text:
Can someone help me identify this Ficus plant?
I have a bonsai with me which I grew from a seedling germinated in my backyard. It's been with me for the last 5-6 years. I definitely know its a Ficus, but I am not able to identify which species it belongs to. I have provided pictures of the specimen below:

I need to know if its F.virens (white fig) or F.ingens (Red leaf ficus). This specimen is from Kerala, INDIA.

There are up to 900 different species within the Ficus genus... you might want to add in some more detail e.g. location, measurements, the shape of different sections of the plants (which can be done by taking more photos of different parts through different perspectives). Also, keep in mind that, without genetic testing, it may be difficult for most people to identify which exact species this is with the absolute certainty.

This is a Ficus Bonsai, size and shape wont be natural. However its from Kerala India


text:
Is chloride necessary for animals?
Of the twelve well-known atomic constituents of our body eleven elements have specific properties obviously relevant to their rôle, making them indispensable. Oxygen (electronegativity and valence), carbon and hydrogen (both elements have virtually unique properties), nitrogen (amino group), calcium (calcium(II) is necessary for bones in vertebrates), phosphorus (use of phosphate in nucleotides and ATP), sulfur (–S–S– bridges), sodium (Na+ is a small cation), potassium (K+ is somewhat larger, together with its companion and presumed substitute Rb+), iron (used in hemoglobin because of properties of a transition metal), magnesium (Mg2+ takes part in the ATP cycle, if not anything else).
What about chlorine? A search resulted in

Chloride is involved in the exchange of oxygen and carbon dioxide in the red cells.
In this, chloride passes into the plasma (chloride shift) and bicarbonate into the cells.

(https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/chloride), certain use by muscle cells and also some mention of ligand-gated chloride ion channels in neurons. Chloride in stomach secretion may be dismissed because is used as a generic acid (that is, to complement H+), not for its own special properties. And no mention of biological chlorine compounds other than ionic (such as, having a C–Cl bound) can be quickly found.
Which cells absolutely need specifically Cl− to function? Is the anion mandatory for animals to live?

I am not sure I am clear  what you are asking, but mutations in the chloride channel are known to cause cystic fibrosis (a major breakthrough in the understanding of this disease)

@user338907 relevant, but again: so named “chloride channels” are not necessarily selective. Whereas a sodium channel hardly can pump anything but Na⁺ (the rare Li⁺, perhaps?), anion channels conduct mostly Cl⁻ because of abundance, but generally who-knows-what.

OK. As regards your second-last sentence, there is Gribble, and chloramphenicol comes to mind. (Extending things to the halogens, there is  fluroacetate)

My answer may be a little basic, but I think it is comprehensive:
Many elements are special; for instance, many metal ions such as iron or cobalt are required as cofactors or in catalytic sites due to their chemistry. Oxygen is highly electronegative, that also grants it some of its functions. But... without delving too much into things... chloride is the most basic constituent of saline, without which it would not be saline. Here are 3 very, very important and yet

It works well with alkali and alkaline earth metals, hydrogen, and many compounds... it's a natural pairing!
You cannot separate positive and negative charges in a solution at a macroscopic level. It's not a feasible thing to avoid harboring chlorine atoms as part of biochemistry.
It accounts for a large portion of extracellular fluid tonicity.
etc...

Thus, most inter- and extra-cellular fluid is relatively chloride ion rich, across the entire bush of life. To my knowledge there is no life, tissue or cell on this planet that does not contain chloride ions as part of its makeup by necessity. It is simply heavily constrained in evolution as a basic component. It's just not practical to obtain K+ or Na+ or Ca2+ ions without Cl-, it is so common in nature.
If you want specific examples, you can always mention its indispensable roles in neuron firing (transmission of axon potentials) and general cellular homeostasis, which is dependent on electrochemistry and osmolarity and stuff like that which is heavily influenced and dependent on the presence of a regulated concentration of solvated Cl-.

Ī̲  didn’t discuss abundance of elements on Earth (or elsewhere in the known universe), nor hinted that natural abundance of nutrients has something to do with the question. Please, keep your stuff to the topic.

Neither did I, as I'm sure you will agree. I see 3 posed questions, perhaps I can restate the answers more tersely. Is chloride necessary for animals? Which cells absolutely need specifically Cl- to function? Is it mandatory? The answers are yes, all, and yes. All animals can and do suffer chloride deficiency. I think the answer can also be extended to most microbes. This does not rule out the possibility that one could engineer a synthetic life to use bromine or fluorine, but I presume you know why neither would be a good elemental substitute. They are very different physicochemical anions.

That Wikipedia article states that so named chloride channels may conduct many different ions. An empty-worded statement about necessity of Cl⁻ may not count to qualify an answer.

There are very many membrane channels that are partially or entirely non-selective, including anion and cation channels. I don't really understand how that is relevant, but I wish you luck on getting an answer that you are looking for! Though I would caution you against looking for answers at bio.SE where the lack of chlorine is a strained, imagined hypothetical. Along those lines, we can speculate and opine all day about silicon-based lifeforms. But that's all fantasy and science fiction until we see a proof of concept. Best of luck!

source: Stack Exchange

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

sort: votes


text:
Is the enteric nervous system found only in vertebrates?
The enteric nervous system is distinguished by being autonomous from the central nervous system and capable of independent action, such as the peristaltic reflex. For this reason the the intestines can be removed from the body of a vertebrate creature and they will still function.
Is this type of nervous system unique to vertebrates, or is it found in invertebrates and insects as well?

A Google search of "enteric nervous systems of invertebrates" yields rich results, such as How To Innervate A Simple Gut: Familiar Themes And Unique Aspects In The Formation Of The Insect Enteric Nervous System. Searching before posting is always a good practice.

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


text:
Thin layers or laminae that make up a single summer band in tree ring, what are they?
I took the photograph below of some tree rings. Each division on the ruler is 1 millimeter:

Each tree ring (the areas between the pizza crusts) represents one seasons worth of growth. The growing season is from about March to October. My question is about the small lamellae or dark bands that make up each ring. I have placed a green box around one set of these bands. What are they?
These small bands all seem to be the same width, so tree rings that are wider (good years) have more of them, and rings that are narrow (drought years) have fewer.
What are these bands?

These are the annual rings that are usually found in areas /regions where environmental conditions are not uniform throughout the year.
These are formed due to the activities of cambium (bundle of vascular tissue in plants showing secondary growth).
In spring it is lighter in color and has lower density whereas the autumn wood has high density and dark in color with higher density.
Spring wood - High activity, produce large no. of cavities
Autumn wood - Low activity, less lumens and cavities.

Read the question more carefully.

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


text:
Why do basil leaves turn black?
I notice that when I buy basil it is fresh and green in the store, but when I take it home it wilts and turns black within 24 hours.
Why does it do this?

That seems pretty fast to me. How is it stored in the store and how do you store it at home? Specifically, is it frozen at any point or bashed around during transport at all?


text:
Strategy for tree and shrub identification
I often find it difficult to identify trees and shrubs even though I have many handbooks and manuals on trees and shrubs in my area (New England). The typical problem is that the species is not in the handbook, or that it is very similar to many other species. For example, hawthorns have many different species which are very similar to each other and most books do not exhaustively list the different hawthorns and their distinguishing characteristics, instead just listing one or two of them.
Web sites are even more fragmented than books and are usually a lot less detailed than the books so even if I search around, the results are often useless.
Am I going about this wrong? What improvements can I make to my strategy for identify trees and shrubs?

Species ID books with pictures, or photos, will generally never be comprehensive enough to include all species, although with some there will be additional information it the text that will give details about other related species, varieties, hybrids or cultivars.
Importantly look for ID books that include an ID key, generally at the start, and learn how to use it. They are usually accompanied with a good explanation of how it works.
The key takes the form of

Does it have this...?
If it does go to [3]
If it doesn't go to [7]

And so on, making successive distinctions until you end up with the species.
They can take some getting the hang of, and you need to know the botanical terms that they refer to.
Also importantly, if you don't already have and use one, you must have a decent hand lense, or magnifying loupe, that you take with you everywhere. Often the deciding features can only be properly be assessed when looking close up, and you need to get to know what the species you are familiar with look like under the lense.
An experienced ecologist friend, an expert in flora and fungi, has a couple of books that have no images in at all, it is just the species ID key, that he takes with him when he is surveying. Granted he already knows his species very well, but you can't remember everything all the time and so you need a book that can tell you the final distinguishing features, even if it is text.
But again a hand lense is a good place to start. My favourite is an Eschenbach 10/40 Pocket hand-held magnifier from Germany http://www.eschenbach.com/cdd40611-ceda-4188-a5c3-882565859296/products-hand-held-magnifiers-pocket-detail.htm
Someone gave this site http://dendro.cnre.vt.edu/dendrology/syllabus/key/key1.cfm?state=&zone= as a good resource for trees in the US


text:
Do all fungi dislike acidic environments?
I know that some fungi prefer mildly alkaline environments and dislike acidic environments. Is that true of all fungi, or do some fungi prefer acidic environments? If so, are such acidic fungi rare exceptions or is it common for there to be acid-loving fungi?

