text:
Is induction and derepression the same thing?
Induction
This is a definition that our professor mentioned in class $-$the process of turning on the expression of gene in the response to a substance in the enviornment is called induction.
Derepression
From wikipedia $-$ in genetics and biochemistry the removal of repression, such as of an operon so that gene transcription occurs or is enhanced, with the net result frequently being elevation of the level of a specific enzyme. This effect is called derepression.
In lac operon when Allolactose molecule is present in the medium (in the bacterial cell) it binds to the monomer of repressor and reduces the binding affinity of repressor to the operator site and the RNA polymerase is free to synthesis a polycistronic mRNA. Thus the allolactose molecule turns on the expression of lac operon by removing repression.
So I conclude that in lac operon induction is same as derepression. But does it hold true for all operons or there are operons in which induction is achieved without repressing the repressor?

what is the purpose of the question? Is there a case when you want to use one of the words or it is just curiosity? This will help with answering

@aaaaaa I am both curious and wish to apply the words to my answers during exam.

@SanjuktaGhosh Don't play with words in your exams. Always use the words that the examiner would understand :P

@WYSIWYG :) I usually write which is most appropriate without bothering about the examiner.

I’d prepared this before I saw that @WYSIWYG had answered in the same vein. So the credit to him. But just to clarify:
Technically you are correct. Although having the same end-result, induction can occur by a direct mechanism, not involving de-repression, the example in the lac operon being the catabolite activator protein (CAP). However, it is quite normal to refer to a de-repressor as an inducer.
If we take a simplistic view and regard the key step in bacterial transcription as the binding of RNA polymerase to the promotor then the situations for de-repression and positive induction are:
De-repression
The binding of RNA polymerase to the promotor is prevented by the repressor (e.g. the lac repressor) binding to the DNA (at the operator). The de-repression occurs when the so-called inducer (allolactose here) binds to the repressor, reducing its binding affinity for the operator and hence allowing RNA polymerase access to the promoter.
Positive induction
Here the affinity of the RNA polymerase for the promotor is sub-optimal and is enhanced by the inducer. In fact, this generally occurs by a protein–protein interaction — in the case of cAMP induction of transcription of the lac operon it is the binding of the cAMP to the CAP that causes it to interact with RNA polymerase and increase the binding affinity of the latter.
Another on-line resource on this topic is at LibreTexts, and this has diagrams I should perhaps have included here.
In eukaryotes  direct induction would seem to be more common than de-repression, with inducers such as steroid hormones binding to specific receptor proteins which then bind to the DNA. However the details of the DNA interactions are much more complex.

Induction is an effect of a stimulus on the cell. During an induction of gene expression a gene is expressed in response to a stimulus.
De-repression is a mechanism of gene regulation which may lead to expression of the corresponding gene. The gene can be expressed via direct activation as well. The action of CAP on lac operon would be an example of direct activation. There are several other examples too.


text:
What Type of Mushroom is this?

Recently in Eastern Pennsylvania, there has been lots of rain and heat (90's) for a couple weeks now, so lots of mushrooms are popping up.
A neighbor posted a picture of this fungus in a community group, and was wondering if it is edible.

I found some images of Amanita rhopalopus that look similar, but I`m not totally convinced they are the same, as some look a bit different. Any one think they are Amanita rhopalopus?

You should not eat it if you don't know for certain what it is! E.g. here is a similar deadly mushroom: https://www.google.hu/search?q=gyilkos+gal%C3%B3ca&client=firefox-b-ab&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiOgqreh57OAhVB3SwKHYyqBDoQ_AUICCgB&biw=1536&bih=730#imgrc=nrVy5g6yIBrD-M%3A

Obviously no one should eat any unidentified organism without the guidance of an expert. Thanks for the possibility.

Mushroom identification is very difficult. As well, post more detailed pictures, including gills and dissected views. Do not ever imagine about eating an unknown fungus identified via web this way. Experts identify mushrooms after collecting a lots of characteristics (including light-microscopy of tissue, spores etc and chemical tests at least), and also there is role of expertise of that experts. Tribal and Rural-peoples when collect mushroom, they very well-know the look ,habit and habitat of mushrooms they eat. Often, they collect fungus from a well-known site or locality.

I am no mycologist, but I think it looks like the false death cap, Amanita citrina var. alba.
I'm basing this mostly on color, size, and the universal veil remnants on the cap.  Here is a picture for comparison:

Amanita citrina is now known to contain the toxin alpha-amanitin;
  however, if eaten in normal amounts it is considered the concentration
  is so low that it is unlikely to have any significant effect on a
  healthy adult. Of far greater risk is the possibility of confusion
  with one of the deadly Amanita species such as the Deathcap, Amanita
  phalloides, or the Destroying Angel, Amanita virosa. For this reason
  our advice is not to eat Amanita citrina, whether it is raw or cooked

Source: First-Nature

It could be an Amenita, another option is a Lepiota.

yes amanita sp. do not eat it at all. They come up in the grass after rain and hot weather.

It would be nice if you could provide a more detailed response, which may include an image of your proposed ID, organism distribution, and/or any other general background info that's relevant to the OP. +1 if you can do this.

source: Stack Exchange

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sort: votes


text:
Computer Virus that infects DNA?
I have watched a talk by Mikko Hypponen (CEO of the security company F-Secure) called Silicon Plague. There, roughly at minute 51 of the talk, he mentions a computer code that is supposed to be able to infect DNA.
I was googling and found the corresponding article posted ~2.5 years, and some c++ codes. Let me cite:
 The computer code, written in C++, hosts the DNA sequence of M.mycoides
 JCVI-syn1.0. At runtime it acts as follows:

 1) Preparing the DNA sequence of M.mycoides JCVI-syn1.0 in the memory,
    (with slightly modified watermarks).
 2) Encoding own file-content in base32. The base32 code is then encoded in
    JCVI's DNA-encoded alphabet.
 3) This representation of its digital form is then copied to a
    watermark of the bacteria's genome in memory. With this, a fully
    functional bacterial DNA sequence including the digital code is
    generated.
 4) Next, it searches for FASTA-files on the computer, which are text-based
    representations of DNA sequences, commonly used by many DNA sequence
    libraries.
 5) For each FASTA-file, it replaces the original DNA with the bacterial
    DNA containing the digital form of the computer code.

 The code has a classical self-replication mechanism as well, to eventually
 end up on a computer in a microbiology-laboratory with the ability of
 creating DNA out of digital genomes (such as laboratories by the JCVI).

As far as I understand, the program tries to go into biology-lab computers with genome files, and modify the content with some content of itself. This sounds scary. Unfortunately, I'm not at the level yet where I would understand whether that could work (undergraduate student), so my question is: Does that idea work? Could there really be a computer virus that infects DNA?

The c++ is here.

I was going to call BS but this looks pretty legitimate. It could of course work in theory, but I don't see any practical application

@MalharKhushu-Well, what is the practical application of any other computer virus ? :)  Unless we call stealing money and destroying data, a 'practical application' :) :)

Hi ACGT. Really nice post. However, the question is a bit ambiguous. Are you asking 1: if this virus could reflect/translate/exist in real-world DNA? or 2: if the virus could INFECT an existing organism (cell)? The answer for the first question is undoubted YES, and to the second question is undoubted NO. There is no evidence that the code is wrong. So, as long as it is in the right machine (craing inst) it WILL work. Your question will be treated more seriously 10 years from now on as we WILL see these kind of viruses more often.

First bacterial genome created entirely with a computer links to PNAS: Chemical synthesis rewriting of a bacterial genome to achieve design flexibility and biological functionality open access.

Computer virus alters cancer scan images computer virus can give you virtual cancer and a real hospital bill.

As I understand from your post, the computer virus you are talking about is modifying database (FASTA files) in genetics. That would have a pretty bad impact on research in genetics and medicine.
If one uses such a database to synthesize/edit sequences and then introduce this DNA into a living organism, then yes the computer virus would have affected a living organism. If the sequence the computer virus has introduced is able to be transcribed into mRNA and go on infecting other cells, and eventually spread, then I guess one could say that the computer virus would have become an actual virus.
However, two things are to be considered. First, I very much doubt such a thing could go unnoticed. Second, anyone could have fun and create novel sequences. The only thing the virus does is corrupting files in a computer. The eventual existence of a man-made virus has no specific relationship with the computer virus and doing too much analogy here would stand little meaning.

This is very silly.
All the computer virus is doing is corrupting a text file in a computer database.
If someone uses the information in the corrupt file to synthesize actual DNA to modify a living organism, the agent is the human. The computer code has no interaction whatever with the DNA.
This is just the same as if the person accidentally or deliberately engineered some pathogenic feature into an organism — a more realistic and worrying phenomenon.
PS
Fortunately this particular C++ code is for a Windows executable, and NCBI is all Unix.

"Fortunately this particular C++ code is for a Windows executable" - So what? The virus could 'infect' a fasta file before you submit it to NCBI DB.

@SolarWInd This PS was meant to be taken in the same spirit as the question.( I leave you to work that out.) However, since you ask, the scenario envisaged NCBI GenBank's database in which the sequence ALREADY resides being infected with a computer virus to corrupt it, not the user uploading the sequence. Of course, one can upload any sort of nonsense — one doesn't need a computer virus to do that — but that wasn't the scenario.

