in a protein are often made up of structures like alpha helices and beta sheets linked by very flexible looping regions. The way these structural elements are connected is generally different in every protein. However some motifs that perform similar tasks can be identified by their 3D shape and order of connection (which I think is what you're asking about). For example the OB motif (images and good starting point here) has a strict order that the beta sheets follow, whereas the helix is optional. Although this is a neat example of protein "grammar", its very much exceptional when motifs like this are identified.
No Obvious Rules.
This following answer is educated guessing, and other peoples comments would be helpful.
Proteins are much more complex than a 2 dimensional language like English or DNA. One way to think about why your question is difficult to answer is considering that protein biochemistry happens in 3D space whereas our other examples, language and DNA, operate linearly in a 2D line.
Any evidence of a linear ordering in a finished protein implies very simple folding and post-translational processing. Most biochemical tasks are not simple and require complex nuances in the enzymes' chemistry (which comes from 3D chemistry, not 2D sequence). DNA is complicated too, but like our language, it is designed to be simple and read quickly in a line. This means if a sequence wants to do something a bit more sophisticated, it needs a specific order. This isn't a problem in 3D space as there is a lot more to variation other than sequence.

"Proteins are much more complex than a 2 dimensional language like English or DNA."  Good point, but what are we to make of the fact that the initial formation of a protein takes place in a linear, 2-d chain of just 20 amino acids?  It certainly seems to start out in a language-like fashion (don't you think?).
If so, should not the question be what are the rules or principles which determine how the transformation is made from a 2-dimensional, language-like system to a 3-d dimensional, functional machine?

I'm going to assume that you mean "are there any rules for which amino acids can follow which amino acids in a protein?" The answer is no. In terms of a protein's chemistry, there is no restriction on the amino acid sequence.
However, not all amino acid sequences will fold into a definite 3D structure, and not all amino acid sequences will be soluble in water. For these reasons some amino acid sequences cannot be produced via the standard in vivo process (i.e. by a ribosome), but there's no reason they couldn't be produced through chemical synthesis.

I hope that I got what are you asking. You give the example of words, it's not good one. Look on the protein like a machine or maybe cupboard. You bought one in Ikea and now you need to follow the instruction to bring together all the elements. If you just paste together all the parts you will not get a working cupboard. What rules the parts of cupboard following? Physic.

Take for beginning the Bohr model of atom. If you want simpler example - planets in solar system. After that put 10 atoms together to from the simplest amino acid. What structure will they get? Bring near another amino acid. How will they interact together?

The rules comes from physics. And they are very very very very complected. To understand what structure some protein will get or how it will interact with another protein - you need to take all the atoms in the system and to know how they will act one with another. Only huge computers can calculate such things - and only the simplest of them.

Edit: answer to the comment:
Thats what so amazing in the nature. The evolution found the way to build all the body proteins just from approximately 20 amino acids. By the way that doesn't mean that there is just 20 a.c. There are more that 500. 240 Of them can be found free in nature and other only only as intermediates in metabolism. (http://onlinelibrary.wiley.com/doi/10.1002/anie.198308161/abstract)

If you want another example - take Lego. You have - lets say - 20 types of different peaces but you can make a lot of different things from them.

The nature must use a minimal amount of building blocks. This giving advantage in the evolution cause it is simpler. Look at the DNA. Its build just from 4 building blocks! And caring all the information of how to form entire body. Isn't it amazing? :)

I agree that the protein is a machine and I understand (thanks answers like yours) that the laws of physics are involved.
Nonetheless, there seems to me a crucial difference between man-made machines and protein machines.  The machines we make (including from IKEA) are not made from 20 fundamental parts which when put together and folded properly give me the end product I need.
But that is how proteins are made -- does that not suggest that there must be some intervening logic or system which mediates between the linking of the fundamental units and the functioning of the 3-d machine?

I posted an edit to my answer.