Fungi that grow in acidic media are well known, here just one reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC518635/pdf/jbacter00651-0183.pdf
About their spread, they are less common in mild environments (like you hands, or your garden soil) but of course in acidic environments, they will be predominant.


text:
Why are tree rings the same if rainfall is different from place to place?
I have looked at data from rain gauges and usually the rainfall levels are very different from place to even. Even in adjoining towns or townships the rainfall can exhibit much different patterns.
Nevertheless, all the trees in an area tend to show the same ring patterns. Why is this?

The rings are not only affected by time but also by location. So no, the patterns are not always the same depending where you are. Climate do affect the rings.
Typically a major factor affecting ring patterns is the seasonality. Depending on the number of rainy season, you might observe one or two rings per year.
If interested, here is an introduction to dendrochronology (from the University of Victoria).

I have a whole textbook on dendrochronology. It does not discuss this issue.

I must say I lack much citation and answer by what I remembered from my Bachelor degree. Citing wikipedia: , the variation of the tree-ring growths provides not only a match by year, it can also match location because the climate across a continent is not consistent. But please, wait for other users input before accepting the answer of someone who knows very little about dendrochronology.

What is your textbook by the way?

Fundamentals of Tree-Ring Research by James H. Speer


text:
Why doesn't the Tsetse fly wipe out all animal life in its range?
The Tsetse fly, which is native to interior West Africa, carries the protozoan that causes sleeping sickness, a disease which was apparently invariably fatal before the advent of modern medications. Since there is no way to prevent being bitten by this insect, why did it not kill off all animal life in its range?

Firstly, as Remi.b points out, although Trypanosoma brucei infection is invariably fatal in humans, the same is not true for all host species. Domestic animals, particularly cattle, are an important reservoir of T. brucei rhodesiense and can also be infected with T. brucei gambiense (although it's not clear how important a reservoir they are for gambiense).
Secondly, just because all hosts in an area get bitten by tsetse does not mean they all become infected with trypanosomes. Even in endemic areas most vectors never become infectious. The transmission cycle for trypanosomes and other insect-borne pathogens requires an incubation period in the insect vector which is often longer than the median lifespan of the insect, so even if all insects get infected early in life, most will never survive the incubation period to become infectious. The later the average time of first infection gets, the higher the fraction of hosts that will have the opportunity to reproduce before dying.
Finally, it isn't entirely accurate to say "there is no way to prevent being bitten"; it is possible to reduce exposure to insects behaviourally. For example, in most endemic areas local residents will know which areas are most heavily infested and should be avoided.

Good answer +1. I think I've upvoted all of your answers so far! It is good to have you on Biology.SE.

Thank you very much! I only discovered the site recently but it seems to be a great community.

Trypanosoma, the parasitic protozoans that uses the TseTse fly as vector to reach its definitive host, a mammal. In wild mammals, Trypanosoma brucei has no noticeable impact (Chatterjee, 2009). I don't know about Trypanosoma cruzi.
Parasite who recently transferred from one host to another are often the most virulent. In the particular case of a parasite that transfer from an animal species to humans is called zoonosis. Ebola virus disease, AIDS, salmonellosis and influenza are all examples of zoonosis. I know little about Trypanosoma evolution but this lab probably have a number of publication that will interest you


text:
Which animals can see (or feel) the Moon’s infrared radiation?
The luminosity (bolometric) of the Moon in infrared is several times greater that its luminosity in visible light. Moreover, it may be rather possible for the Moon to be obscured by some fog or haze which lets only the infrared radiation through. It is known that some snakes have “pit organs”, but the decent Moon’s infrared flux can, probably, be detected by something more crude. Can any other animal (than snakes) take benefit from its sensitivity to medium-wave infrared to see (feel) the Moon?

It is notoriously hard to find reliable information on the Moon’s infrared flux in Internet, although its density at Earth’s surface should be several µW/cm² (or tens mW/m²). My estimate is about 30 to 40 milliwatts per square metre under favorable conditions, which is probably not high enough to be detected with every pit organ (crotaline snakes are claimed to have threshold at about 107 mW/m²). Research on Agkistrodon contortrix (see graphs) states that 60 mW/m² and as little as 15 mW/m² (albeit not in infrared) produce a nerve response in receptors. On the other hand, pit organs are optimized for such localized and agile sources as small animals; some other sensory system might be more appropriate for nearly stationary sources producing more incident energy (heat).

Welcome. You seem to assume snakes can sense the moon by IR, but can you provide evidence that that is so?

@AliceD: probably not with every pit organ, but Ī̲ deem 90 mW/m² high enough to be felt by anybody claiming an excellent sensitivity. Some research on Agkistrodon contortrix (see https://journals.physiology.org/doi/full/10.1152/ajpregu.00024.2002#_i2 , graphs) states that 60 mW/m² and less (albeit not in infrared) produce a nerve response in receptors. Those having threshold at 110 mW/m² (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080012/ ) are probably not among most sensitive.

Please include that information in the question proper - it makes the post a lot more substantial. Thanks! Interesting question.

@AliceD: tried my best. Sorry for delay.

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


text:
What is the relationship between a "main" strain genome and its variant genome in archaea?
I am going to analyze DNA sequencing data in order to try to extrapolate some information about the survival strategy of Pyrococcus Furiosus to gamma irradiation, as maybe you already know from all the previous questions that I published .
In particular, among my previous posts there was the one titled as What does genetically tractable strain mean? in which I asked the meaning of genetically tractable strain because I was reading the article about Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome in which they compare the Pyrococcus Furiosus reference genome sequence (the one that was firstly sequenced in the year 2000) with the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption of the pyrF gene (I have clarified the meaning of this process here What is targeted gene disruption?).
Now, what I still can't really understand is why do they compare the "modified" genome sequence of the variant with the reference genome sequence ? I would have aligned the "modified" genome sequence of the variant with its sequence before the targeted gene disruption. Then, of course, I would have all the properties of the variant and not of the "main" strain ( the reference Pyrococcus Furiosus genome).
Instead, in the article they compare first the reference genome sequence with the one of its manipulated variant and then they also compare the sequences of some particular genes, obtaining some properties as if they were discussing of the same genome. For example:

the protein products of 102 of the total 2,134 genes in the NCBI reference sequence are disrupted in COM1 at the translational level through nonsynonymous mutations. These result in amino acid changes, insertions and deletions introducing premature stop codons, and frameshifts producing longer or shorter products with alternate coding sequences. These were subdivided into 36 major changes (Table 4) and 66 minor changes (see Table S1 in the supplemental material) based on the Needleman-Wunsch global alignment identity compared with the protein sequences in the NCBI reference sequence.

This and many other extracts show that they compare the reference and the variant as if they were, respectively, the "control" and the sample that has been treated, ignoring the fact that they were actually distinct genomes.
In the post What does genetically tractable strain mean?, the answer to the question "why do they do this comparison?" was essentially that results obtained by manipulation of the tractable strain can inform your understanding of the reference form. But why are we allowed to treat them as if they were the same genome? And so, can we consider the properties refered to the COM1 valid also for the reference Pyrococcus Furiosus and for all its existing variants ? For instance, here they say:

a number of genes involved in DNA repair, including an uncharacterized RadA domain protein (PF0872), DNA repair helicase Rad3 (PF0933), 5'-to-3' exonuclease NurA (PF1168 [23]), and DNA repair helicase (PF1902), could potentially be inactive in COM1 as they fall into the minor protein-level differences category (see Table S1 in the supplemental material). However, COM1, Parent, and DSMZ showed no significant differences in their ability to recover from exposure to UV or gamma irradiation under conditions previously reported for P. furiosus (14).

Can I say that this could be valid also for the reference Pyrococcus Furiosus, in the sense that if the mentioned set of DNA repair genes are inactive, it will show no significant differences in its ability to recover from exposure to UV or gamma irradiation ?
My conclusion, months ago, was that a variant can be considered as if it was the main strain since the definition that I read in Wikipedia is:

In microbiology and virology, the term variant or "genetic variant" is used to describe a subtype of a microorganism that is genetically distinct from a main strain, but not sufficiently different to be termed a distinct strain.

Now this conclusion does not satisfy me anymore and I would like to really understand the reason of this comparison and how to interpret the relationships between genomes. Can we consider the main strain and its variant simply the same since the last one is not "sufficiently different to be termed a distinct strain"? Are all the phenotypic properties observed for the variant COM1 (like for example the fact that although a set of DNA repair genes are inactive, the ability to recover from exposure to UV or gamma irradiation, under certain conditions, is still the same) valid also for the "main" strain (that is the NCBI reference genome) ?
Thank you in advance.