The computer file does NOT contain DNA. It is a computer file. And the virus is NOT targeted at the Craig Institute (not that that is relevant). It contains a TEXTUAL REPRESENTATION of DNA bases (not even the sugar and phosphate) which can be interpreted (by someone reading it) in a different code than the genetic code — like a cipher. He could have devised a code in which he had written a message "Don't forget to feed the cat", but this one can be typed out by a human being and compiled into a Windows executable. (Glad I don't run Windows. Prefer the cat.)

"All the computer virus is doing is corrupting a text file" - You just contradicted yourself. If the virus can infect a computer file containing 'DNA' strings (you said it can) and the file is used to synthesize REAL DNA, then yes, the virus worked! And the virus is targeted to Craig Institute, which happens to synthesize DNA (from computer files). Voilà!

@SolarWind you don't know what you're talking about here. Please stop before you embarrass yourself further.

"This is very silly." I think at one point this was said about the idea of proteins being infectious, or that surgical instruments should be sterilized.

@uhoh — There must be a name for the type of guilt by invented association in your criticism. However I went on to explain why I thought the proposition was silly. I suggest any criticism should be directed at that argument.

It's 5PM Friday here, I'm going to read through again tomorrow morning. I hope it's not a case of the DNA saying the RNA did it, and the RNA saying the ribosome did it, and the ribosomes saying the protein... or should it be...

@uhoh — Are you confusing suicide with homicide? And wouldn't it be better to find the body before concluding that there had been a crime?

It's 7:30 AM and still on my first cup of coffee, I'm going to need at least three neurons firing before I can respond, give me a few more minutes...

okay we've got three neurons going strong and two more will be on-line shortly. I still see this as 100% non-silly. To me a conceptual virus exploits existing behavior. It doesn't matter if that's molecular behavior, OS behavior, or human behavior. The currently discussed virus exploits all three, which makes it quite a "clever" virus. So no, I don't see this as silly at all.

You’re entitled to your view and your down vote. The poster accepted an extended version of my argument in another answer two years ago, so the world moves on, unimpeded by computer viruses infecting its DNA. I suggest we do likewise.

I already have a fasta for a XDR tuberculosis strain on my computer.  It's not hurting anyone, nor will it.  If someone wrote a script that changed the fasta file I have of drug sensitive strains to put in resistance-granting mutations, that's going to screw up some analyses, but it's not going to kill anyone.

It's theoretically possible that a particular DNA sequence could trigger a bug in one of the programs that deals with sequenced DNA and inject executable x86 code into the computer's memory that then causes it to insert that DNA into something that's then going to be synthesised... producing an organism that contains the computer virus in its DNA and might will then, eventually, be sequenced again...
But if that were actually possible, it probably would've happened already! At the very least, some DNA sequences would cause a crash, and then the bug would be fixed. But if it weren't... it's theoretically possible for a gene to evolve that uses that. Wouldn't that be cool? (But yeah, that's never going to happen.)

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text:
Identification of an insect (?)
This one was found in the woods of northern Poland. It was about 5 cm long and crawling pretty dynamically. For me it seemed a little too big for a butterfly larva.

What is it called?

Related: What kind of creature is this?

It's an  elephant hawk-moth, Deilephila elpenor. Here is an image from Wikipedia to compare with:

Agreed; that's definitely it. Since OP saw it in Poland I don't know if a (British) 20p will be helpful for scale; for non-UK readers, the coin is 21.4mm in diameter so size is spot-on.

I think it is the larva of the sphinx purple butterfly.

Size of the larva is arround 70 mm

I haven't heard it called that before but from the photo it sounds like this is an alternative common name for Deilephila elpenor. Nice photos!


text:
Why bananas accumulate a radioactive isotope of potassium (K40)?
A quick google search reveals many pages that intend to calm consumers down and assure them that quantities of radioactive potassium in bananas (K40 isotope) is not sufficient to be concerned about, e.g. http://www.raw-food-health.net/Natural-Radiation.html. I am not worried that bananas may be harmful, but I wonder if bananas are actually enriched in K40 relative potassium in soil? Maybe bananas are not enriched, and so every potassium-rich food is equally radioactive... but if specifically bananas are particularly enriched in K40, then what is the mechanism of this process?

The reason, at least suggested for other food, is a high potassium content in general. In the last paragraph (on wiki), you might find that plants w/ high potassium content are also likely to have a high content in radium...perhaps K+ transporters / uptake mechanisms have a slightly higher affinity for Ra2+ as well ?


text:
What are the consequences of drinking water with food?
Does drinking water with a meal release lesser energy/glucose into the blood stream due to a diluted digestive mixture ?
For simplification : If a person eats 100 grams of cooked jasmine rice with no water in take, when digested in 90 minutes  releases, say, a 100 calories. Then, if  the person eats 100 grams of cooked jasmine rice and drinks 50 ml of water along with it (during/after) (basically, halving the power of the digestive juices) then will the energy released be 50 calories ?

Cooked rice or dry rice? Cooked rice absorbs water, so even if you didn't 'drink' any water, you still would have ingested it.

@XaNaX edited question

A moderate amount of water while eating will not dilute digestion
...according to Michael F. Picco, M.D. and the Mayo Clinic:

There's no concern that water will dilute the digestive juices or interfere with digestion. In fact, drinking water during or after a
meal actually aids digestion.
Water and other liquids help break down food so that your body can
absorb the nutrients. Water also softens stool, which helps prevent
constipation.

Water, after all, is the "universal solvent" which should help break food and organic materials down further.
Effect of Stomach Acid Dilution
This is a total myth, especially if you consider it from totally a chemical perspective.  Stomachs secrete about 400 to 700 mL of gastric acids per meal. Just to be conservative, let's say 500 mL.  Also, the average stomach has a pH of about 2.  Now let's look at the formula for pH and what the effects of adding water might be:
pH = log(1/(mols/volume))
2 = log(1/(mols/0.5L))

Now solve for mols, and we get mols = 0.005
Now let's assume our meal contains about a quarter of a liter of water in it.  We'll also assume that our food is completely pH neutral.  This is probably a little high on water concentration, but let's see its effect on our stomach's pH.
Since it has a neutral pH, the mols does not change, but our volume does (0.5L [previous contents] + 0.25L [from the food] = 0.75L).
pH = log(1/(0.005 mols/(0.5L + 0.25L)))

Now solve for pH and we get pH = 2.18.  No problem here, since normal digestion occurs between a pH of 1.5 to 3.5.
Finally, let's say we drink a lot of neutral pH water with our meal now.
pH = log(1/(0.005 mols/(0.75L + 4.25L)))
pH = 3

So we are still within a normal pH of digestion, even though we just drank over 4.25 liters (~1.12 gallons) of water with our fairly liquid meal of 0.25L!  We would need to drink about another 45 L of water to knock our gastic pH above 4.  But don't worry, we would die of water intoxication well before that ever happens.
Furthermore, our stomachs (and digestive tract) are incredibly good at adapting their secretions to the consistency of a meal.
Water and Speed of Digestion
Perhaps another way that water may change caloric intake is to increase the speed at which solid foods exit the stomach.
This is thought to reduce the meal’s contact time with stomach acid and digestive enzymes, resulting in poorer digestion.
As logical as this statement may sound, no scientific research supports it.
A study that analyzed the stomach’s emptying speed observed that, although liquids do pass through the digestive system more quickly than solids, they have no effect on the overall solids’ digestion speed.
Bottom Line
Water during meals should not decrease the amount of calories absorbed.  With all that being said, digestion is a very complex system, and there are still many unknowns as well as individual responses.  Before making drastic changes concerning your health and digestion, you should consult a medical professional.  This answer should in no means necessary replace any medical advice or treatments, but rather aid in your understanding of how digestion works.
A Final Word of Caution
I feel obligated to include that however you found this question/answer, staying hydrated to aid in digestion is a very healthy function, especially in considering weight loss and 'feeling full for longer.'  However, obsessive water consumption aimed at decreasing food consumption/appetite ("fluid loading" or "water loading") is a common symptom of eating disorders.  If this is a concern for you or someone you know, please, seek professional support and help.

Sources:

NCBI - Adaptive Secretions

NCBI - Digestion Speeds

www.mayoclinic.org

water.usgs.gov

Thanks for answering. I am more interested in know if somehow (say by drinking half a litre of water) I am able to dilute digestion - will the process of digestion release only half the energy (carbs/fats/etc) from the food ?

@happybuddha no, drinking water will not decrease the amount of energy released from food by digestion. Any excess water will simply be absorbed by your body. There are no magic tricks.

I would suggest removing/rewording the last few sentences of your "Bottom Line" section - that's bordering on medical advice, which is off-limits on this site. If you are going to keep it, please add some supporting citations to show that the majority of acid reflux cases improve with more stomach acid. You also need to support your statement that one should delay drinking water until after a meal - neither one sounds scientifically accurate.