I suppose you are not asking how does DNA code for mRNA which has codons (sets of 3 nucleic acids) when read in the correct reading frame (where 3 base pairs each are read beggining from the start codon) a ribosome then translates this into protein... theres a lot more details then what I said... that is called translation:
http://en.wikipedia.org/wiki/Translation_%28biology%29
Afterwords the protein is folded into a 3d shape
http://en.wikipedia.org/wiki/Folding_funnel
Other stuff (other than amino acids) can be added, like a a lipid for anchoring into the membrane (GPI anchor or prenylation) or sugar (glycosylation) amoung other things, this is called post translational modification.
http://en.wikipedia.org/wiki/Posttranslational_modification
if you are asking about the evolution of proteins, here is another article:
http://en.wikipedia.org/wiki/Protein_family
wikipedia can get pretty detailed, also there might not be a lot of pictures... lippincott's illustrated biochemistry has lots of great pictures... but it's a book for health science students, not very abstract/theoretical/philosophical so you won't get much on evolution of protein families among different life forms...
If you are asking which amino acids can go together and which stuff can't, I dunno, I'm not a biochemist...

authors: Данило Омельченко


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What type of Gorgonzola cheese fungus/bacteria is this?
I have purchased a gorgonzola cheese and it came with some orange/yellow fungus/bacteria in the cheese's surface. Anyone know what kind of fungus/bacteria it is, and if it's safe to eat?

I highly doubt if the nature of type of fungi can be identified just by looking at it.


text:
Trying to identify an Ontario bird photographed in Spring in the Don Valley

Any help is appreciated! I think this may be a juvenile bird? I thought it might be a brown-headed cowbird, but the plumage and head markings don't seem quite right (compared to examples on the internet)? Any assistance is greatly appreciated.!
Rob aka orbitrob

Based on the location, timing and picture, this bird is a female Red-winged Blackbird (Agelaius phoeniceus)
In the spring in Ontario, it would be unlikely to have juveniles around, as breeding has just begun unless this photo was taken near the end of Spring. Male Red-winged Blackbirds would be in their dark black plumage with the yellow/red wing patch. Here is a photo of a pair with the male on the left and female on the right.

You can find more information about them here

That's very helpful. Thank-you! Makes sense as there were a lot of the 'showier' males around. :)


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Can anyone identify this mystery caterpillar?
I found this caterpillar in in El Cerrito, CA and was wondering what kind it is?

Best assumption, Gulf Fritillary Caterpillar (Agraulis vanillae). I could be wrong though.

The larva is a caterpillar which grows to approximately 4 cm (1.6 in) in length. It is bright orange in color and covered in rows of black spines. The spines are soft to the touch and do not sting, but the larva is poisonous if eaten. Source: Wikipedia.

Thanks! The caterpillar looks like a close match and the adult butterflies do too!


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Simulating substitution rate of neutral mutations
I am trying to computationally simulate a population based on the Wright-Fisher model I would like to get to the classic result of the neutral theory of molecular evolution that the rate of neutral substitution equals the rate of mutation. However, the results of my simulations never show that. I will briefly explain my simulation process and how I calculate the mutation and substitution rates. Please let me know if there is something wrong in my procedure.
I have a non-structured haploid population that grows in discrete time steps. I start with a population of N individuals in an environment with carrying capacity K. I use a K-allele model of mutation. At each generation, every individual will reproduce n offsprings and it will immediately die afterwards. A u fraction of offsprings will be chosen randomly to have a single mutation in each generation (u is mutation rate per gene per generation). At each generation, I record how many mutations have occurred and how many mutations have reached fixation in the population (reached frequency of more than 99% of individuals). Thus, mutation rate and substitution rate per generation is calculated as the number of mutations and number of substitutions divided by population size, respectively. With this set up, even with hundreds of repetitions, the rate of fixation will never be as big as mutation rate u.
Where do you think is the problem?
I have struggled with this a lot and I appreciate any help.
Edit:
My code is written in Python. This my pseudo-code:
Parameters: population size, genome_size, mutation_rate, generation_number, fixation_threshold.

'''
Population_size: Here it is 1500
Genome_size: the number of loci that can be mutated. Each locus can be mutated to any of ACTG. Here 10^4
Mutation_rate: number of mutations per genome per generation. Here 0.05
Generation_number: The number of generations that the population grows. Here 1000
Fixation_threshold: The fraction of individuals having an allele in the population so that the allele is considered fixed. Here 0.99
'''

The initial population is created. All individuals are the same without any mutations
A vector to hold the number of mutations and a vector to hold the number of fixations is created

For each generation:
    I determine how many individuals in each generation should be mutated. Here 8.
    I randomly choose  (uniform with replacement) the individuals to be mutated
    For each individual in the population:
        It will produce an offspring. The offspring inherits the genome of its parent, i.e. the mutations of the parent.
        If the individual is among the ones to be mutated, the offspring will receive a mutation that is randomly picked.
            The mutation can be a back mutation
        The individual will die
    I record the number of mutations that occurred (it will always be 8 in this case)
    I record any mutation that has a frequency in the population of more than 0.99 of individuals. This is the number of fixations

I run this code for at least 100 times. I expect that the average number of fixations to be equal to the average number of mutations in each generation, or they converge over generations. Because the neutral theory of Evolution by Kimura predicts that for neutral sites in the genome, substitution rate is equal to the mutation rate.