... I was reading the article about Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome in which they compare the Pyrococcus Furiosus reference genome sequence ... with the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption.

Instead, in the article they compare first the reference genome sequence with the one of its manipulated variant and then they also compare the sequences of some particular genes, obtaining some properties as if they were discussing of the same genome.

I think this is from where your confusion originates. From my reading, the paper you link is a comparative genomics paper, and the authors do not perform any genetic manipulations of the tractable COM1 strain. All mentions of "disrupted" genes are referring to the effects of naturally occurring insertion sequences or nonsynonymous mutations. "Natural", here, meaning not purposefully disrupted. Based on the comparison with the Parent and DSMZ strains, it seems like COM1 accumulated its various disruptions and rearrangements while it was propagated as a wild-type lab strain.
For more on how the COM1 strain was "discovered", I suggest reading the original paper in which it was described.

Thank you for your answer @acvill but I do not understand many things: 1. Where is the term "natural" that you mention ? 2. So coming to the main question: why do they do this comparison ? Is it just to describe the difference between the two genomes ?

@Manuela (1) "natural" is in reference to my use of "naturally" in the previous sentence. I wanted to avoid confusion concerning the origin of the COM1 mutations. I'll italicize for emphasis. (2) Yes, they are describing the differences between the COM1 genome and the reference genome, as well as structural variants in the Parent and DSMZ genomes.

Ok @acvill in fact it makes sense, thank you. But I am still confused because in the part of the article that I posted, when they align the COM1 with the reference they say something like "these proteins in COM1 could be inactive because the protein sequences are different with respect to the protein sequences of the reference". Why do they expected to be the same ?

Let's continue this discussion in chat.

Finally, I do not really understand the utility of what they do (both the original paper and the latest one).

@acvill Moreover, when I said "the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption." I wanted to say that the COM1 strain was obtained by targeted gene disruption of the pyrF locus (PF1114) using a plasmid designed for double-crossover recombination (37) which are words written in the article. I did not want to say that they purposefully "disrupted" genes...

Then I found this definition in Springer about targeted gene disruption that tells that it is Experimental replacement of an endogenous gene by a mutated (non‐functional) version within the otherwise unchanged genome is called targeted gene disruption. So I said that they did genetic manipulations . But honestly now I do not understand if this was done by the authors of the original paper that you linked or it occured naturally. The original paper is too much complificated for me :/


text:
What are the causes of gene amplification in archaea?
I was studying this article about Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome in order to try to extrapolate some features that could explain, at least in part, the survival strategy of Pyrococcus Furiosus exposed to gamma irradiation.
In this article, they compare the Pyrococcus Furiosus reference genome with the genome of a variant designated COM1, which is a genetically tractable strain.
In the Introduction they say:

The COM1 strain was obtained by targeted gene disruption of the pyrF locus (PF1114) using a plasmid designed for double-crossover recombination (37).

I would like to see if, after this targeted gene disruption, there is some amplification of some genes that I suspect they are involved in the servival strategy of these extremophiles to gamma irradiation, because then in the article they say that a number of genes involved in DNA repair could potentially be inactive in COM1 (as they fall into the minor protein-level differences category) but nevertheless it shows no significant changes in its ability to recover from exposure to UV or gamma irradiation.
For this reason, I would like to see if maybe some other genes involved in genetic material protection are amplified in response to this targeted gene disruption (in the sense that there are more copies of a gene being present in the genome). In fact, since I saw from NIH that:

cancer cells sometimes make multiple copies of genes in response to erroneous signals from other cells or because of signals they're getting from the environment.

Could this be valid also for my situation? In the sense that now I am not considering cancer cells but Pyrococcus Furiosus cells and as signal from the environment I consider the targeted gene disruption ?
Thus, my question leads to: what are the causes of gene amplification in archaea ? In few words, I need to understand this last question in order to see if it makes sense to try to detect gene amplification with the DNA sequencing data that I have. Anyway, I gave you all the background I am working with because I hope that, in this way, you can understand better what I want to know.
Thank you in advance.

Re: "what are the causes of gene amplification in archaea ? " I suspect trying to answer that would make for a good research career! :) I'm not familiar with archaea, but I think the NIH "signals" statement above only means that pre-existing signal-based gene amplification systems are induced in those cases.  However, perhaps Pyr. does have mechanisms to detect loss-of-function in a gene and respond as you suggest. Sounds like an interesting research project!

Thank you very much for your opinion :) ok I do not really understand the meaning of pre-existing signal-based gene amplification systems but knowing that it is not a completely nonsense reasoning is already something very important!  I think that there are few people studying archaea and I do not know why... They are so interesting, as you say .

The best science often comes from reasoning that gets close to "nonsense", but not quite. You've got an interesting idea to pursue -- good luck!

Just to clarify, are you interested in gene amplification (more copies of a gene being present in the genome), or increased gene expression (more copies of a gene being transcribed into mRNA and/or translated into protein)? In a pure culture system (clonal lineage), I think it makes more sense to look into transcriptional regulation before looking for gene amplification, though gene amplification can be favored at times (some forms of acquired antibiotic resistance in bacteria, for example).

@MikeyC I am interested in the first one: gene amplification (more copies of a gene being present in the genome). I have already studied gene expression... not really in this exact context. I made statistical data analysis of quantity of mRNA produced from some particular genes when P. Furiosus cell coltures were exposed to gamma irradiation. Now the idea is just to check if the genes, that in that study increased the mRNA production after the irradiation, are amplified if you do targeted gene disruption .

I really would have analysed this in the same context in which I studied gene expression... so for example to see the genome of the irradiated cell cultures and the not irradiated (control) and check if there is amplification of some particular genes in the irradiated one. The problem is that I do not have those kind of data. I can not find them. I do not even know if someone has done such experiment.

I see. Definitely an interesting topic. I know that viral insertion is one cause of non-essential gene duplication. Maybe looking for viral genetic signatures could provide some relevant insights. I can also imagine how viral excision or insertion might be triggered by a stress response to radiation exposure.

Ok, thank you @MikeyC . So maybe do you mean that some viral insertion mechanisms could be analogous to the targeted gene disruption...?


text:
Biological modeling languages - some basic issues
I am trying to get used to with couple of modeling languages in biological context like SBML, BioPAX, Kappa and BEL. Some basic issues came up to my mind that are unclear to me even after a lot of related studies I read.

Are there any causal reasoning algorithms available for SBML? If yes please give me the reference.
Which "framework" supports modeling and mining (e.g. candidate mechanism identification / identification of upstream controllers) in Kappa?

Anyone has any idea about these?
Thanks in advance!


text:
What is the "anatomy" of transcriptional regulation in Archaea?
I want to know what are the DNA elements that are recognized by transcription factors in Archaea and so what is the "anatomy" of transcriptional regulation in this case.
I found in this paper by Alexandra M. Gehring et al. that the process of initiation of transcription in archaea is governed by TATA-binding protein (TBP), Archaeal transcription factor B (TFB), and Archaeal transcription factor E (TFE). These constitute the basal transcription factors and transcription initiation is regulated by DNA elements that are recognized by basal transcription factors that recruit the enzyme RNA Polymerase (RNAP) that will copy DNA into RNA. There  are  four  DNA  elements  currently  known  to  regulate  archaeal  transcription  initiation: the TATA-box located approximately 25 bp upstream of the site of transcription  initiation;  the TFB  recognition  element  (BRE) located immediately upstream of the TATA box; the initiator element (INR) located  within  the  initially  transcribed  region,  and  the promoter  proximal  element  (PPE) located  between  the  TATA  box and the site of transcription initiation.
This seems very similar to the eukaryotic system and, in fact, also the Wikipedia page tells that  the core machinery is more similar to eukaryotic transcription (with respect to bacteria).
Moreover, the first paper that I linked also tells that it is probable that some archaeon-specific factors await discovery for the elongation and termination steps of transcription.
Now, I started to search if Archaea have enhancers and silencers like the eukaryotic genes but I could not find anything. Since the core machinery is more similar to eukaryotic transcription, can I assume that there are enhancers and repressors and that the main pattern of DNA elements necessary for transcription and transcription regulation is that of eukaryotes? Maybe, the reason why I do not find the answer to my question in Google is that some archaeon-specific factors await discovery. Indeed, Archaea are, in general, often called the "blind spots" of natural diversity because of lack of knowledges about them.
Also if you have a look at the Promoter (genetics) Wikipedia page, there is a list of elements of promoter relative to Eukaryotes and Bacteria, but nothing about Archaea... So is it completely wrong to look at the eukaryotic elements and explanations of this page, for example, as (at least) probably valid also for Archaea ?
Thank you in advance.


text:
What is the meaning of NF-kB (transcription factor) "activity"?
This article discuss about the NF-kB activity and its mathematical modeling Understanding NF-κB signaling via mathematical modeling. The NF-kB is a transcription factor mainly involved in the regulation of inflammatory genes. However, I do not really understand this: what do we mean by NF-kB activity ? For instance, if we consider this graph (that is figure 1A in the paper that I linked):

by NF-kB activity on the vertical axis, do we mean the number of RNA molecules produced by the target gene regulated by the NF-kB over time ? Or it depends on the kind of experiment ? In the article it tells: this prediction was confirmed by using EMSA on wild-type cells. What does EMSA effectively measure ?
P.S. The idea that by activity I mean the number of RNA molecules produced comes from the fact that I read some thesis works about NF-kB activity in which Cignal Lenti Reporter System (QIAGEN) is used for the experiment and I read in  Reporter Gene Assays that a reporter gene assays are typically used to measure the regulatory ability of an unknown DNA-sequence. This is done by linking the unknown promoter sequence to an easily detectable reporter gene whose product can be easily detected and quantifiably measured. However I do not really understand how EMSA can experimentally give us information about NF-kB activity (maybe because I did not understand how it works).
I thank you in advance.