Now edited.  I originally included that part as a way to indicate this answer should not be interpreted as medical advice and there is anecdotal evidence (albeit, no peer-reviewed articles from my cursory search) suggesting the contrary - that water during meals has impeded their digestion, such as perpetuating their acid reflux.  Apparently this inclusion did the opposite of my intention.  These edits now directly state that this answer is not medical advice.

@MattDMo I am not looking for magic tricks - just a definitive answer !


text:
Drug and antibiotic resistance in organism
Out of gram positive or gram negative or both which one is having a higher resistance to drug or antibiotics? How the organism gains that gene for drug or antibiotics resistance.? Kindly explain it in detail.

This is basically a homework question (simple question without any effort to solve it yourself), you are lucky that this slipped through. It is also kind of broad. Please do some research yourself in the future and state what your problems are.

@Chris it can still be downvoted and closed as homework, even if it was answered. These kinds of "do all my work for me" questions are unacceptable on this site.

@MattDMo Correct point. It will not disappear, though.

Sorry people.. !!  I'll not do it again..!!

The major effect of drugs or antibiotics on bacterium is on its cell wall.
Gram positive bacteria have a thick outer layer of a polymer called peptidoglycan (formed by repeated units of a disaccharide: NAG-NAM) which has many cross-linkages. Beta-lactam antibiotics such as penicillin, cephalosporin etc. competitively inhibit an enzyme called transpeptidase (also penicillin binding protein); which forms the cross-linkages in peptidoglycan; and thus weakening the cell wall. As a result of which osmotic pressure now becomes enough to cause lysis of cell wall and hence the bacterium dies. Also drugs such as Vancomycin inhibit the formation of peptidoglycan polymer.
On the other hand, gram negative bacteria have an outer layer of lipopolysaccharide (endotoxin) beneath which lies a thin cell wall of peptidoglycan. Hence beta-lactam antibiotics do not have much of an effect on the gram negative bacteria.

To conclude, gram positive bacteria are much more sensitive to beta-lactam antibiotics and lysozyme than gram negative bacteria. Also it is worth mentioning that gram negative bacteria are more sensitive to the lytic action of anti-bodies because lipopolysaccharide in their outer membrane produces a high immune response (read about Sepsis for more details on endotoxin).
Hope this is helpful.

Yea thank you.. simple and good explanation...!!

Is there any drug or antibiotics which can be effective for gram negative organisms?

Yes. Gram negative bacteria are sensitive towards detergent like antibiotics which dissolve the outer membrane. Example- Polymyxin disrupts the integrity of the outer membrane (but it has some toxic effect too).

Hey, remember there are many other ways to inhibit the bacterial infection which do not involve degradation of bacterial cell coat.


text:
Is Melanin a PCR Inhibitor?
I have been growing B16F10 Mouse Melanoma cells. I need to extract the genomic DNA and do PCR to amplify a specific region. However, no matter what temperature or magnesium concentration I use, I have no luck.
I obtained mouse DNA from someone who was genotyping mice. I tested the PCR oligos with that DNA, and the reaction worked, so it's not an oligo problem.
The genomic DNA had poor 260/230, about 0.6. I thought the EDTA levels may have been high, so I did an isopropanol precipitation to clean it up. This made the 260/230 ratios about 2.1. But the PCR still didn't work.
What I had noticed during the precipitation however was that the DNA pellets were gray to black. I assume this is melanin, because the cells are melanoma cells, and turn black.
Could this melanin be a problem in PCR?

Melanin is a potent inhibitor of PCR - when you use B16 cells (or any other cell line that produces melanin) you have to purify your sample from it. Unfortunately a simple Phenol-Chloroform extraction or an ethanol precipation won't do the magic, since melanin co-precipitates with the nucleic acids.
I recommend following the following paper: "CTAB–Urea Method Purifies RNA from Melanin for cDNA Microarray Analysis".
The protocol derived from the paper can also be found here.

just use a protease to break the melanin

@4DNeuron Have you ever tried this? Besides this, melanin is not a protein.

I don't have much expertise in PCR (so please do not ask me technicalities). A research has proven that melanin is a PCR inhibitor as it forms complexes with thermostable DNA polymerase and inhibits its activity, thus inhibiting PCR. See this paragraph below:

We found that both RNA and cDNA preparations derived from melanocytes contain a RT-PCR inhibitor that copurified with nucleic acids. Investigation of the candidate inhibitor melanin revealed that it potently blocks PCR at concentrations below 200 ng/ml, whereas 100 microg/ml melanin was required to inhibit reverse transcription. Melanin and thermostable DNA polymerase preferentially formed a distinct complex with reduced migration velocity as compared to pure polymerase in nondenaturating polyacrylamide gel electrophoresis. Our findings demonstrate that melanin is a potent inhibitor of thermostable DNA polymerase in vitro and that the inhibitory effect is conferred by a direct and reversible polymerase-melanin interaction.

The same paper also gives a solution to your problem as:

The inhibition of the enzyme by melanin could be reversed by diluting solutions of preformed complexes or by adding excess amounts of other proteins such as bovine serum albumin or dry milk.

Reference: http://www.ncbi.nlm.nih.gov/pubmed/10814530

Thanks, I'll take a look at the paper, and maybe try adding BSA to the PCR mix. I have no idea how concentrated the melanin is, but if it's concentrated to turn the sample black, it must be pretty high.

Yup it makes sense. I hope it'll work, else you can also try the method suggested by @chris.

There are many suggestions how to avoid melanin-caused PCR inhibition. Some we have found helpfull (like using smaller amount  of DNA sample + increasing number of cycles or adding BSA to PCR reaction), other (like trying different DNA isolation and PCR kits, purification columns etc.) are good only for profits of biotech companies. The solution is in fact very simple: using proper procedure for DNA isolation.
Rutinely we prepare DNA using high-salt lysis buffer (250 mM EDTA, pH 8,5, 1% SDS and 100 ug/ml proteaseK) and, after incubating at 50°C, single extraction step with phenol/chloroform, followed by precipitation with 1 volume of EtOH (not more, otherwise you precipitate EDTA). Under these conditions melanin remains with DNA.
For samples containing melanin we include one extraction step with phenol only before phenol/chloroform extraction. Melanin gets extracted into water/phenol interphase and falls throught phenol during centrifugation; this does not happen when you extract with phenol/chlofoform mixture. For efficient melanin extraction the high salt is important. If you need to eliminate melanin from ready-made DNA samples, add LiCl to 2M concentration and extract with phenol.


text:
Alignment of sequenced fragments in Next Generation sequencing (sequence assembly)
The NGS (Next Generation Sequencing) involves fragmenting the DNA to be sequenced. This is followed by attachment to beads or flow cells and then a localized PCR is conducted. Modified bases are added and with addition of each base, a detection is made (by fluorescence for instance) for the type of base bonded. After complete sequencing of all the fragments, how are these reads of fragments assembled in the way they were in the original non-fragmented DNA? (in short: How sequence assembly works?)

There are different methods of sequence assembly. To get an overview you can read this: http://www.nature.com/nrg/journal/v14/n3/full/nrg3367.html

Possible duplicate of What exactly are computers used for in DNA sequencing?

Assembly and alignment are generally used to refer to two different algorithms that work in two different ways.
Alignment takes your sequence fragments, and compares them to a reference genome, and tells you where that read aligns and how closely it aligns.  For a while, popular aligners used Burrows-Wheeler transform algorithms to make special indexed versions of the genome, this made alignment to the index far faster.
Assembly is when you have no reference, and use the overlap of the reads to build large contigs.  For a while De Brujin graphs were a popular algorithm for that.


text:
Retrieve all predicted cds from NCBI
Please apologies if this has been answered somewhere else, but I couldn't find an answer to this problem.
I would like to retrieve all the predicted coding sequences on the NCBI ftp for a given species. Let's say my interest species today is Stegastes partitus and that I go here. I know how to get all the predicted mRNAs (./RNA/Gnomon_mRNA.fsa) or all the predicted proteins (./protein/protein.fa) but I cannot find how to get the CDS... if ever it's possible? This can be done on the Ensembl FTP.
Thanks for any insight!

EDIT: The output would ideally be a multifasta file like this:
>Stegastes_partitus_gene1_cds
ATG(.................................)TAA
>Stegastes_partitus_gene2_cds
ATG(.............................)TGA
>Stegastes_partitus_gene3_cds
...

One QA site, which specializes on detailed bioinformatics questions is biostars.org

I'm downvoting because the readme file already tells you that the GNOMON folder should contain the files you want.

The GNOMON and the GFF folder. As per as the text mining goes, you can use excel and awk...awk is more of a stackoverflow question...but I don't think you are on linux.

@Koustav Pal So you're downvoting because you know the answer? You could at least provide a proper answer ;) Thanks anyway! PS: I'm on Linux, which does not mean I know everything of text mining -- hence my question.