There's not a lot we can do without your code or at least a pseudocode outline. Why are you expecting the fixation rate to be exactly the same as the mutation rate?

I will put here a pseudo-code outline. I expect the fixation and mutation rates to be equal, because that is what the neutral theory predicts for neutral sites. Am I not correct?

Wait, if I'm reading your pseudo code correctly, each organism produces exactly one offspring and the only way to reach fixation is have all 1500 individuals develop the same mutation independently. Either n, the number of offspring needs to be sampled from a distribution, or you need to sample with replacement from the current population of parents N times to create the next generation. What kind of results are you seeing? From this pseudocode, I expect fixation rates of almost exactly zero.

You are correct. I can either have more than one offspring per individual or sample with replacement. I have tried both scenarios. What I observe when I plot the data is constant mutation rates across the generations, and few burst of fixations. See the image below. The x axis is generations and the y axis is frequency. .

That is about what I expect from your model and simulation. Kimura predicts that the rate of fixation is related to the mutation rate, but that actual relation depends on genetic drift and the distribution of offspring and the population size. The probability of an individual mutation reaching fixation is very small in nearly all cases. The probability of seeing a fixation event is always increasing, but it will never reach the mutation rate(or even really get close in a population of 1500).

Thanks. But the theory does exactly say that k=u, where k is fixation rate and u is mutation rate. It explicitly says that fixation rate is irrelevant of population size, because mutations arise with rate Nu and fix with probability of 1/N, where N is the number of chromosomes.

Do you have a link to the text of the theory?

Yes I used this paper which you have cited yourself.
Kimura, M. (1968). Evolutionary rate at the molecular level. Nature, 217(5129), 624–626.

What an insidious misunderstanding about a single variable. My word. Do you have any other related questions or points of clarification you would like?

Thanks for your help. That was all my problem. With the following procedure, the mutation rate equals the substitution rate: I calculate the mutation rate for each generation as the number of mutations divided by the population size. For all generations, I take the mean mutation rate for each generation. Now for the substitution rate, I divided the total number of substitutions over all generations by the number of generations. This will give the substitution rate per population per generation, which equals mutation rate per individual.

This just got too big for a comment and I think might actually qualify as an answer.
Can you give me a source for what you're reading? According to this, which matches the definitions you are using, K=(Nu)/N=u where K is the substitution rate, u is the mutation rate in the population, Nu is the individual mutation rate, and N is the population size.
I went back to Kimura's original paper in Nature in 1968 and he derives that u(p), the substitution rate in the population, is (almost exactly) the same as the mutation rate in an individual(p). But this follows from a different paper(prolific guy) where he shows that the fixation probability for a given allele is roughly 1/N, where N is the population size. Your individual mutation rate in your model is not u, but Nu.
You are confusing the mutation/substitution rate in the population, which is used for molecular clocks and other things, and the individual mutation rate. If the molecular mutation rate, is say, 1/20 (as you assume in your model) then you are expecting a fixation rate per mutation of 1, essentially. If the substitution rate is going to be the same as the molecular mutation rate, every single mutation must reach fixation. If the same locus mutates twice in the same generation(quite possible with enough individuals), then both must somehow reach fixation, even though the first to reach fixation will necessarily destroy the other.
I hope that helps you sort out why Nu will never equal K, and helps the results of your model make sense.
(sidebar: Nu isn't the raw molecular mutation rate but the individual mutation rate, which is actually higher because while growing to adulthood the average human gamete is involved in about 50 cell divisions, which leads to a few more mutations per person.)

I don't fully understand how your model works
I don't fully understand how you model your population. Is it a standard $oop$ (object-oriented programming) where you simulate each individual? Or is it a simulation where you already use some mathematical model? You could eventually copy-paste your code. it is probably not very long, right? What language did you use? Do you have only one locus? Do you simulate several positions within these locus? Do you allow for back mutations?
It seems that you allow the population size to change over time and I don't quite understand how your parameter $K$ does limit the growth rate though. You should write down some equations about that. In any case, change in population size will modify the probability of mutation fixation.
Here is probably some important modifications to do on your code
It is a bit hard to comment on your simulations without actually seeing some equations or seeing the code but I really think that you'll need two important modifications in your code.

fix population size $N$.
To simulate reproduction, randomly choose (uniform distribution) individuals (with replacement) from the population. The chosen individuals form the new generation. For example:

In R:
new_pop = sample(old_pop, N, replace=T)

or directly
pop = sample(pop, N, replace=T)

In Python:
from random import randrange
new_pop = []
for i in xrange(N):
    new_pop.append(old_pop[randrange(N)])

When you get your results, don't forget that you're talking about a stochastic process and you may want to run enough simulation or enough independent loci in order to be able to compare with the predictions from mathematical models.