The word activity has at least two meanings in biochemistry. One is chemical activity as in the effective concentration of a chemical. This comes up a lot because biomolecules often behave non-ideally.
The other sense, relevant here, originates in the description of enzymes. As catalysts, enzymes accelerate the rates of chemical processes. Enzyme activity characterizes the rate of an enzyme catalyzed reaction, so these activities are quantities that include time dimensions (Cornish-Bowden, p. 81).
This leads to a definition of the activity of a transcription factor, a biomolecule that catalyzes the initiation of transcription. The activity of a transcription factor is its enhancement of transcription (which, since uncatalyzed transcription has an effective rate of 0, is the same thing as the observed rate of transcription).
Usually this is only indirectly measured, and usually the absolute activity (in, say, transcription initiations per cell per hour) isn't needed, only the relative activity. That's why activity is often illustrated on axes with normalized/absent units; the raw units are often arbitrary. So, yes: activities in this case could be literally measured by the number of mRNAs transcribed when NF-κB is activated. But anything proportional to that mRNA population is also suitable as a measure of activity.
From the reference in question:

NF-κB enters the nucleus, denoted by the suffix ‘n' (k1). This leads to synthesis of IκB mRNA transcript, denoted by the suffix ‘t' (tr2).

So, synthesis of the IκB transcript is the main response variable they're interested in tracking in term of NF-κB activity. But that's not the definition of activity, just a convenient measure of the promotion of transcription. NF-κB promotes many transcripts, not just IκB!
In 5, electrophoretic mobilility shift assays are referred as follows:

As time-course data, derived from electrophoretic mobility shift assays (EMSAs), indicated that the three IκB proteins had differential dynamic control, we set out to construct a mathematical model of NF-κB signaling to study the specific roles of each IκB isoform in regulating the temporal control of NF-κB (Hoffmann et al, 2002)

A biomolecule has a certain mobility in this experiment and the mobility shifts when the shape or charge distribution of the biomolecule changes. So here the raw signal is the migration distance of a given band (somewhat arbitrary as a measurement, but proportional to activity).
I have not yet checked the Hoffmann et al 2002 paper. But if we assume that, here, "EMSA" summarizes experiments 1) comparing nuclear and whole cell extracts (key for deciding that NF-κB is activated) and 2) using Western blotting for confirming protein bands, perhaps the "confirmed by EMSA" phrases are less opaque.

Thank you very much for your answer! I have one question: I like that you give a formal definition of activity of transcription factor as The activity of a transcription factor is, narrowly, its enhancement of transcription. However, can I find this definition in some literature material or is something that you can know only by reasoning about what a transcription factor does ? And second question: by "titrated" you mean bound to DNA sequence of target gene ?

I've added some explanation but will find references too

Wow, congratulations on your education ! So I wait for references, thanks.

My answer now has some references and I think should help with your direct concerns about activity. I took out the unnecessary language about titration, and explained it directly. I will improve the EMSA part.

Thanks now the answer is very helpfull ! So I would enjoy also the EMSA part.


text:
DNA Replication And Primer
Why does nature rely on RNA primer for the start of DNA Replication? Why not simply use DNA primer and make life simple !

Biochemically none of the DNA-dependent DNA polymerases involved in DNA replication have the ability to begin elongation without a 5' to 3' primer.
The only DNA Polymerase that can catalyze elongation without a 5' to 3' primer is Reverse Transcriptase, however Reverse Transcriptase is an RNA-dependent DNA polymerase, and that accounts for the difference.
And if your next question is, but why, the answer is that that is how the systems evolved. Also DNA Polymerases have a much higher rate of fidelity due to error checking than RNA Polymerases do, and as the RNA primers get removed anyway and replaced with DNA, an error here or there in the primer will not matter.
The RNA-DNA duplex is also less stable than the DNA to DNA duplex, so it makes it easier for FEN1 to remove an RNA Primer than it would a DNA primer, assuming that the mechanism of primer removal and replacement after the complementary leading and lagging strands have been synthesized remained in place.

Main reason is that DNA pol needs template while RNA pol does not. Hence DNA pol need initial primer (which is made by RNA pol or primase ). That is why there is RNA primer not DNA.

@Dexter Did you read my answer? "... none of... have the ability... without a 5' to 3' primer. Third paragraph addresses your 2nd point.

I am still unclear from your answer. You gave fact not reason. I think reason should be "need of template" as question was asked why RNA primer not DNA. And how is error correction is contributing to RNA primer not DNA ? I think, error correction is output not reason.

@Dexter The reason is that is how the system evolved. But as to make the answer little more than a comment, the reason DNA Polymerase needs any primer is the answer that addresses the first question, "Why does nature rely on RNA primer for the start of DNA Replication?" And the reason is that the DNA-directed DNA Polymerases involved in DNA replication do not have the ability to begin elongation without a 5' to 3' primer. That answers the first question.

@Dexter, I will concede I could have been clearer, but the basic thing I was getting at with the third paragraph is that DNA-directed RNA primers are sloppy replicators, but as the primer is removed and replaced, you can sustain errors in the primers without detriment to the organism. I would guess that the energetic cost of using RNA primers is less and it works faster than an equivalently abled DNA polymerase could in laying down a primer, which is why we have Primase as an RNA Polymerase and not a DNA Polymerase.

@Dexter. The final paragraph just states that RNA-DNA is less stable, so that probably makes it easier (less energy required) for the enzymes to remove the primer, which, if that is why it evolved this way, would be another reason that nature uses RNA instead of DNA for primers.

Asking why question in evolution make life difficult :P
I doubt sloppy replicator is good explanation. See explanation of this phenomenon in Biochemistry by Stryer. On other point on energetic, some calculations have been done here. Going by that logic, I don't think it will matter if it is DNA or RNA. Nonetheless all these points are valid in light of "Evolution" :P


text:
By What Mechanism Does Heat Cause Muscle Relaxation?
Heat is commonly used "loosen" muscles, but what exactly is happening to relax the muscle? It wouldn't make sense that increased blood flow alone would relax muscle.

Read this it was very helpful to me as a Reiki Practitioner who wants to know how the heat generated by my hands on therapy with my patients for Hospice brings such relaxation to them.
http://healthyliving.azcentral.com/effects-temperature-muscular-contraction-11504.html

Please add some more details to your answer. Your answer may become invalid if the link expires or gets broken.

There may not be one because it may not have any effect.
It appears to be a placebo effect. There is not a lot of clinical evidence heat does anything beneficial, in fact cold may actually be more effective. Evidence of an effect appears to be mostly anecdotal or unscientific "studies".


text:
What Effect Does Skin Redness Have On Underlying Tissue?
When someone applies a rubefacient ( something that increases blood flow to the skin, turning it red), what effect does this have on the underlying tissue? Is blood supply increased radially from where the rubefacient was applied and thereby increasing blood flow to underlying tissue (I'm thinking up to a few centimeters of muscle) or is blood supply essentially being stolen locally in order to bring it to the skin?

Rubefacients cause cutaneous vasodilation (hence the redness), but they are a very broad group of drugs, and have multiple modes of action. They have different effects and side effects (locally and/or systemically). You need to specify the drug. Whatever it is it probably won't be an effective way to improve muscular blood supply, and if this is a medical question you really should talk to a doctor before applying topicals willy-nilly.


text:
Difficulty in finding protein inhibition drugs
I was reading an article on a recent identification of a PARP-14 protein in cancer cells that is responsible for production of additional glucose which keeps cancer cells from dying, and that a PARP-14 inhibiting drug is still a long way from becoming reality.
Would like to ask any medical researchers/anyone with adequate knowledge, what is the difficulty in producing drugs that inhibit production by a certain protein? Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it? As how other types of drugs are made? Please give some specific examples regarding this topic. Your help is much appreciated.

Can you please link to or cite the article?

Basically the problem is finding or designing compound that can either competitively bind to the active site of a protein or an allosteric regulatory site that does not also interfere with proteins necessary to maintain cells elsewhere in the body.