My point is, read the readme. I didn't even read the readme, I only did a ctrl+F for CDS and found out that they were inside the GNOMON and GFF folders

The GNOMON and GFF folder contains the files you want, the GNOMON if you check the README relates to the GNOMON gene predictor and the GFF I think links back to the same file. I think the file you want is ref_Stegastes_partitus-1.0.2_scaffolds.gff3.gz which contains the coordinates on the scaffolds.
And as you stated you are on linux, so the best and geeky way to go is awk.
awk '!/#/{if($3=="CDS")print}' ref_Stegastes_partitus-1.0.2_scaffolds.gff3 > SomeFile.gff3

UPDATE

This part is from python. With reference to the previous user's answer if you fetch the GBK file, rna.gbk, this should allow you to fetch CDS using biopython
You should also check out Peter cook's tutorial on handling genbank files in python
from Bio import SeqIO
from __future__ import print_function

Genome = SeqIO.parse("Examples/rna.gbk","genbank")
handle = open("Examples/rna.faa","w")
for genes in Genome:
    i=1
    for Feature in genes.features:
        if Feature.type=="CDS":
            FASTA=Feature.extract(genes.seq)
            print(">"+genes.id+"_CDS_"+str(i),file=handle)
            print(FASTA,file=handle)
            i += 1

I would recommend that you install anaconda, it is a package management software, which when installed installs its own python version and alongside it installs some 400 different packages. Instructions are available on the link. So these packages should come with the link.
After you have installed anaconda, put all that code from up there into a Myfile.py and execute on the command line with python Myfile.py.

I cannot upvote (not enough rep), but +1 anyway. "I would like to retrieve all the predicted coding sequences on the NCBI ftp for a species." --> we're getting closer! :)

do you mean any species?

Yes, for instance this one (Stegastes partitus). (See my edit)

CDS are a bit different, because this particular annotation is provided with GFF files on the genomic coordinates. And the genomes themselves have many versions in different stages of assembly primarily contig, scaffold, assembled chromosome with unknown chromosomes, but the files should be inside ./GFF/ and the name will change according to version and stage of assembly of the genome the gff file relates to

Ahh so you want the sequences!

Yes! Apologies if this was not clear.

check the edits

Brilliant! Many thanks :) And indeed, Peter Cock's webpage is really helpful, I'll keep this in mind.

The RNA folder of your link provides several annotated file formats. These include reference to the CDS for every transcript.
Stegastes_partitus/RNA/
Download and unzip the rna.gbk.gz file and open it.  You will see CDS location information for every entry.

Yes but this does not provide an "easy" access (such as a multifasta file) to all the cds of this species.

No, true. That would require some text mining skills, but would be pretty easy for someone that has that expertise, if you had them or knew someone that did. I'm just a hack.

A web-based way of getting this data:

Go to the NCBI Assembly page: https://www.ncbi.nlm.nih.gov/assembly and search for the species of your interest. Here, the query would be something like "Stegastes partitus"[Organism] which would return only one hit that is the latest reference version of the assembly. Since there is only one hit, you are directed to the 'Full Report' page by default. Click on the link at the top left corner and change the 'Full Report' format to 'Summary'
At this point, you will see a 'Download Assemblies' button. Click on that, choose the data source as RefSeq and file type as 'CDS from genomic' and you are good to go!

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


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How to confirm pure-breeding parents
I was reading Genetic Analysis (Sanders, Bowman) and saw the following figure summarizing the 1909 work of Herman Nilsson-Ehle in describing the genetic control of kernel color in wheat:

How did Nilsson-Ehle determine that the original pure-breeding parents were in fact homozygous for each allele?

Welcome to Biology.SE. They were probably inbred lines for many generations.

If they are "pure-breeding", that means that they are homozygous.  If they were heterozygous, the offspring would not all have the same color as the parents.  But tree-breeding" means they all do.

These genes are additive. No dominance relationship is assumed to exist between allele $A_1$ and $A_2$ or between allele $B_1$ and $B_2$.

In Campbell Biology (2021) 12th edition it says that
"True-breeding" (or pure lines) can be verified over many generations of self-pollination. If they produce only the same variety as the parent plant, then they are homozygous.

There are more complicated situations, such as if being homozygous at a locus is fatal. You then end up with pure-breeding heterozygotes.


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Does Human being have potential to perform parthenogenesis?
Wikipedia says:

Parthenogenesis can occur without meiosis through mitotic oogenesis. This is called apomictic parthenogenesis. Mature egg cells are produced by mitotic divisions, and these cells directly develop into embryos.
In 1936, Gregory Goodwin Pincus reported successfully inducing parthenogenesis in a rabbit. In April 2004, scientists at Tokyo University of Agriculture used parthenogenesis successfully to create a fatherless mouse.

Since human is mammal,does not the success of the experimentations hints at the possibility of parthenogenesis in humans,naturally?
If not,why is  parthenogenesis not possible in human beings?

'Possible' is a tricky word here. There are a lot of things that are possible that just don't happen, because they are so exceedingly rare; or that happen but are unknown because they are hard to spot.
As it happens, we know that parthenogenesis-like effects can be induced in humans, because we've done it. If you remember the cloning debacle around Hwang Woo-suk, it turns out that while he didn't clone anything, he did manage to induce parthenogenesis, so … good for him, I guess?
Whether or not it happens in the wild… we just don't know. It's possible that it does, but it's really difficult to look for, since women have sex and then subsequently have babies, and a vanishingly small proportion of them are ever DNA tested; so even if one in every one million live births (which is a lot) were the result of parthenogenesis, we might never, ever know.
Basically, it's definitively possible with external meddling; it may or may not be possible without, and it may or may not actually ever happen.


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In terms of differentiation, how many generations of asexual reproduction, will usually be equal to 1 of sexual?
As far as I understand, in sexual reproduction, there is a mix of 50/50 genes from parents. In how many generations of asexual reproduction, will offspring reach differentiation level that of sexual one ?

Welcome to Biology.SE!
Clarification of the question
It is unclear what you mean by differentiation? I will assume that the question is

For what value of $n$. is the number of pairwise differences between any two siblings under sexual reproduction is equal to the number of pairwise differences between any two $n^{th}$ cousins under asexual reproduction?

Answer
The answer to this question mainly depend on (1) the mutation rate and (2) the amount of genetic variation present in the sexual population (which itself is a function of the mutation rate).
Assuming a panmictic population of constant size $N$, assuming equal sex-ratio and non-overlapping generation (and a few other assumptions), we can make some estimations. Let's assume that the sexual and asexual populations that we are comparing have the same mutation rate $\mu$.
Sexual population
Using coalescent theory, one can show that the expected number of pairwise difference between any two individual in a sexual population is $4 N \mu$. It would be off-topic to explain why this is true. I let you open a population genetics book and/or open a different post.
Asexual population
Assuming an infinite site model (just like coalescent theory does), the number of pairwise differences between $n^{th}$ cousins is $2 n \mu$.
Comparison
Let's set the equation
$$2 n \mu = 4 N \mu$$
and solve for $n$, we get
$$n = 2 N$$
In words, $2N$ cousins in asexual populations have the same number of pairwise differences (on average) than two sibling in a sexual population of size $N$.
Remarks
Please note that the conclusion is drawn from important (but common) assumptions. Note also that drawing conclusions from the above calculation such as "sex helps retain genetic diversity" would be wrong, as we are comparing sibling to $n^{th}$ cousins and not randomly chosen individuals in the population.

excellent answer, thank you. The reformulation is good


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What made *silphium* difficult to domesticate?
I tried this question at Worldbuilding SE, and was told that perhaps this place would give me a better chance at an answer. So, leaving aside the worldbuilding aspects of the issue, I am interested in the now-extinct plant called silphium, which was widely used as a contraceptive in the Classic world, and was overharvested into extinction at the beggining of the Middle Age, being apparently non-domesticable.
So, why exactly was it non-domesticable? Was it actually non-domesticable, or its domestication, like that of strawberries, just depended on some techonolgical innovation that was not available at the time it become extinct? If it was really impossible to domesticate, what measures could be taken, in a pre-industrial society, barring it not being used as contraceptive, to at least protect it from extinction?
More generally, what factors lead a plant to being non-domesticable?

Welcome to Biology.SE. From wiki: we cannot even accurately identify the plant we cannot know for certain whether it is extinct. and The cause of silphium's supposed extinction is not entirely known. Because we know nothing about this plant (but the name people gave it in the middle age), it impossible to make much speculation. I am voting to close for this reason.

The factors that make anything hard to domesticate rely largely on factors that make it difficult to artificially select domestic traits. Perhaps it was long-lived or germinated infrequently, or needed a different kind of space or environment than the people at the time were giving it, or had some other unseen condition that civilization at the time wasn't able to rescue. For example, it's hard to domesticate elephants because they only birth every 5 years and sexually mature after about 15 years. By the time you select for a trait, you may very well have died many times over!

Have you found any reliable sources for this plant's existance? The wikipedia page seems to be from that era when wikipedia wasn't exactly trustworthy... Note that there are many extant species going by the name of "Silphium" [wiki ; article].


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Length of anopheles chromosomes?
Where can I find the length of each anopheles chromosome? I've obtained data in which the length of each 2L chromosome for several anopheles is 39101648. I'm looking for an article that gives the length of 2L so I know my output is correct.

I came across this paper (Holt et al. 2002), does this answer your question? Look at Table 2 and 3. In this paper the lenght of 2L is  52393056 bp.