Thanks for your answer. I have updated the question and implemented your suggestions to my code. But it does not meet the expectations yet.


text:
What is an aromatic cage and what does it do?
Epigenetics, 2. ed, Chapter 3.6:

Similarly, methylated lysine residues embedded in histone tails can be
  read by “aromatic cages” present in chromodomains, or similar domains
  (e.g., MBT, Tudor) contained within complexes that facilitate
  downstream chromatin modulating events (see Ch. 7 [Patel 2014] for
  structural insights

I understand it is something like a protein motif, but I cannot find a good definition using google.

googling "chromodomain aromatic cage" leads to this paper : "Epigenetic Virtues of Chromodomains" (Crit Rev Biochem Mol Biol. 2011 Dec; 46(6): 507–526.) which references "aromatic cage" as "Structure of the HP1 chromodomain bound to a lysine 9-methylated histone H3 tail." (Science. 2002;295:2080–2083.). See figure 3c in the first paper : " The peptide sits on the DNA minor groove, with its methyllysine inserted in the four-residue aromatic cage."

Sentence from same book: ...The chromodomain forms an aromatic cage that has been well documented as a specific binding pocket to methylated histone residues.

It refers to the structures in the PHD-finger domain and chromodomains. The aromatic amino acid residues form a cage like structure which covers and interacts with the methylated ammonium of lysine via a cation-pi interaction.

The BPTF-PHD structures reveal the main characteristics of PHD fingers that can read H3K4me3. The binding occurs through an aromatic cage where a trimethyl ammonium group is stabilized by van der Waals and cation-–π interaction, which is similar to the ones observed in chromodomain, MBT, PWWP, and Tudor domains. This aromatic cage is composed of one Trp and three Tyr residues; and it has three faces and a 'lid' that is beyond the tip of H3K4me3. Subsequently determined structures of other fingers in complex with the H3K4me3 peptides show that the cage varies and can contain a combination of two to four aromatic and hydrophobic residues.

 Margueron et al., 2009

Interesting, so in the image on the left, the cage is supported in a 7-propeller fold, but it is also found in this minimal PHD-finger domain (eg 1WEN) which is much smaller. cool.


text:
Can two proteins sharing a few domains be considered homologous?
I wonder when to say two proteins are homolog. In the current example I checked the sequence of these two proteins in pfam and as you see they have some shared domains but all domains are not shared. Can I say that these proteins are homolog? How can I be confident about my decision?

Did you do a sequence alignment of the two proteins? Homology is often judged on DNA/protein sequence similarity. Other relevant information might be the source species of the two proteins (and their evolutionary distance).

It would be better if you can summarize the PFAM results in the form of text.

I thought that PFAM visuall result better explains my purpose.

@MySky It is difficult to search the content shown in the images. You can keep the image but a text summary would be good

Worth mentioning that this was cross-posted to BioStars.

Yes this question is cross posted in BioStars: https://www.biostars.org/p/335210/

Homology means shared evolutionary ancestry. Sequence similarity is often used as a proxy for homology but inferences should be made with care.
The similarity between two genes/proteins should not just be good but has to be statistically significant (metrics like E-value) for the two genes/proteins to be considered homologous.

INFERRING HOMOLOGY FROM SIMILARITY
The concept of homology – common evolutionary ancestry – is central to
  computational analyses of protein and DNA sequences, but the link
  between similarity and homology is often misunderstood. We infer
  homology when two sequences or structures share more similarity than
  would be expected by chance; when excess similarity is observed, the
  simplest explanation for that excess is that the two sequences did not
  arise independently, they arose from a common ancestor. Common
  ancestry explains excess similarity (other explanations require
  similar structures to arise independently); thus excess similarity
  implies common ancestry.
However, homologous sequences do not always share significant sequence
  similarity; there are thousands of homologous protein alignments that
  are not significant, but are clearly homologous based on statistically
  significant structural similarity or strong sequence similarity to an
  intermediate sequence. Thus, when a similarity search finds a
  statistically significant match, we can confidently infer that the two
  sequences are homologous; but if no statistically significant match is
  found in a database, we cannot be certain that no homologs are
  present.
Pearson, 2013