@canadianer I am not sure that the link to the article is necessary. The OP gives a specific example and then asks a more general question about developing chemotherapeutics that target proteins, not necessarily why it would be difficult to find one for PARP-14. No?

@AMR It's not necessary, but I'd like to read it.

@canadianer http://www.ncbi.nlm.nih.gov/pubmed?LinkName=gene_pubmed&from_uid=54625
Sounds like it makes some form of modification to histones in DNA damaged cells that rescues them and contributes to their survival.

@AMR Yes I read that, which is why I'd also like to read the paper that says it produces glucose.

@canadianer This one? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179111/

Drug production is very long, tedious and costly process. It generally takes more than 10 years to make entirely new drug. It has various iterative aspects. take a look at following cartoon showing various steps in drug design ( Taken from Anderson 2003 )

Now coming to your questions,

what is the difficulty in producing drugs that inhibit production by a certain protein?

First of all you need to know other effects of that protein which might be essential for normal cell function. For example, there are many genes overexpression patterns which have correlated with cancer. This suggest excess quantity of these proteins/factors leads to cancer. Now one would like to block these proteins with inhibitors. However if you block these proteins, they might also affect regular cellular function. For example, SHC1 overexpression is correlated with breast cancer. However that protein is very important in apoptosis regulation, EGFR pathway, Oxidative stress and many more functions. Now if you inhibit this protein, your normal cells will also get damaged.

Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it

It is not that simple, for this you need inhibitor which can specifically either bind (it can be competition also) specifically with given protein. Most of the time there are other problems like , there might be other proteins with that structure which can affect other protein's function. There will be other important problems like

Delivery of inhibitor
Specificity (Inhibitor need to act only on target cells)
Sensitivity (Inhibitor need to be sensitive enough to get full response in low concentration)
Side effects (There might be side effects of this inhibitor which should be minimized)
Cell resistance (Many times cell becomes resistant to inhibitor)

Above mentioned points are actually major issues in all cancer treatments like Chemotherapy  , Radiation therapy, Immunotherapy , Hormone therapy etc.

Nice, but whether the protein is important for normal cell function was not part of the question I think. One thing is to figure out how to specifically inhibit a given protein with a drug (which is hard enough in itself). Whether this is a good idea at all, given the various functions the protein might have in the body, is a separate problem.


text:
Rationale behind washing off unbound protein antigen in indirect ELISA
My question is with regards to the usability of the indirect ELISA in measuring protein concentration. Suppose we want to quantify the concentration of a protein. The indirect ELISA method would require one to coat the bottom of the well with protein antigen and wash off unbound antigens.
My question is that wouldn't washing off unbound proteins mean you are 'diluting' the actual protein concentration? Your resulting colour intensity will not reflect the actu protein concentration. Thanks!

The method is based on the principle that the amount of antigen bound to the plastic will be proportional to the concentration in the sample being tested. And of course an ELISA will usually be run with a calibration in parallel so that the signal from your sample is compared to that from standards.
The wells will be rinsed anyway in subsequent steps to remove unbound antibody molecules: if you didn't wash off unbound antigen it would simply compete for binding the antibody then disappear later in the procedure.


text:
How do similar environments on islands in close proximity result in allopatric speciation?
I would like to ask a question on the very classic example of allopatric speciation seen in the Galapagos finches. Adaptive radiation occurred because the finches flew from island to island, so there is gene flow, and the different environments on the different islands provide different selective pressures that causes relative fitness of the same species of birds to change. Over time, more drastic changes occur and speciation event occurred.
What I am doubtful of is the extent of different selection pressures on speciation. Given that the islands are so close to each other, wouldn't it be safe to assume that these islands generally have similar types of plants, similar types of insects, similar climate, similar predators. If gene flow between populations of finches can occur across islands, why can't it happen for the other biotic factors "contributing" to the islands' characteristics? So how can such similar conditions/environments provide selection pressure that is different enough to result in speciation?
Your clarifications are very much appreciated!

The question is a bit confusing because it seems to be built on at least 5 misunderstandings.
Allopatry and gene flow

[..] allopatric speciation seen in the Galapagos finches. Adaptive radiation occurred because the finches flew from island to island, so there is gene flow [..]

By definition, an allopatric speciation is a case of speciation where there is no gene flow. If there is gene flow, then you may still end up with a reduction of gene flow and a speciation event but that would not be called allopatric speciation.
The first event leading to isolation (that is to an allopatric scenario) might be caused by birds flying over to another island but this does not mean that the divergence between populations occurred with gene flow.
Relative fitness

[..] the different environments on the different islands provide different selective pressures that causes relative fitness of the same species of birds to change.

It makes little sense to talk about relative fitness of a species. The relative fitness of an individual is the absolute fitness of this individual divided by the absolute fitness of a reference individual (generally a theoretically super fit individual) in the population.
Did you want to talk about competition between species? I don't think so as I don't know how this concept would fit in the rest of the question.
Assumption of similar ecology

[..] wouldn't it be safe to assume that these islands generally have similar types of plants, similar types of insects, similar climate, similar predators.

No, it really is not a good assumption. In some extreme cases, climate can actually radically differ between two locations at less than 20 meters apart! The same is true for other variable making up the ecological conditions.
Species dependent migration abilities

If gene flow between populations of finches can occur across islands, why can't it happen for the other biotic factors "contributing" to the islands' characteristics?

Because birds have wings! It is easier for a bird to fly to the next island than it is for a mouse.
Implicit assumption that selection is needed for speciation

So how can such similar conditions/environments provide selection pressure that is different enough to result in speciation?

Speciation can happen in absence of divergence selection (esp. in allopatry). Genetic drift alone yield to population divergence too and can lead to reproductive isolation.
To my knowledge, the relative role of selection vs drift in causing speciation is not well understood though.


text:
Meaning of ‘motif’ in molecular biology
I would like to understand the meaning of the term motif as used in molecular biology.
In an article in Nature Biotechnology, Patrik D’haeseleer states:

Sequence motifs are short, recurring patterns in DNA that are presumed to have a biological function. Often they indicate sequence-specific binding sites for proteins such as nucleases and transcription factors (TF).

Does this mean that in the DNA sequence of a gene there are recurring patterns/subsequences of DNA which are presumed to have a biological function? If so, can such motifs be found simply by using a software that detects recurrent substring in a string?
In relation to the biological function of such motifs, I would like clarification of this extract from
a paper by Williams et al.:

P. furiosus ORF PF1193 displayed up to 12-fold increase in mRNA level at 20 min following irradiation (Table S1). PF1193 contains a ferritin-like di-iron motif found in ferritin- and Dps-like proteins and bacterioferritins and was found to belong to a new subclass of ferritin-like di-iron carboxylate superfamily (Ramsay et al. 2006; Tatur et al. 2005).

By “motif”, do the authors mean that the gene PF1193 has a subsequence which is found many times in the DNA sequence of the gene that encodes ferritin- and Dps-like proteins, and that this may indicate that they (genes and the related proteins encoded) have similar characteristics/properties?
How does this relate to the sentence in the extract from the Nature Biotechnology paper?

Often they indicate sequence-specific binding sites for proteins such as nucleases and transcription factors (TF).

They certainly mean a not too bad alignment, you should blast (the AA of) your protein or some parts of it to see how good it is.

In the excerpt from your linked paper, "motif" is referring to a protein sequence pattern as opposed to a DNA sequence pattern.

@reuns does AA stand for Amino Acids? I have "Blasted" the protein and I have found some similarities with the Ferritin-like protein of Pleurocapsa (and other DNA protection protein of other bacteria). Then I aligned the DNA sequence of the PF1193 gene and the DNA sequence of the gene that encodes Ferritin-like protein of Pleurocapsa and found similarities also there...

I have edited your question so that it conforms to English scientific style. I have changed biology to molecular biology as ornithologists would understand something quite different by motif.  I simplified the very last part because I could not understand what you were trying to say. You will see how the question is now more compact and readable.  Please note that in referring to published papers, the statements therein should be attributed to the authors and not to the journal. Only attribute opinions to journals when they appear in editorials.

@David thank you .

@David thank you very much ! I would really like to fully understand the questions of my post that you have italicized .