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Why is black eumelanin black even though it consists of black AND brown molecules?
In dogs,eumelanin consists of molecules of DHI and DHICA. DHI and DHICA are made from dopachrome. DHI through DHI oxidase and DHICA through DHICA oxidase also known as TYRP1. When TYRP1 has a mutation through which it loses its function, mostly DHI is produced which gives brown eumelanin.
Now, if TYRP1 is functional, are both DHI and DHICA produced? If no, why not? If yes, why does the eumelanin appear black and not a dark brown?


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How to get the average number of pairwise differences among populations?
I have genetic data in .structure and .vcf format (and can easily reach other formats with PGDSpider). The population of interest is structured and I would like to calculate the average number of pairwise differences (over a given window) between any pair of populations.
Is there an existing tool that would do it?

With relation to the other bioconductor question I would point you towards these packages;

VariantAnnotation: Provides functionality for reading and manipulating vcf files.
GenomicRanges: Provides functionality for creating genome intervals. Also provides overlap functions for calculating overlaps between various ranges.
rtracklayer: Allows you to easily change formats between different biological file formats.
AnnotationHub: Makes many common and uncommon annotation files available in the R terminal in various formats such as TxDb, OrgDb etc. etc.

Here's a tutorial very similar to what you are asking for. It utilises some of the packages mentioned above. Principally, AnnotationHub, GenomicRanges and VariantAnnotation.
If you want the manual of these packages, they are available on the linked pages.


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Did the Hela cells leave John Hopkins
Did John Hopkins let people outside of the university use the Hela cell-line that was isolated from an immortalised cervical cancer?

Perhaps more biology-inclined people know what those are, but I personally do not... Could you expound a bit on what those are and what they were used for?

The HeLa cell line is fairly famous - I think 'Hela cells' is enough to identify the line. The Wiki is here: https://en.wikipedia.org/wiki/HeLa

If you are interested in learning more about HeLa cells, there is a very nice book : The immortal life of Henrietta Lacks which tells the story of life of Henrietta and also of the cells

Cultures of HeLa cells are used in many labs around the world, and were widely shared from very early on. From the Wiki:

In the spring of 1953, a cell culture factory was established at
  Tuskegee University to supply Salk and other labs with HeLa cells.

It may be worth noting -- since many non-biologists seem very unclear on this point -- that HeLa cells were not the first immortal cell line, and they have not been unique for many decades since there are now tens of thousands of human immortal cell lines

But it should be noted that HeLa cell line is very easy to grow compared to other cell lines. In fact there was a period just after DNA finger printing became affordable, that  researchers realized just how easier it was for HeLa to grow. Many cell lines turned out to be contaminated by HeLa or were HeLa (as the HeLa cell had outgrown the cells of the original cancer line).


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Why we need an egg cell donor and a surrogate mother in an organism cloning process?
Could a whole set of artificial organism-cloning process only be operated on the  somatic nuclear donor ,which means for example ,can we extract the somatic nuclear from animal "A" and put it into the egg cell plasma also from animal "A"  then implant it into the animal"A"'s uterus to clone "A" ?

Could a whole set of artificial organism-cloning process only be
  operated on a somatic nuclear donor?

No, this would not be possible. Single-cell reprogramming would enable you to reset the potency status of that cell up, yielding an embryonic stem cell (ESC). However, ESC do not have the ability to generate extra-embryonic structures (e.g. placenta), which are known to be required for providing oxygen and nutrients to the embryo, amongst other relevant functions.
Theoretically, it could be possible to replicate the embryological environment, and I think this is the second part of your statement. Nevertheless, in practice this is not possible... the amount of signals and parameters that one would need to control simultaneously is far too extensive.
I don't quite see the point of having an enucleated egg and performing somatic cell transfer, when you're not really interested in implantation in utero. Somatic cell reprogramming would be sufficient (see iPSC)

thanks ! Now I gain some new knowledge now , but there is a little bit misunderstood , what I mean is that ,for example ,if we get a somatic cell from animal "A" , can we just transfer that cell to animal A's uterus to clone animal"A",instead of finding another surrogate mother or egg cell donor?

@Snake From your comment and your newly edited question I see what you mean. You are wondering whether it is possible to clone an animal by using its own somatic cells AND eggs.
I do not have extensive experience with transgenic production, but I have a hypothesis on why the same female is not used as a donor and for implantation: oocyte extraction is an invasive method that may be destructive (i.e. the donor female dies). Therefore, it is not possible to use the same female and a foster mother is required.

the trick is ovum come with a whole package of signal pathways built in before fertilization that you need to trigger implantation and embryonic development. In theory you could engineer these (search artificial ovum)  but it is drastically easier and less expensive to just use existing ovum organisms produce for essentially free.
could you use ovum and somatic components from the same organism that is the surrogate mother, sure, but there is not much reason to do so. You still need a donor egg and surrogate mother they just all happen to be the same individual.


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How does a spider's legs not get caught in silk when wrapping prey?
When a spider catches a prey, it wraps it up in silk. It uses its legs to do this. So how does its own legs not get stuck on the silk?
Note: I'm not talking about walking around the web. There are non-sticky anchor strands of silk to walk on. I'm talking about when the spider actually wraps something up.

There are two parts to this answer.
Spider Legs
First, I would like to mention that spiders avoid sticking to their webs by more means than just non-sticky anchor strands to walk on.  To help keep the glue from sticking to their legs, an oily substance apparently covers spider legs.  Furthermore, the same study found that:

In addition, Eberhard and Briceno also noted that the spider’s gait seemed specially designed, such that it “reduced the area of contact between the sticky droplets and the setae [spiny leg hairs].” This, combined with the fact that the thread touched many (rather than only a few) branching hairs, made it very unlikely that any glue would slide all the way down the hairs to make contact with the main part of the leg – which would have made permanent adherence more likely.

Spider Wrapping Silk Fiber is Different
The main reason spiders do not get stuck to their silk when wrapping prey is because wrapping silks are different from silks used to make webbing.  There there are seven known types of silk that spiders can produce.  Aciniform, or wrapping silks are the strongest silk from a spider and specifically designed for wrapping.  This silk is typically dry, and does not contain the high amounts of N-acetylgalactosamine which give the distinctive quality of being sticky.   For a very detailed study on wrapping silk architecture, please see this recent study from 2015.

There there are over seven types of silk that spiders can produce. So does that mean there are 8 forms? Please be precise. I assume you are taking this information from your last link, which states Spiders can produce up to seven types of silk [...] in the first sentence of the introduction.


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Is it okay to scale the RNA-Seq counts after log-transformation?
On an RNA-Seq dataset, I want to apply a clustering algorithm which requires zero-mean uni-variance gene expression levels. I am wondering whether it makes sense to use "scale" function in R after taking logarithm of the counts. For microarray data, I was actually using the scale function which (as far as I know) makes sense; but this is the first time I am using RNA-Seq. I heard about "voom" normalization (in "limma" library on CRAN), but I don't really want to use that since I am not really familiar with the details.

What are the datasets; different samples? The analyses and the statistical procedures that you use depend on what kind of data you have. There are several (infinite) distributions that can have 0 mean and 1 variance. The question is, what is your expected distribution i.e. the null model. Certain data are known to follow certain models. So the question boils down to what is your data.

My data is gene expression data and the algorithm assumes a zero-mean uni-variance Gaussian distribution.

So you just have one sample? Technically, the different genes are different random variables. Moments like mean and variance are for one random variable. Comparing different genes is like comparing apples and oranges. Moreover, the expression of all genes is not expected to follow gaussian. For more details see this post.


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What does curated gene mean?
I see in databases "curated" or "not curated" for genes. What does that mean?

https://www.google.fr/#q=curated+genes

Welcome to Biology Stack Exchange. Could you provide an example of a database where genes are classified this way?

Thanks! For instance: http://www.wormbase.org/species/c_elegans/gene/WBGene00009562#0-9g-3
I also saw some genes that mentions as "not curated"

"Curated" is mostly synonymous with "manually curated", which means that these genes have been experimentally validated. Most non-curated genes are just predicted by a software.

In Bioinformatics, the term "curated" indicates that the information has been validated either experimentally or using predictions from a software. Often the manually and experimentally curated sections are more dependable than the ones by software. When a gene is curated, it means certain desired information about the gene such as its location on the chromosome, its function, the proteins it encodes for are known.

Welcome to BiologySE... thanks for your contribution, but can you please add some links/citations that back up your claims? We always appreciate references on the site and it will increase your reputation much more than comments/answers without any citations/references.


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Interchromosomic vs Intrachromosomic Recombinations
What is the difference between interchromosomic and intrachromosomic recombinations?
I did a research about them and saw some videos (e.g. this and this) with animations on YouTube. But I'm still lost between them and can't differentiate between these two expressions.

Welcome to Biology.SE. It always help to show what you found. Linking to the youtube videos you've watched would be could.

The link should be added in the question (using the 'edit' button) not in a comment and especially not as an answer. I edited your post to add the link. You can now delete your comment and your answer.