Members of a protein family are descendants of a common ancestor and are hence homologous. However, in the course of evolution they would have acquired new domains or reshuffled their domains such that their sequences are no longer similar. Proteins that have full length sequence similarity are called homeomorphic (Wu et al., 2004). Therefore, members of a protein family may be homologous but not homeomorphic. However, homeomorphic proteins can evolve independently and therefore may not be considered homologous.
Identifying homologous proteins is, therefore, not a simple task. Machine learning algorithms are used for better identification of homologous proteins. Some of these algorithms are mentioned in the linked papers.
In general, global similarity, rather than local similarity should be considered for identifying homeomorphs. See What is the difference between local and global sequence alignments?

This is the definition of homology that disturbed me. you say we must consider global similarity rather than local similarity. accordingly, we can't say these two proteins are homologs, because just about 60% of their lengths have significant (above 80%) similarity and the rest of their sequence is not similar. But actually, we see that they share 4 exactly similar domains, and have 3 nonsimilar domains. according to shared domains we can say those are homolog (at least in part of their sequence). I am really confused.

Wikipedia (Protein family): Proteins in a family descend from a common ancestor (see homology) and typically have similar three-dimensional structures, functions, and significant sequence similarity. The most important of these is sequence similarity (usually amino acid sequence) since it is the strictest indicator of homology and therefore the clearest indicator of common ancestry. Proteins that do not share a common ancestor are very unlikely to show statistically significant sequence similarity.

Could you please lead me to some good papers that give me a deeper understanding of the definition and concept of homology? As I previously said, I am really confused about this.

I have updated the answer @MySky


text:
Downloading specific yeast genes in an automated manner?
I have 6 genes of Candida albicans yeast namely orf19.723, orf19.5908, orf19.610, orf19.2119, orf19.4998 and orf19.4056. And I have found the corresponding ortholog genes from Broad Institute website of other 16 species of yeast. So I have all gene names. Now how would I specifically download these genes and from where can I do this, preferably in an automated manner?
Also is there any standard naming convention? Because the ORF names given have other names too like BCR1, EFG1 and NDT80.
The list of gene names I have :
The orthologs of C. Albicans with S. cerevisiae
orf19.2119  YHR124W
orf19.4998  YBR033W YKL034W
orf19.5908  YBR083W
orf19.610   YMR016C YKL043W
orf19.723   NONE
orf19.4056  YMR136W

The orthologs of C. Albicans with S. paradoxus
orf19.2119  spar33-g1.1
orf19.4998  spar197-g23.1   spar324-g3.1
orf19.5908  spar200-g4.1
orf19.610   spar184-g1.1    spar324-g10.1
orf19.723   NONE
orf19.4056  spar165-g2.1

The orthologs of C. Albicans with S. mikatae
orf19.2119  NONE
orf19.4998  smik146-g12.1   smik109-g17.1
orf19.5908  smik83-g2.1
orf19.610   smik571-g2.1    smik109-g10.1
orf19.723   NONE
orf19.4056  smik1535-g1.1

The orthologs of C. Albicans with S. bayanus
orf19.2119  sbayc514-g9.1
orf19.4998  sbayc611-g22.1  sbayc652-g20.1
orf19.5908  sbayc678-g131.1
orf19.610   sbayc638-g23.1  sbayc652-g27.1
orf19.723   NONE
orf19.4056  sbayc657-g41.1

The orthologs of C. Albicans with S. castellii
orf19.2119  Scas697.24
orf19.4998  Scas625.4
orf19.5908  Scas718.27  Scas635.12
orf19.610   Scas106.1   Scas709.52  Scas625.8
orf19.723   NONE
orf19.4056  Scas680.22d

The orthologs of C. Albicans with C. glabrata
orf19.2119  CAGL0L13090g
orf19.4998  CAGL0L01947g
orf19.5908  CAGL0M01716g    CAGL0F04081g
orf19.610   CAGL0M07634g    CAGL0L01771g
orf19.723   NONE
orf19.4056  CAGL0I00902g    CAGL0L06776g

The orthologs of C. Albicans with S. kluyveri
orf19.2119  SAKL0E11330g
orf19.4998  SAKL0A09812g
orf19.5908  SAKL0B06578g
orf19.610   SAKL0D13442g
orf19.723   SAKL0A03476g
orf19.4056  SAKL0E04862g