Meaning of Motif in Molecular Biology
In English the word, motif (borrowed from the French), has a variety of meanings in different areas. The one that is borrowed in molecular biology is that of pattern together with a hint, perhaps, of emblem or badge.
The word pattern indicates both repetition and a master mould from which copies are made. In molecular biology this indicates that this is not unique, it occurs repeatedly. The word emblem suggests a means of identifying the group to which something belongs. In molecular biology it is associated with a shared function for members of the group.
Types of Motif in Molecular Biology
Here the word motif is applied mainly to the three related macromolecules, DNA, RNA and protein. All of these are linear chains of restricted varieties of defined components (four nucleotides, 20 amino acids) arranged in defined ways which we refer to the sequence of the macromolecule. Within the overall sequence there can be sub-sequences, which, if they repeat represent patterns, and which may have functional significance. We refer to such patterns as:

DNA sequence motifs
RNA sequence motifs
Protein (or amino acid)sequence motifs

The first of these is what D’haeseleer is referring to. It should be noted that these sequence motifs can be absolute, or consist of consensus sequences, such as the one for the ROX 1-binding site in the article cited:

However the nucleotides or amino acids are not the only components of macromolecules the arrangement of which can produce a pattern. Motifs in molecular biology can be composed of structural components. This is expressed in the following definition of protein motif:

Protein motifs are small regions of protein three-dimensional
structure or amino acid sequence shared among different proteins. They
are recognizable regions of protein structure that may (or may not) be
defined by a unique chemical or biological function.

And a similar definition that considers only structural motifs in proteins adds: “An example… is a helix-turn-helix motif.” This is a motif in certain proteins that bind DNA.
Identifying Sequence Motifs by Computer
The limit of the approach suggested is that statistically one would expect any small sequence pattern to recur in DNA, and the problem is how to tell which recurring patterns have biological significance. It should be realized that is not the sequence motif alone that makes it functional, but the context in which it is found. Thus, a TATA box or other DNA motifs that act as binding sites for transcription factors were discovered (and are differentiated from other random or non-functional occurrences in the genome) by their proximity to the positions where transcription is initiated. Their function was confirmed experimentally, e.g. by binding RNA polymerase to the DNA. (This, I hope, answers the last query about the function of motifs as protein-binding sites.)
So, in general, no. Although I admit that I have personally use computational approaches to discover new small hydrogen-bonded protein motifs (a somewhat specialized area).
The ferritin-like di-iron motif
This is not a DNA sequence motif. It is not even a protein sequence motif, but a structural protein motif. The definition can be found on InterPro:

This entry represents a group of proteins, containing ferritin-like
domain, which is an about 145-residue domain made of a four-helix
bundle surrounding a non-heme, non-sulphur, oxo-bridged diiron site.
The diiron site is contained within a twisted, left-handed four-
helix-bundle constituted of two anti-parallel helix pairs connected
through a left-handed crossover connection.

It is shown here with the helices coloured yellow and the iron atoms red spheres:

[From deMare et al. (1996)]
Footnotes

The helix–turn–helix is also referred to as a domain. The distinction between motif and domain is one of size (note the small in the definition of protein motif). However InterPro does refer to the ferritin-like di-iron pattern as a motif, so this can be regarded as acceptable usage.

One might argue that as the sequence and structure of proteins are specified in the DNA, the motif should also be in the DNA. This is a fallacy. The information is there, but in a cryptic form. The redundancy of the genetic code means that protein sequences are far more conserved than the corresponding DNA sequences, and the three-dimensional structural patterns are not evident from inspecting amino acid sequences.

Thank you very much @David . The situation is more complicated than I thought. But are there some softwares that discover motifs ? Like if I give as input the DNA sequence of the gene and gives me them... I read about "SSR" locator in this forum https://biology.stackexchange.com/questions/38913/how-to-interpret-the-simple-sequence-repeat-ssr-on-the-coding-sequence-but-no

Some software that has implemented the biological context that you need and the experimental evidences (so that it is a sort of "database" of motifs).

Finally, Just to definitely clarify this important point: when you say The word emblem suggests a means of identifying the group to which something belongs. In molecular biology it is associated with a shared function for members of the group. Does it mean that if two genes have in common DNA sequence motif, they share the biological function relative to this motif ?

@Manuella DNA sequence motifs generally relate to recognition by proteins — for binding and perhaps cleavage or chemical modification. We don’t generally talk about the function of the biological function of a DNA motif, and, as I tried to imply, such motifs may be necessary, but not sufficient to initiate transcription. This topic is covered in many reviews of transcription, some of which, no doubt, will have tables of motifs.

@Manuella The prediction angle is more to the fore in proteins, where specific sequence motifs might suggest a protein is tagged for transport to a particular organelle. Thus, sites like SwissProt have databases of particular protein motifs, and allow you to enter a protein sequence to find out what motifs it contains. 3D structure is somewhat different. There have been a number of projects determining the structure of unknown proteins. A putative function is often based on the structural motifs revealed, generally using expertise, although 3D structure comparison software exists.

Ok thank you very much. So DNA sequence motifs generally relate to recognition by proteins... thus I think my initial idea was completely wrong. So a very last question @David to officially confirm that my assumptions were unfortunately nonsense.

By biological function I simply meant that if two genes have a DNA sequence motif in common, maybe their encoded proteins could have some "functional" properties in common... for instance if I consider the gene that encode the Ferritin protein, I know that the Ferritin protein has the capability to avoid the production of free hydroxyl radicals, that can catalyze the oxidative damage of biomolecules, because they can store Iron and avoid Fenton reaction.

So if I consider an other gene that has a subsequence in its DNA gene sequence that is a motif for the gene that encode ferritin protein, can I say that this last gene could encode a protein that has the same nice property of Ferritin protein of storing Iron and avoiding free hydroxyl radicals production ?

One point that I did not emphasize in my answer (which I may include in a later revision) — most DNA sequence motifs fall outside the region of a gene that specifies the amino acid sequence. So if two genes have such a motif in common it implies some sort of similarity in the control of their expression rather than their protein products. I am not a transcription expert, but for example many genes are transcribed in response to interferon and these share motifs — interferon sensitive response elements. However the genes encode many different types of proteins that are needed to fight viruses.

Ok ! @David That was the point that I wanted in really few words... if these motifs are found in the CDS (whose sequence determines the sequence of amino acids in a protein) what happens. Are the encoded proteins similar in their functions ? This discussion made it clear to me that I want to know this.

@Manuela — See Footnote 2. Then it is better to look at the amino acid sequences. Sequence motifs in proteins can indicate function, as in the protein kinases, but can also be transport tags. SwissProt will generally tell you.

Re:

When they say "motif", do they mean that the gene PF1193 has a
subsequence which is found many times in the DNA sequence of the gene
that encodes ferritin- and Dps-like proteins ? And this may involve
that they have similar characteristics/properties ?

Yes, although motif sequences may not be exactly identical, as what really matters is the 3-dimensional structure produced and thus its function (whether binding, enzymatic, or whatever). You can think of them as recognizable functional units, often but not always self-sufficient. For example, a promoter sequence in DNA would be considered a motif, as would be a zinc finger in a protein, as would be a poly-A tail on an mRNA.
A problem in using motif sequences to identify genes of related function is that during evolution, sequences may have changed even as 3-D structure (and function) remain similar. Here's a paper working on that problem from about a decade ago:
J Biol Chem. 2012 Jun 8; 287(24): 20565–20575.
Published online 2012 Apr 25. doi: 10.1074/jbc.M112.367458
PMCID: PMC3370241
PMID: 22535960
"Use of Structural Phylogenetic Networks for Classification of the Ferritin-like Superfamily"

Blast the protein and see if the 1st results are ferritin-like!

Thank you @Armand ! Yes I also read in ncbi that motifs are used as base of proteins classification. But so, since you have confirmed what I wrote (the extract that you reported) at least conceptually , as rough estimate can I find motifs with a Python code that finds recurrent substrings in a string ? (where the string is the DNA sequence of the gene)

This answer is incorrect regarding the ferritin-like di-iron motif cited in the question. This is a protein structure motif, not a DNA motif. Identification of gene families from DNA sequences  is, of course, important, but it is done on the basis of overall sequence similarity, not usually on the basis of particular motifs, and I don't think this is what the poster was asking about in terms of computer analysis. I interpret her question as using computers to discover motifs, rather than identify them in DNA sequences.

@David actually I was particularly interested in identifying motifs in DNA sequences... but yes the answer was lacking of some things .


text:
What is the typical arrangement of amplified genes in archaea genome?
I have to check if some genes are amplified with bioinformatics tools, but, in order to do it, I need to know what this means from a biological point of view.
It seems not so difficult to understand, in fact the definition from NIH is simply the following:

Gene amplification is an increase in the number of copies of a gene sequence. Cancer cells sometimes produce multiple copies of genes in response to signals from other cells or their environment. The term also can refer to polymerase chain reaction (PCR), a laboratory technique that is used by scientists to amplify gene sequences in a test tube.

So my question is: if I have the complete DNA sequence of the organism's genome that I am studying (like this), that belongs to Archaea domain, what I should do to check for gene amplification is to see if the sequence of the gene (that I suspect that it is amplified) is repeated more times ?
I thank you in advance.

Could you clarify a few points to produce a focused question on the biology rather than the bioinformatics. (Of course a question on the bioinformatics is acceptable, but one at a time is how this site works. The two are separate questions.) When you say "how gene amplification is present in the genome" what do you mean? Do you mean how does it occur mechanistically, or what function can it serve? And it would be good to say whether you are interested in prokaryotes (as it appears) or eukaryotes, because the situations are rather different in the two cases.