The prefix inter- means "between two or more", and the prefix intra- means "within one".
So interchromosomal recombination means recombination between two different chromosomes (for example, it normally and often occurs between each homologous paternal and maternal chromosome pair during the Prophase I stage of meiosis).
Intrachromosomal recombination would mean recombination within a single chromosome.

Thnx alot beautiful explanation


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C to T Transition Mechanism
I am seeing C to T transitions in my sequencing data, but also some strange signatures that follow along with that. I am trying to understand the biology of what is occurring. In the data I see more C to T changes than G to A changes, when it would be expected that these numbers would be relatively the same.
So, in vivo when a C to T transition occurs, does the complementary base get changed to ensure watson and crick binding, or will you end up with a T-G pair? This would explain the phenomenon that I am seeing but I don't know if this happens. (Andy references would also be super helpful. Thanks.)

Depending on how your sequencing data is being presented to you, this may not be an issue. Are you looking at FASTQs, BAMs, VCFs? In my experience (human resequencing), variants are generally reported from one strand instead of both -- that is, a variant, which really causes two paired bases to change in tandem, is represented in the results by just a single letter change. When a C to T transition occurs, I would assume it's a C-G pair transitioning to a T-A pair, unless your biological or sequencing situation is unusual somehow. Give us a bit more detail about your file format and sequencer.

You have not told us what kind of sequencing data you are using, for example in bisulfite sequencing you change non-methylated C to U which are read as T. The context is very important here.

@KoustavPal This is deep genome sequencing from an Illumina 4000.


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Are our ears more sensitive to low or high pitched sounds?
I am a Physics student who also love music and learned a little bit about Medical Physics. I know that the basilar membrane in the cochlear duct enables us to distinguish different frequencies. The different parts of the basilar membrane have different resonance frequencies and this leads to frequency dispersion.
I've also learned that the pitch of a tone is determined by the fundamental frequency, and the overtones just add timbre to the sound, and are difficult for common people to hear separately.
I think the above implies our ears are more sensitive to lower frequencies. However, this is obviously not true when we listen to a symphony, in which I think most people are more "sensitive" to the higher parts. And I think this is the reason while the melody is usually in the highest part in a song.
So I am confused. Are our ears more sensitive to high frequencies or lower frequencies? Is there a biological explanation of why we usually tend to hear the highest-pitch part of a piece of music?

Short answer
Our ears are most sensitive to the mid-frequencies.
Background
There are different ways of assessing sound level. The physical one simply determines the physical sound pressure level (SPL) in which all the frequencies weigh equally. This is referred to as C-weighting and is expressed in dB SPL.
Our ears, however, are most sensitive to intermediate frequencies, peaking at around 4 kHz (Fig. 1). The frequency weighting that takes this into account is dBA weighting.
The reason why we are most sensitive to mid-frequencies can be sought in the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.

Normal equal–loudness-level contours for pure tones. source: Duncan (1996)
Reference
- Duncan, High Performance Audio Power Amplifiers
For Music Performance and Reproduction (1996): 1-18

Maybe "high middle" frequency  , as I remember middle "C" is 512 Hz.


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Learn Bioconductor the hard way!
I came to analyzing population genetics data from the background of a theoretician and a computer biologist but not with the standard tools that a bioinformatician (or empiricist in population genetics) know of. I have a fairly good knowledge in R and in programming in general.
I am looking for a course/tutorial for learning bioconductor (and other R tools for analyzing genetic data). A course/tutorial that is short, dense and assumes the user has good knowledge in programming. I am happy with both a video or a written tutorial although I would slightly prefer a written tutorial. I typically aim at analyzing data on structured populations such as the average number of pairwise differences among population, or graphing the site frequency spectrum per population, etc..
There are a fair number of such tutorials. Can you please give me recommendations?

bioconductor is a source for packages, You can ask for tutorials to bioinformatics packages in bioconductor, those would be the vignettes. But, I don't understand what you mean by tutorials for bioconductor. Of the top of my head if you have population genetics data, then most probably you are dealing with normal distributions. There are statistical packages which are far more robust than most packages on bioconductor. This question is a bit unclear as to what you want to do and what sort of data you have.

I recommend the DESeq2 tutorial at:
http://www.bioconductor.org/help/workflows/rnaseqGene/
I think this is a good start for you because:

DESeq2 is a very popular package. You'll learn how exactly a bioinformatician works.
The workflow starts from alignments, and show you how to connect command-line tools with the R-package
It shows you how to generate MA plot, PCA plot etc. You'll appreciate how easy to do such things in R.
Testing for differential gene expression is very important
You'll learn how R does the programming. For example, in R it's a good idea to create a data set object, and do something like this:

obj <- .... # This is my R-object
obj <- fun1(obj) <- # Function 1 adds information to the object
obj <- fun2(obj) <- # Function 2 adds more information to the object

I'm not able to fix the format. Can someone help me?

I tried to fix the formatting, but the formatting looks bugged.

@bli Sorry, I tried to answer the question as best as I could, but I somehow screwed the formatting.

I mean, it doesn't seem to be your fault that the formatting is screwed: Normally, 4-space indentation works and it seems to me you did it right. Or maybe code-formatting is not expected to work after listings ?

@bli Yeah. I was trying to do code formatting, but I couldn't get it working...

It seems to be happening because of <. Don't know why. Possibly because it indicates the beginning of xml/html tags.


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Do other young mammals turn their backs to their parent when upset?
I have noticed that upset toddlers turn their back to someone who wronged them and huff. Most adults don't do this, so I don't know how this could be a learned behaviour. Do other animals express this behaviour? I do not see how this could be specific to culture.

Other Primates
Sulking is the behavior you are refering to and it is seen in orangutan, Chimp and Bonobo. Likely in other primates but I am not aware of any published works. I have heard about it in baboons but have not read the papers myself.
Source
Source2
Source3
Source4
Also adult humans DO do this on occasion, it is just often more subtle.
It is amazing how many identical social behaviors are seen in our close relatives, especially the ones about conflict and conflict resolution.

could you provide the citations for these papers directly in your post in case the links die? Also, a quick note/summary about what each states would be beneficial (not even entire abstracts but perhaps even a 1 line summary so people know what they're clicking on). thanks!


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E. coli bioreactor or E. coli fermenter?
I have a Requirements Specification in Russian for a "Fermenter" that would be used for "E. coli cultivation". This E. coli strain would be used to make a generically-engineered drug. The "fermenter" would consist of two "reactors" of 200 and 2000 liters, linked by a "pipeline system for transferring the half-finished product between them".
Would the whole thing be called a "Bioreactor" or "Fermenter", or are the two terms interchangeable here?

I don't think that there is a clear division between bioreactor and fermenter and the terms are often used interchangeably, but they do carry a difference in connotation (and marketing). The term "bioreactor" implies complexity, research driven, and/or maximal cell growth. Bioreactors are more state of the art and are used primarily for studying microorganisms or producing difficult to grow cells or for peak production of cells- while the term "fermenter" implies production of a substance besides or other than just the cells and might have the connotation of utility.  Fermenters also carry a historical connotation of brewing beer, wine, and other fermented food stuffs or materials. Also, it's important to bear in mind that bioreactors are used for fermenting, because bioreacting is not a real word.
If you just need a simple design for producing the bacteria or a bacterial product, then the term fermenter might be more appropriate. If you need computer control, or if you are using it to investigate/research growth and/or production parameters then you could call such vessels bioreactors without the risk of looking foolish. I think the best way to describe the difference is probably by example, but instead, I tried to itemize some of the distinguishing details, as follows:
Fermentors commonly have all or some the following elements: Agitator (of simple design), pH meter, temperature control (jacketed vessels are common), pipes for transferring nutrients, water, etc., and a sampling port (maybe). It may be made out of wood or clay, but if it is made from steel, plastic, glass, or other modern materials, that certainly wouldn't disqualify the term fermenter, but I would probably not call an oak barrel or a clay pot a bioreactor.
Bioreactors generally have the same things as fermenters, but bioreactors also usually have some or all of the following additional elements: oxygen probe, air or oxygen pump(s) and diffuser(s), other gas ports, additional ports/pipes for pH monitoring and control (often a programmable computer controlled pump is used for multiple solutions), electrolyte balance, radial or axial impellors- which operate at hundreds or thousand of RPMs, a vapor condensor (maybe), spectophotometer (for cell density measurements), nutrient processing data, and any variety of data measurement and/or recording is the often the point of interest, or when growth of tricky or finicky cells is necessary (especially like hybridomas, phytoplankton, or perhaps generally eukaryotic cell culturing). Also, there are different kinds of bioreactors like wave bioreactors (often in bioreactor bags on shaker tables instead of having an impellor).

In general, sterility is more important for bioreactors whereas many fermenters (or fermentation products, like yoghurt) can kind of take care of themselves, or a certain "cleanliness" will work. In both cases, steam sterilization is common. Again, the division is a bit blurry, and the terms might be used interchangeably by some people, like a jacket (light) versus a coat (heavy).
So, for your specific example, it would definitely be a fermentation system (not a bioreaction system), but regarding whether to call the vessels bioreactors or fermenters is more of an opinion, I'm afraid; but personally, I would probably say the fermentation system has two fermenters, since the idea is to produce a product and it sounds like they may be simple vessels. However, if the system has on-the-fly computational checks and balances, then I might be tempted to call the vessels bioreactors (if dazzle demands it).
Also, the smaller (200 L) vessel could be called an inoculation vessel without any connotations.