The orthologs of C. Albicans with K. lactis
orf19.2119  KLLA0F24420g
orf19.4998  KLLA0F25674g
orf19.5908  KLLA0E12507g
orf19.610   KLLA0F04840g
orf19.723   NONE
orf19.4056  KLLA0F17116g

The orthologs of C. Albicans with A. gossypii
orf19.2119  AGR347W
orf19.4998  AFR275W
orf19.5908  AER177W
orf19.610   ABR055C
orf19.723   NONE
orf19.4056  ADR249W

The orthologs of C. Albicans with K. waltii
orf19.2119  Kwal33.14699
orf19.4998  Kwal26.8099
orf19.5908  Kwal27.12423
orf19.610   Kwal26.8176
orf19.723   NONE
orf19.4056  Kwal47.17849

The orthologs of C. Albicans with C. tropicalis
orf19.2119  CTRG01097.3
orf19.4998  CTRG03636.3
orf19.5908  CTRG02294.3
orf19.610   NONE
orf19.723   CTRG00608.3
orf19.4056  CTRG04523.3

The orthologs of C. Albicans with L. elongosporus
orf19.2119  LELG01178
orf19.4998  NONE
orf19.5908  LELG02666
orf19.610   LELG05390
orf19.723   LELG03123
orf19.4056  LELG01761

The orthologs of C. Albicans with C. parapsilosis
orf19.2119  CPAG04608
orf19.4998  NONE
orf19.5908  CPAG01691
orf19.610   CPAG00178
orf19.723   CPAG00564
orf19.4056  CPAG05034

The orthologs of C. Albicans with D. hansenii
orf19.2119  DEHA2A07282g
orf19.4998  NONE
orf19.5908  DEHA2G13794g
orf19.610   DEHA2E10978g
orf19.723   DEHA2E05984g
orf19.4056  DEHA2E07172g    DEHA2F25916g

The orthologs of C. Albicans with C. guilliermondii
orf19.2119  PGUG02096.1
orf19.4998  NONE
orf19.5908  PGUG04378.1
orf19.610   PGUG03651.1
orf19.723   PGUG05571.1
orf19.4056  PGUG05533.1

The orthologs of C. Albicans with C. lusitaniae
orf19.2119  CLUG00404
orf19.4998  NONE
orf19.5908  CLUG04694
orf19.610   CLUG02047
orf19.723   CLUG00627
orf19.4056  CLUG05535

You could check out biopython if you are comfortable with Python programming

What OS would you do this on? Do you have access to UNIX tools? Also, please show us the rest of the gene names. What identifiers do you have? The answer will depend on what database the identifiers point to.

@terdon : I have unix tools (debian is the os). OK I will list the genes.

It would be quite easy if you have Refseq/ENSEMBL ids for those genes.

@terdon : I have updated the question.

These sequences do not have any standard i.d. The information in Saccharomyces Genome Database is also obsolete (2005) and does not have these identifiers.
These sequences can be found here (in the same site).
Each species has a short name:

ORGANISM        Short Name
S.cerevesiae    Scer
S. bayanus      Sbay
S. paradoxus    Spar
A. gossypii     Agos

.... and so on.
First letter of genus name in uppercase + first 3 letters of species name in lowercase.
The fasta file (for all ORFs) is:
 www.broadinstitute.org/regev/orthogroups/nt/<Shortname>.fasta
From there you can use grep to retrieve the sequence.
So, if you have saved shortnames and gene names two separate files you can do something like this:
for shortname in `cat shortname.txt`; do wget -O tmp.fa "http://www.broadinstitute.org/regev/orthogroups/nt/"$shortname.fasta; grep -A 1 -f ids.txt tmp.fa >> $shortname"_Select.fa"; done

@dexterdev The searching code can be made better and faster depending on what you really want as output.

Do you know what is the difference between http://www.broadinstitute.org/regev/orthogroups/nt/Scer.fasta and http://www.broadinstitute.org/regev/orthogroups/aa/Scer.fasta

@dexterdev The first is Nucleotide sequence and second is protein sequence. I gave the first link because you said you wanted nucleotide.

Sorry for the dumb question. I did looked at it , but did'nt noticed that. Sorry.

OK, the first step must be to map all these IDs to the same database. Try using http://uniprot.org if you want protein sequences else, look for each of them and find the corresponding Refseq ID. Since you have IDs from multiple databases, you might need to google them individually. If you know the ID type of each identifier you have, you can use a tool like DAVID's gene name converter to automate it.
Once you have a list of IDs from the same database, save them in a file (one ID per line). Then, for UniProt accessions, you can get the FASTA protein sequence by running:
while read name; do wget -O - http://uniprot.org/$name.fasta; done < names.txt

For RefSeq IDs, you can use the batch retrieval tool of Entrez.