@David ok I will correct it but with the  "how gene amplification is present in the genome" I mean how the genome DNA sequence is after gene amplification... so I am not interested in how it occurs mechanistically or what function it can serve (unless it is needed to understand what I want to know)... so in the sequence that I linked, should I simply find the sequence of a gene more times if it has been amplified ?

I appreciate the linguistic usage problems with the English word “how” for non-native speakers (French, German and Italian, rather than Spanish which I assume  is not too different). The usage you employed seems logical (= “how are amplified genes arranged/disposed in the genome?”) but is never employed. I would perhaps write something like “What is the typical arrangement of amplified genes in bacteria, especially those features that one might regard as indicative (or signatures) of amplification?”. It is not my particular area or I would answer.

Thank you very much @David for the suggestions

You ask "so in the sequence that I linked, should I simply find the sequence of a gene more times if it has been amplified ?"
Yes. There are many ways, both natural and artificial, to end up with more copies of a certain gene or genes without a proportional increase in copies of the other genes in the cell. Thus, there is no generally expected arrangement of the amplified genes.
One aspect to think about is the criteria for determining whether two given genes are copies of the same gene or are two distinct genes.

Thank you for your answer but I do not understand when you say One aspect to think about is the criteria for determining whether two given genes are copies of the same gene or are two distinct genes, because, if they have the same sequence, they should be certainly the same, right ?

I added a new post focused only on the second question, so if you want to have a look here https://biology.stackexchange.com/questions/101133/what-are-the-causes-of-gene-amplification-in-archaea you can understand better what I meant . Sorry for these jumpings :)

@Manuela Re: " if they have the same sequence, they should be certainly the same, right ?" Right, but many (most maybe) processes that produce gene amplification will result in mutations in one or more copies, either immediately or over time. For example, a duplicated segment of chromosome may initially have the same genes, but absent strong selection those will diverge over time. Maybe the copies still function the same, maybe they don't.

Thank you ! Things are much more complicated than I thought. Is there a criteria to enstablish if they are copies of the same gene, as you mentioned in the answer ? And, moreover, can you suggest some books or material that explains with more details what you said to me in the answer (so about the fact that we should see in the genome sequence different copies of the gene duplicated) ?

@Manuela My perspective is gene duplication in mammals over evolutionary time, so I would give an example of something like "Evolution of olfactory receptor genes in the human genome"  doi: 10.1073/pnas.1635157100 and the follow-on work. Your perspective seems to be much more short-term oriented (and not eukaryotic!), so something like "Bacterial gene amplification: implications for the evolution of antibiotic resistance" Nat Rev Microbiol. 2009 Aug;7(8):578-88. doi: 10.1038/nrmicro2174 might be more to your interest.


text:
Why are there different gene expressions that are refered to the same gene in microarray experiments results?
I am studying gene expression profiling considering a dataset available on NCBI website. I do not understand the following: why are there some genes that have different profile and different ID numbers but they refer to the same indentical gene ?
The dataset that I am analysing is here .
For instance, we have that ID-8938, ID-1870, ID-7323 and ID-15 refer to the same gene called RadA but the gene expression profiling is different for each ID. So I ask which is the difference between these ID if they represent the same gene ? Moreover, how can I understand which is the one that has to be chosen for the analysis ?

Why would you expect only a single profile measurement to be in the database for a gene?

@mgkrebbs because if you do the measurement of the mRNA produced in those time points for that gene, how can I obtain other measurements for the same time points ? Do they take other cellular cultures of the same organism and make the same measurements at the same time points to check if the values are consistent ?

What you are looking at there is a microarray dataset (see the description here).
Microarrays are chips that have many sequence specific probes on them and sometimes they have multiple probes for the same gene.
Readout differences between the probes of the same gene could be caused by either noise in the data or biological effects like expression differences between transcript isoforms - other reasons could be possible as well.


text:
Hayflick limit and hair or nails
I am not a bio major but I have heard about Telomerese shortening in each cell division which leads aging and cellular death. I also read that Hayflick limit is about the number of divisions a cell can make before it dies.
So my question is, how is it possible for us to have constantly dividing cells such as in our hair or nails. They are also cells right? They constantly divide almost our entire life, so how come they do not die out of Hayflick limit?
Or is it like, when a cell divides for the first time, it loses one unit of Telomere but the second cell also have the same number of Telomeres as the first one? I mean if Hayflick limit is 50 for the first cell, is there like 49 and 49 for both cells after division? And when do they decide to divide, is the first cell waits its child to reach Hayflick limit before it divides again? Is this just too complicated to explain in layman terms or are we just not sure yet?
Please do not go hard on me if I have conceptual mistakes, I am just really curious about this.

IIRC, hair follicles/nail beds don't create hair by cell division, but instead by producing the keratin directly.

And Adult Stem Cells replenish the tissue and have Telomerase turned on to extend the telomeres to overcome the 3' replication problem which causes telomeres to shorten. The net effect is that Adult Stem Cells do not lose telomere length.

Let's do some math.
Also, let's ignore your examples, and use a clearer one - instead of fingernails, let's look at the cells that line the intestine.  Intestinal epithelial cells are shed and replaced constantly and very rapidly, roughly every 5 days.  So that means about 50-70 cell generations per year.
Each time the cell replicates, it loses a little bit off the end of its telomeres.  How much does it lose?
We know that for lymphocytes, adults lose roughly 30 base pairs of telomeres per year.  Lymphocytes don't replicate as fast as the colonic mucosa, though.  The estimate for these rapidly-dividing cells is about 44 bp/year. We can say 50 for a round number.
That doesn't tell us much unless we know what we're starting and stopping with.  Humans start life with about 10,000 bp of telomeres.  At least in cultured cells, once telomeres reach 1000-2000 bp, cells become senescent and stop, or greatly reduce, their growth rate.
So we start at around 10,000, we can lose up to 9000, and we lose around 50 per year. That means that the intestinal epithelium, which have about the most rapidly-dividing cells in the body, are good for about 180 years of life, assuming that the loss remains constant.
(I don't know if loss does remain constant in these cells, but in lymphocytes, the loss of telomeres accelerates in elderly people, from about 30 to about 60 bp/year in people over 60. However, it's likely that reflects increased lymphocyte turnover in older people, not something intrinsic to the age per se.)
So bottom line, we're good for it.
More generally, keep in mind that the popular media have seized on telomeres as a simple answer for everything related to aging.  Obviously, that's not reality.  Telomeres certainly reflect aging; in some cases, perhaps many cases, they may be one influence on aging; but in most cases, telomere shortening is probably only a minor aging factor, and many other causes are more important.

Is there a clean explanation for why telomere length decreases roughly linearly with time (or with number of cell divisions) rather than exponentially? Or is this mostly an empirical observation?

The end-replication problem means that there is a loss of a constant number of telomere bases, not a fraction of the length.  Hence, linear loss

I'm sorry, but your answer is wrong. The cells that are lost are replaced by adult intestinal stem cells http://www.nature.com/nrm/journal/v15/n1/fig_tab/nrm3721_F1.html Adult stem cells keep telomerase active so that telomeres are extended with each replication.

I admire your confidence in not even reading the references I helpfully linked for you before your attempted correction.
While embryonic stem cells have active telomerase, adult stem cells (which is what we're talking about here) do not have enough to maintain telomerase length.


text:
Relationship between turgor pressure and osmotic pressure?
I would like to know if there is a relationship between osmotic pressure (inside and outside of a cell) and turgor pressure. If so, is there a way to formalize it mathematically?
Thank you in advance,
Eorn