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why did capacity of regeneration decreased in evolution?
When we consider trend of evolution the ability of organisms to regenerate decreased as the complexity of body structure increased.

acetabularia-can regenerate whole body even if 1/100th part of body is left
small pieces of sponges can grow complete individual.
hydra-interstitial cells are totipotent.
planarians-neoblasts are omnipotent
crustaceans-heteromorphosis.
lizard-regenaratetail..........what is the reason you expect for this ?

Evolution made life more and more complex. The more complex the "bodyplan" of an organism became, the more different tissues and cell types it has, the more difficult it is to regrow them.
For example a sponge has about 3 different cell types. If you take a small piece of a sponge, these 3 cell types well still be present and once they grow they can form a whole new sponge.
The more complex you go, the more different cell types you need, and thus the harder it becomes for a few cells to represent a full organism.
It also has to do with symmetry. Sponges have none, cnidarians have radial symmetry, mammals bilateral. To put it simple: if you slice a piece out of a jellyfish like you would out of a pie, it's easy to imagine it can 'close' itself with new tissue coming out of the border tissue, because it's the same tissue as the one you removed. If however you cut of a foot of a human, the cells of the leg won't produce new foot cells, because they are (a lot of different) 'leg cells'.
As for the lizards, they can "regenerate" a tail but it is never the same tail as before, it will always be shorter than the one they lost. Also the tail is still pretty 'simple' (if you can put it that way). If you would cut of a lizards leg it would not regrow...
I hope this has somewhat answered your question!

Well, you right. Still some lizard can grow limbs too if I remember it right

Also, cancer. Larger, more complex animals have to balance regenerative ability with the danger of uncontrolled proliferation. The more stem cells and stem-like cells you have floating around, the more likely one of them is to become immortal in a way you don't want it to. I would elaborate more, but I think the original post is a homework question anyway.

Seriously? I get voted down just for not elaborating more? I thought the answer was useful as it stood...I just figured the OP might not be needing it now that it's been two days. Sigh.


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Why is there a difference in the orientation of my imagined body vs. my physical body?
My Personal Experience
When I visualise a specific aspect of my body, the inner mental image does not seem to be aligned with my actual physical form in space.
What I mean by this is:
Say I identify a pain in my right ankle, and in my imagination I conjure a mental picture of my ankle to help me pinpoint the exact location of the pain ...
... in my mind, the orientation of my body in the mental picture seems to be slightly forward of my actual physical body, and slightly turned or rotated towards the right.
This is a two part question:
Firstly:

Do other people share this experience ?

Secondly

Is there any accepted explanation for the effect ?

My best guess is that it could be related to the lateralization of eye movements accompanying brain activity during different cognitive tasks.
http://www.nlpu.com/Articles/artic14.htm

In 1977 Robert Dilts conducted a study, at the Langley Porter
  Neuropsychiatric Institute in San Francisco, attempting to correlate
  eye movements to particular cognitive and neurophysiological
  processes. Dilts used electrodes to track both the eye movements and
  brain wave characteristics of subjects who were asked questions
  related to using the various senses of sight, hearing and feeling for
  tasks involving both memory ("right brain" processing) and mental
  construction ("left brain" processing). Subjects were asked a series
  of questions in eight groupings. Each grouping of questions appealed
  to a particular type of cognitive processing_visual, auditory,
  kinesthetic, and emotional (visceral feelings). Each was also geared
  to either memory (non-dominant hemisphere processing) or construction
  (dominant hemisphere processing). Dilts' recordings tended to confirm
  other tests which showed that lateralization of eye movements
  accompanied brain activity during different cognitive tasks. This
  pattern also seemed to hold for tasks requiring different senses.
  Looking upwards and the right can indicate imaginative construction of
  a picture.

(snip)

Eyes Up and Right: Dominant hemisphere visualization - i.e.,
  constructed imagery and visual fantasy (Vc).

So my interpretation of my experience in terms of the above would be:
When I imaginatively reconstruct my body as a mental image, my inner gaze is upwards and to the right.

the upwards would explain why I visualise my feet slightly forward of my physical body
the to the right would explain why I visualise my feet rotated slightly clockwise with respect to my physical body

Does anyone have any views that would confirm this ?

Parietal lobe is generally responsible for the perception of the body space. There are some conditions in which people perceive their body spaces differently. Also read about phantom limbs.


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Kegg in Cytoscape: how to get plots with reaction IDs in place of EC numbers using KeggScape?
I found a KeggScape manual page representing Kegg reactions in Reaction ID format, but I couldn't find how to get a Kegg plot with reaction IDs in place of EC numbers. Does anyone know?

Welcome to Biology SE. I think you will need to provide more information if you hope for an answer. I do not use Cytoscape, but believe it is a general networking tool that has nothing intrinsically to do with Kegg. I see there is something called Keggscape. If that is what your question is about, you should edit it to say so, and provide a link to the documentation. Your title doesn't indicate you are talking about Cytoscape so I have edited it for you, putting your old title as a first line. If this is not correct, modify it.


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Metazoan branching: Placozoa or Porifera?
Of Placozoa and Porifera, which branched off first? (Conversely: which are closer cousins to us?)
I've heard both suggested as our most distant cousins with bodies, so was wondering which ordering is currently considered most likely. Of suggestions that Placozoa branched off later, I've heard some saying that the branching was even post-Cnidaria/Ctenophora. This seems very unlikely: is it?

Currently we don't even know which of the Porifera or Ctenophora branched off first. However, between the Porifera and the Placozoa, the Placozoa are more similar to Cnidaria + Bilateria.

@entonio Does this resolve the Ctenophora v. Porifera debate? (It does for me, but I don't know if that's because of my bias towards Porifera - like many, I've been very uncomfortable with the analyses that put Ctenophora as the most distant)

Bertie, thanks for the paper, it echoes a lot of what I think about this myself - many recent phylogenetic 'upheavals' are in fact methodologically unsound, and this is probably one of them. Still, my issue is with the whole 'this settles it' discourse - I just don't see that the data is enough to settle some things, but people are eager to have the last word on them. I think one day these times will be looked upon with some condescension, we got a lot of new toys to do phylogeny with, but so far we've been sloppy and dishonest using them.


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Do pet animals and humans perceive good and bad smells differently
As the title says, just wondering if there is a difference in what animals like dogs and cats perceive as good smell vis a vis humans. Example : Smell of some flowers - great . Fart smells - bad.

When I see dogs and cows roaming in stinking garbage, I feel like the answer is no.

Humans perceive colours differently from each other, so why wouldn't the same be true of pets/dogs/animals in general, for smell? Even humans don't like the same smells. My mother despises the smell of daffodils. They make her gag, and if she is around them enough, vomit; But plenty of other people seem to love the smell.

Thank you for your comments. XaNaX, I understand your point. What do you think the reason for this difference is ? I am not an expert in understanding how the nose senses smell, but is this perception of good and bad smell physiological or is it psychological ? With eyes, the differences are the rods and cones right, so is the perception of good / bad  smell similar?

This article suggests that when we first smell something, we link it to the emotions we feel at the time. Those emotions are then associated with that smell, the article says, and depending on whether or not the original emotion/event was a positive or negative one, we then have a reaction that reflects the original emotion when we again smell that something.

TL; DR Mostly no.
On a molecular basis, cats' and dogs' noses look quite similar to ours. Most of what we know about smell comes from studies on non-human mammals, and is supposed to apply to humans too. So, big similarity, but...

Cats and dogs distinguish far more kinds of than humans. It's likely they know more kinds of bad smells and good smells, possibly including from things that we think lack odour.
Many animals also have a working vomeronasal organ, that is, a sensing organ similar to the olfactory mucosa we use for sensing common smells. The vomeronasal organ detects pheromones, the smell-like signals used for communication between animals. We, humans, are at least deficient, if not completely unable to use the vomeronasal organ and pheromone signals. It is debatable whether animals conflate regular smells with pheromones. Pheromones are very efficient in conveying information about potential sexual partners, rivals, and so on. So these are a completely different set of bad and good smells, available only to animals. That is, if we can call those sensations smells, a big if.
On the other hand, humans evaluate smells culturally. Some people learn to enjoy offensive smells that people from other cultures carry on disliking. Since dogs have limited ability to manipulate smells and to convey information to another dog, I doubt they can form these cultural constructs of smell. We sense sensuality in a perfume; the dog senses a bunch of pungent flowers, neither good, nor bad.

Thanks for the detailed answer Nick and also XaNaX for the link.