Helpful answer. One thing , I am not working on protein sequences, but just nucleotide sequences.

When I googled these ids I couldn't find any match in a database. I checked SGD but their repository (from MIT) is obsolete (2005). Even then the orf fasta file (S.paradoxus) did not have an identifier like spar* or SPAR*. Example; first fasta header: ORFN:24882 YPRWsigma4, Contig c301 66351-67256. These are not even from complete assembly; it says contig.


text:
General time reversible model of evolution and Felsenstein model
I would like to get suggestions for the books related to General time reversible model of evolution and Felsenstein model etc. Specifically the mathematical treatment of these topics and concepts related to general balance and detailed balance etc. Can someone point out any books, links etc related to these.

I never heard of these terms. To satisfy my curiosity and assuming that you have some reference, can you please provide a link to the definitions of these things (or to the original articles)? Time reversible model of evolution kinda sound like coalescent theory. Are you sure those are not the same thing? There is a very good book by John Wakely called Introduction to Coalescent Theory.

You can find some information, with references to the original papers, on this Wikpedia page: https://en.wikipedia.org/wiki/Models_of_DNA_evolution#GTR:Generalised_time-reversible.28Tavar.C3.A9_1986.29.5B9.5D (I won't try to offer a summary, because it's not by field.)

The classic answer would be Joe Felsenstein's Inferring Phylogenies. It has substantial technical discussion of GTR and Felsenstein models, among others.
However, it does not have any index entries for "general balance" or "detailed balance". I was not familiar with these terms, so I googled them and they do not appear to be common terms in the phylogenetics field.
These terms do pop up in the MCMC literature a bit regarding transition probabilities, so it seems likely that it is somewhat related in terms of underlying math. However, I think that you are more likely to find phylogeneticists talking about "stationary" or "equilibrium" models rather than in terms of "balance". Possibly a difference in terminology between fields.
It might be helpful to know more about what you mean by these terms and why you are interested in them, in the form of links or otherwise.

I was curious to read about these when I was doing course work. Thanks for the response. Now I have moved into a different field. But I will go through it when I find free time.

Of course- I have started answering older unanswered questions because I think it's useful for future users at least. It is understandable you might have moved on, this is from 5 years ago after all!


text:
How can I compare the STRIDE and DSSP output files of a particular pdb file?
I have the pdb file of H-ras protein 5P21.pdb. I am supposed to compare the output of DSSP and STRIDE files after feeding this pdb file to respective servers. My question is how to make a quick comparison between these two results?

Here a solution that does not require you to upload the files to the servers: You can graphically visualize DSSP and Stride at the Sequence Page at RCSB PDB:
http://www.rcsb.org/pdb/explore/remediatedSequence.do?structureId=5P21&bionumber=1
"add annotation" -> Stride and look at the graphical comparison between DSSP and Stride.


text:
How to estimate the DNA density in human sperm head?
I have got an estimate of sperm head volume from internet.Like consider it as a disk of order 4-5µm. Now I wanted to find the DNA density in the sperm head. How to find that?

I don't understand what the value 4-5 microns refers to. If it is supposed to be a volume it should have units of volume.

figure out if 4-5 um refers to the diameter or radius, then calculate the volume of the sperm head, then figure out the volume of a chromosome, assume it as cylindrical and then figure for 23 chromosomes how much space is filled hence you would know the density

@Bez I assume the aim is to get pg per um3 or something similar.

Find, or calculate, a value for the volume of the sperm head.
Find a value for the size of the human genome (haploid or diploid?)
Convert the genome size, which will probably in Giga basepairs, into mass (I suggest picograms).
Divide mass by volume to get a density, pg μm-3
Refinement - does the sperm nucleus take up all of the head volume? Do you need to factor this in?


text:
What is the fate of the typical tree?
Walking through the local established broadleaf forests dominated by oak and tulip poplar (Eastern U.S.), it is common to find patches of young tree saplings, say 10-20 oak or tulip poplar saplings growing in close proximity. The obvious restriction on living space means that probably at most one of these trees will make it to maturity. In fact, judging by the apparent lack of mid-aged trees of these types in the woods, it seems very possible that none of these trees will last much longer. I'm curious: at what point and how would these trees die? The answer might also help me take better care of trees I've planted in my yard.
I can easily speculate about some causes:

Competition for water/nutrients in the soil
Not enough sunlight
Animal predators
Pathogens

But these suggestions don't answer the how or the when. And it's not clear which accounts the biggest impact. Clearly, the above factors didn't prevent the trees from growing in the first place. And the first suggestion (competition for nutrients) puts a limit on their growth but doesn't say per se why a plant would die.