Turgor Pressure(T.P) is defined as the amount of pressure inside a cell solely due to its water content, whereas Osmotic Pressure(Pi) is defined as the pressure required to stop osmotic flow between the cell and a pure solvent when the pressure exerted by water is zero.
Osmotic Pressure is often given as the negative of the Osmotic Potential(or Solute Potential) of the Cell.(Because more the solute, more pressure will be required to stop the osmosis, but against the gradient). (1)
Therefore, it can be easily seen that Osmotic Pressure is solely dependent on the solute concentration of the cell.
The Total Suction Pressure(S.P) of a Cell is the pressure required outside of a cell to stop the water flow in a pure solvent.
The T.P in such a situation would try to reduce the S.P (More the T.P, less would be the pressure on the outside). Whereas, the O.P in such a situation would try to increase the S.P (More the solute inside a cell, more would the water on the outside try to get on the inside)
Hence, Mathematically (considering no other pressures to be responsible for Total Suction Pressure)
S.P = Pi - T.P
This can Also be proved in the following way:
Water Potential(Psi W): Total Pressure inside a Cell.
Solute Potential/Osmotic Potential(Psi S): Reduction in Water Potential Magnitude due to addition of a Solute(solute reduces kinetic energy of water due to bonding)
Pressure Potential(Psi P): Hydrostatic Pressure, i.e, pressure exerted by the water present inside a cell if there were no solute particles.
By definition
Psi W = Psi S + Psi P
(We know, Psi S = -Pi) As written above in (1)
Psi W = -Pi + Psi P
(We know, Turgor Pressure is the same thing as Psi P)
Psi W = -Pi + T.P
Suction Pressure is the negative of Total Pressure inside a Cell
(S.P = -Psi W)
(Water flows from high water potential to low potential, but from low Suction Pressure to an area of High Suction Pressure)
Therefore
-S.P = -Pi + T.P
multiplying by -1
S.P = Pi - T.P


text:
Extraction of RNA from algae
I have used a standard protocol (I will give the bibliography below) to extract RNA from an algae (Posidonia) but I have get literally nothing, since I could not even see traces of the two rRNA. I think that I have failed because the huge quantity of salt and/or carbohydrates in algae in comparison with terrestrial plants. My final objective is to get mRNA and then sequence it, so I need a very good extraction.
Any ideas of paper I could read to go above this problem?
Gambino, G., Perrone, I., & Gribaudo, I. (2008). A rapid and effective method for RNA extraction from different tissues of grapevine and other woody plants.Phytochemical Analysis, 19(6), 520-525.


text:
Why do water molecules diffuse along axons direction?
I am studying tractography technique which aims to reconstruct bundles of axons in brain by following the diffusion direction of water. It is very interesting because it is non-invasive. It exploits the difference between grey matter and white matter: in white matter (axons) we find an anisotropic environment since there is a preferential direction of diffusivity of water molecules that is along the axons direction, while in grey matter the environment is isotropic since molecules do not move with a preferential direction. The diffusion of molecules is generally given by a difference of concentration of molecules between two points but they should move even though this gradient is not present because of the temperature so because of the fact that they have a certain thermal energy. Therefore my question is: why do molecules move along the axons direction ? Is there a biological aspect that causes like a difference in concentration between the starting point and the ending point ? Maybe the answer is trivial but since I am not a biologist I do not know it :) and I am not able to find something on web . It seems that I find only explanations for diffusion of water molecules from outside the cell to inside... I would like to know the reason why they move in the same direction of the axon.

The movement is just the thermal energy motion you describe, not due to any concentration difference.
The anisotropy is due to the geometry. White matter tracts are effectively a dense bundle of thick, fatty hoses. Water can freely move in the tubes but cannot move as freely through the dense walls, so you see more movement along the axon length rather than perpendicular to them.
You can read more at https://en.wikipedia.org/wiki/Diffusion_MRI


text:
Why do genes, encoding the same proteins and in the same conditions, have different expression?
Is it possible that two genes, which come from two different cell cultures and which encodes the same protein, produces different quantity of mRNA? If yes, why?
My question comes from the fact that I am doing statistical analysis of a microarray dataset for the hyperthermophilic archaeon Pyrococcus furiosus exposed to gamma irradiation. Microarray experiments measure relative quantities of mRNA in a cell. My file has values, for each gene of the genome, that are positive or negative since the scientists who performed the experiment made the log10 ratio between the fluorescence intensity of the sample that was irradiated and the reference sample (not irradiated). Indeed, in the microarray experiment we have two channels that typically are one for the "controls" and the other for the cells which are stimulated by an event (in this case the event is gamma irradiation), in order to make a comparison.
In my dataset there are two columns (that are indicated as "reference") that refer to the case in which they should have put the cell cultures not irradiated in both the two channels. I would expect that the values in the file corresponding to these two columns are 0 (since they are the log10 ratio between the intensities of the signals of the genes which encode the same protein and that are in the same conditions). Instead they are different from 0. Therefore I wonder what is the reason for which there is different quantity of mRNA produced from two equal genes?
I made a graph of relative mRNA produced (calculated as I explained before) vs time, in which you can notice that the relative mRNA produced of the reference  (I called them as "Ref" on the horizonal axis) is not 0.

Is it only due to some noise or are there biological reasons ? (the picture refers to a gene which encodes Ferritin-like proteins but it is the same story also for other genes).
Even though I think that my interpretation of the data is correct, I tell you that the dataset I am talking about is here, if you want to have a look.

Please edit your post to make it clear what you mean by "which are equal". More importantly how are these "equal" genes different — is the mRNA labeled differently? If so, does that give you any clues as to why you might see differences? In addition, I have edited your post to try to make your question clearer — please check to make sure I have not broken anything. Finally, please proofread your future posts and also use a spelling and grammar checker — this should help you improve your writing. Thanks!

@tyersome the fact is that it is not easy to explain but I will do the best say it better. Thank you anyway.

I agree I had a bit of trouble following this. Is it that there is a systematic difference, or that there is variability? In biological experiments measurement error and trial-to-trial variance are often relatively large compared to signals of interest.

@tyersome I tried to make it clearer and your edits are ok.

If I understand your question and graph correctly, your Y-axis is log(x/REF), where REF is some external standard. Your "Ref" on the x-axis you expect to be the same as REF, so that log(Ref/REF) "should be" zero, but you find it is not.
However, it looks like the mean(log(Ref/REF)) is still approximately zero. This is what I would expect: values that deviate a bit from perfectly 0, but having an average around 0 (and this average should approach 0 the more samples you have per the law of large numbers). You don't expect to have zero variance in data like this, which is why you repeat the experiment a number of times. You'll notice you have variance in all of your categories.

Ok thank you, indeed now I notice that they are close to 0. But the variability is due to noise due to experimental setup or something like this for instance ?

@Manuela Unclear, but there are lots of places where "noise" is possible in this setup: in production and degradation of mRNA, which are going to be stochastic processes, in imaging of the microarrays themselves which are subject to noise in the camera and digitization, any optical aberrations, stochastic bleaching of fluorescent molecules to non-fluorescent compounds, etc.

Another source of noise is hybridization of labeled cDNA to the microarray chip. It should happen under standard conditions and evenly across the chip - but in physical world nothing is realy ever exactly even. If you have the raw data with coordinates of the probes you should be able to display fluorescence intensities across 2D chip (There are R libraries for that). I once analyzed a chip with what looked like bubble in one corner. Even without bubbles one side could be warmer during hybridisation or other things.

It is entirely possible that different cell-lines express the same genes at drastically different levels.
The proteinatlas provides data and analyses on differences between certain tissues or cell types / cell-lines.
If your cells are of the same line/tissue, then they might still differ dependent on the cell-cycle, age and external factors. There are chemicals that facilitate cell-cycle synchronization.
But I agree to the other answer, that your observations could be within margin of error.


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

How are you defining "data types"?

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

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

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

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

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


text:
Simple computational biology project for AP Biology class. Ideas?
Our teacher assigned us a project to do with an extremely open-ended prompt and it should be completed within a month.
I was planning on doing something related to computation and evolution in terms of biology although I'm not really sure where to start. I say simple because I'm not a professional programmer, rather, extremely interested in the field and I hope to use this as an opportunity to stretch by skills.
Any ideas on a project or where to start would be greatly appreciated.

Welcome to the site. Unfortunately, Biology.SE is not a forum, and your question is quite opinion-based. From the [help/dont-ask], If your motivation for asking the question is “I would like to participate in a discussion about ______”, then you should not be asking here. However, simple Google searches will turn up plenty of hits for project ideas as well as sites where this type of discussion would be on-topic, such as Reddit or Quora. Good luck!

This could be an appreciated discussion at Reddit bioinformatics. Ask where to start, what are easy to use and quick tools, and how to get something meaningful out of the results.

You can use BLAST or NCBI resources to do an analysis of something like the duplication of a gene in the HIV virus, for example. If you're looking for a place to start, I would recommend just learning the NCBI database resources.

In addition to what Ham Radio suggested, checking out Galaxy might not be a bad idea for doing any sort of computation/analysis that would otherwise have to be done on the command line. In particular, check out tools for sequence alignment (BWA and Bowtie), genome assembly (Velvet, Spades, IDBA-UD), and variant analysis (Freebayes, Mpileup, GATK). Good luck!


text:
How do you call the species that gives its name to a upper-level clade?
Just a silly question: I don't remember how the species giving its name to an upper-level clade is called.
e.g. the name of family Canidae derives from Canis lupus
You could say it is the "name-giving" species, but I'm certain a specific term exists.

I guess you are looking for the type species.
Although it is defined to be a "name giver" for the genus or subgenus level you could potentially extend this to higher up levels.
EDIT: After looking this up and actually reading the full article myself, yes, at least in zoology you can extend it to higher levels by for example using the type genus.

Hmm... Thank you
I guess "type genus" is closer to what I was looking for, since it concerns supra-generic clades.
Although I recall once using a term of somewhat greek origin, like blahblah-nymic... but I don't recall what it was...
Maybe "hyponymic species"?