I think this is really too big to answer, since a lot depends on the kind of tree, the climate, ecosystem, and more.  E.g. in my local (Sierra Nevada) forests, lots of small conifers sprout where there's open space and enough (but not too much) water.  As they grow, the weaker get crowded and die.  The dead trees may be fuel for a fire, or cut for firewood by a human like me.  The survivors may grow for centuries, unless killed by fire or toppled by winds.

@jamesqf We could narrow question down by considering my own locality: broadleaf forests in the Eastern U.S. and more specifically "peak" trees growing in already established forest. Here, oak and tulip poplar seem to be the main ones; I seem to find many mature trees and many very small saplings, but virtually nothing in between. You're suggesting competition for space as the main limiting factor?

In the future, please [edit] that narrowing into your question — comments are both ephemeral and often overlooked so they should not be used to convey information essential to understanding the question. ——— Please also consider taking the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

This is a great question.
Without going into too much detail, there is a series of studies done in northeastern US temperate forests (specifically at Great Mountain Forest in Connecticut, USA) on the growth, survival, and dispersal of canopy trees. In this particular community, light appears to be the primary limiting factor. Seedlings and saplings in low-light environments (i.e. stuck under the canopies of mature trees) grow slowly and have poor carbon balance, which makes them susceptible to mortality (probably from pathogens, although the proximal cause of death of seedlings and saplings is rarely known). Early successional tree species (in GMF, white ash/red maple/red and white oak) grow especially slowly, and hence are more likely to die, in low-light conditions; late successional (hemlock and beech) grow slowly even in high light, but are tolerant of slow growth, so are likely to survive until the adult tree above them dies and falls down.
The exact answer to "at what point do these trees die" is a little tricky, but here's a figure from Kobe et al. showing estimated survival probability for different species as a function of light availability (the assumption is of independent mortality probabilities, given light availability, at each time step, so there is no particular stage at which individuals die in the model).

Kobe, Richard K., Stephen W. Pacala, John A. Silander Jr, and Charles D. Canham. “Juvenile Tree Survivorship as a Component of Shade Tolerance.” Ecological Applications 5, no. 2 (1995): 517–532.
Pacala, Stephen W., Charles D. Canham, John Saponara, John A. Silander Jr, Richard K. Kobe, and Eric Ribbens. “Forest Models Defined by Field Measurements: Estimation, Error Analysis and Dynamics.” Ecological Monographs 66, no. 1 (1996): 1–43.
Pacala, Stephen W., Charles D. Canham, and John A. Silander Jr. “Forest Models Defined by Field Measurements: I. The Design of a Northeastern Forest Simulator.” Canadian Journal of Forest Research 23, no. 10 (1993): 1980–1988.
Pacala, Stephen W., Charles D. Canham, John A. Silander Jr, and Richard K. Kobe. “Sapling Growth as a Function of Resources in a North Temperate Forest.” Canadian Journal of Forest Research 24, no. 11 (1994): 2172–2183.

Interesting; I have seen sugar maple seedlings dominate the low light understory in a mature woods. And red maples die after a few years in a modest light woods; Although both are maples they have different light requirements as shown in the graph.

also see https://www.jstor.org/stable/3450004 (red oak/red maple/tulip tree experiments)


text:
Indian Spider Identification
Today I saw this curious colorful spider on its web near a sapota tree in my garden.
I have never seen any spider like this,its around 2cm or a little less.
The most curious part is this part of its exoskeleton which looks like when a moth rests.Like a cape.

here's the underside and the yellow patterned legs.

But the spider was bothered by my presence and was trying to crawl away,and I took this angled shot:

I live in South India.
So what is this spider ?
Is there any advantage of the wing like part?
Links to websites with details of the spider are also appreciated.

That’s maybe an oriental spiny orbweaver (Gasteracantha geminata), according to its appearance and location. You can find many more observations of such spiders on iNaturalist: https://www.inaturalist.org/taxa/207992-Gasteracantha-geminata?locale=en-GB
However, I don’t know what advantage there is to the “spines”. They are not the only species. There’s a whole genus of them with at least 70 known species, according to Wikipedia: https://en.m.wikipedia.org/wiki/Spiny_orb-weaver