@VarunBKothamachu: On another side note regarding point 3: my cats absolutely dislike the new brand of antiperspirant I use. The old one seemed to be more okay to them. Additionally, one of my cats hates the smell of ginger and cumin (she even makes a sound that expresses her aversion and jumps away from it), while the other one clearly does not like it but is not really freaked out when she comes into contact. There must be a thousand anecdotes like that. :)


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siRNA designing problem
I have a gene sequence with 15 alternative splicing forms. I want to design a siRNA for 1 isoform, I select the exon intron junction that is unique for this isoform, and I must design siRNA for this sequence or this unique isoform, but this sequence has a similarity with another sequence when I blast it, also this sequence doesn't have features for siRNA design. With this condition how can I design siRNA for my sequence?

Can you show how the sequences align? A rough illustration is sufficient if you do not want to share the details. Plus why are you targeting intron-exon junction? You can simply target the exon that is retained in the desired isoform.

i aligne these sequences with clustal omega, and also i have this schematic picture in the literature.my desired isoform is the smallest sequense between another isoforms with two exons,and all of the isoforms have both of above exons.therefore  i have to select exon intron junction , that its the uniqe sequence.

Have you extended the siRNA to 25 bases (usually considered the longest) and moved it up and down the junction to try to find a more unique sequence?  i.e. have at least 7 bases on each side of junction, but vary it from 7 to 18 on one side and see if you get more unique blasts. I assume you are blasting RNA and not DNA?

Can you show the alignment? siRNAs have to be perfectly complementary and the 5' pairing is the most crucial. There are other rules too. Also, please tell what were your BLAST parameters. Edit your question to include all necessary details otherwise it would not be possible for us to help you.


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Use of beta-2 microglobulin staining to assess frozen tissue sample integrity
In a Russian paper I'm reading the authors use staining for beta-2 microglobulin (B2M) to make sure that a variety of frozen tissue samples still express antigens on their surface, so that these samples could be used to assess the activity of an antibody they are researching.
The authors write that "since virtually each cell expresses B2M on its surface, this assay ensures that other antigens have remained on the surface of the examined cells as well".
Is there a special term for this kind of check? Is this anti-B2M staining a routine procedure, and are there papers dedicated to this procedure? I haven't found relevant papers.

I'd say it is not common practice to look for B2M, although I guess there will be heavy users would would disagree.
Without seeing the paper I cannot be sure, but I guess they are using B2M as a housekeeping gene, that is, a molecule whose presence and quantity is largely unregulated in living cells, and which is commonly used in labs as reference. Biological samples vary greatly in their content. It is hard to tell if a molecule is made or destroyed in response to a treatment, by merely measuring, and finding more or less of it. But if the ratio between the aforementioned molecule to an unregulated molecule goes up, you can be more sure it responded to the treatment. That is called an internal control. You may be familiar with "normalization to actin" or to GAPDH in immunoblot and qRT-PCR.
The use you are describing is diverging from the typical use of housekeeping genes in a lab, and not optimal for what they were trying to show. Since it's there in pretty much any tissue measured by immunoblot, B2M is expected to be present in any tissue assayed by microscopy. If a tissue slide lacks B2M, it is likely spoilt. But if it has B2M, it doesn't make it 100% certain that other, scarcer, more unstable molecules have been preserved as well. It would be ideal if they looked for the specific molecule they were studying; but if many of their samples were supposedly devoid of the latter, they had to replace the ideal with something more practical.
Note that I am using "molecule" in an ambiguous manner. With antigens in the referenced paper, it's obvious B2M is used as a reference protein. But housekeeping genes, including B2M, are also used as internal control for mRNA measurements ("gene expression").


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trp operon repressor
Does trp repressor form a tetramer or a dimer before it binds to its corepressor tryptophan?
I've been reading BIOS Molecular biology it says that it is a dimer

The repressor is a dimer of two subunits that have structural similarity to the CAP protein and lac repressor.

but according to wikipedia it is tetramer. What is correct?

Revised answer summary
My original answer provided evidence that the trp repressor is a dimer, and that conclusion stands, especially as regards its functional form. I still regard the statement in Wikipedia that it is a tetramer as incorrect, although I now see how it might have arisen. It seems to be a misinterpretation of results in vitro that show an equilibrium can exist between dimer and tetramer (not tetramer only). I have expanded on this in an additional section.
A functional dimer
The functional form of the is certainly a dimer, as originally reported by Schievitz et al. (1985). The summary of this paper includes the statement:

“The crystal structure of the Escherichia coli trp repressor has been solved to atomic resolution. The dimeric protein has a remarkable subunit interface in which five of each subunit's six helices are interlinked.”

It was crystallized in combination with the operator DNA, and the structure deposited in the Protein Database (PDB) as 1TRO. I reproduce an image from the PDB entry below. Many other DNA-binding proteins also have dimeric structures.

A dimer–tetramer equilibrium observed in solution
The statement in Wikipedia probably arises from a report by Fernando and Royer (1992) — subsequently confirmed — that in solution there is an equilibrium between the dimer and higher oligomers (the tetramer predominating). Tryptophan was found to shift the equilibrium to the dimer. The authors claim that this has physiological relevance, although this still seems a moot point.

I have revised my answer, explaining the situation with the tetramer. Wikipedia is incorrect, but it is important to realize that Wikipedia consists entirely of the voluntary work of people like us. It doesn't claim to be correct, only correctable. I feel that it is an obligation of those who find mistakes to correct them (if they can do it easily and with authority) and I shall do so myself in this case. I encourage others to do likewise.

I have now edited the Wikipedia page. I also deleted a reference to nucleoplasm in this section, which should have been removed long ago. Needless to say, bacteria have no nuclei and no nucleoplasm.

I saw you editing today. The original article was poorly written.

@SanjuktaGhosh — Unfortunately many of the articles on transcription  in WIkipedia are poor or out of date. The main article is terrible, failing to distinguish between eukaryotic and prokaryotic systems. The problem seems to be that when Wikipedia started there was an initial surge in enthusiasm, but the updating has been very uneven across topics. Younger people who try to help are often brought up on eukaryotic molecular biology and are unaware of the older work on what then were the only tractable systems — prokaryotes. Specialists generally have little time or incentive to contribute.


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Is "cell proper" considered a biology term / well defined concept?
I am asking this question after writing an answer on English Language & Usage sent me on an expedition through the internet. The originating question asked about the meaning of the word proper after the word cell.
At first I was certain that it was a biology term, describing some sort of cell. I am not a biologist. After some pushback, I researched a bit and found what seems to be the original definition in a book from 1853.

It is a mistake to apply the word cell sometimes to the cell with a membrane, sometimes to the cell without a membrane, and sometimes to the membrane without the cell. Since the contents of the cell constitute the essential part of it (see p. 155), since it forms, before the secretion of the (cellulose-) membrane (pp. 156-167), a separate entity, possessing its own, essentially proper, membranous boundary (the primordial utricle, pp. 169-173), we must call this internal body the cell proper, unless we restrict the term cell to the enclosing wall or chamber, and give the internal body another name. If the name is restricted to the internal body, we cannot, in the great majority of cases, say that new cells are formed in the old, but merely that they are formed out of the old, for even the primordial utricle shares in the division, in the propagation of cells by division. Therefore when daughter-cells are said to be formed in the mother-cells, or to slip out from the mother-cells, or mother-cells are said to be dissolved and absorbed, these phrases must be admitted only as conveniently abbreviated expressions, "mother-cell" being here used instead of maternal cell-membrane.
(bold emphasis added)

My question is: Is cell proper considered a biology term or concept that would be understood by an expert of cellular structures?

I have never heard this term - so it most likely never catched.

this sounds like an old term that, to my knowledge, is no longer used - not surprising given how much more we know about cellular physiology/structure and functions

This isn't a special biology term, it's just an English usage thing. "The X proper" just means "the X, strictly speaking". As well as the question you quote, see also this question on ELU.SE. I would expect this use to be understood by many biologists who speak English as a first language, but there are certainly clearer ways of saying it.
Regarding this particular example, the author appears to be proposing a way of defining a vacuolated plant cell. It sounds like he is proposing a definition that excludes the cell wall, but he confusingly calls the cell wall the "(cellulose-)membrane" (the 'primordial utricle' is the cytoplasm, I think). However, I am afraid I am not an expert in the history of plant cell biology and can't really comment on whether it is a useful contribution to, or synthesis of, the state of knowledge at the time.

I agree with the suggestion that this is mostly just a standard usage of "proper."  However I would caution that most scientists would probably not understand "the cell proper" to exclude the cell membrane! If I ever wrote that, it would be in a sentence like, "The extracellular matrix, while not part of the cell proper, is an essential aspect of a cell's behavior."

@AJK absolutely. Although I would probably need to read more of the original text to work out exactly what the author is describing - it seems he's talking about something to do with the membranes of vacuolated plant cells, and I haven't studied plant cell biology since first-year undergrad. That said, I can think of very few biological definitions from 1853 that remain helpful today!

@AJK have read a bit more around it and added what I understand of his proposed definition, with caveats. Please do feel free to elaborate on it.


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Using UV to kill bacteria in shoes
I see that UV-C is the best to kill bacteria generally. We are interested in using to kill off odor in shoes.
What illuminance is needed to kill most bacteria with UV-C?
Thanks!

Welcome to Biology.SE. Only the last of the three questions relates to biology. The others are questions of material physics.

Do people still use the foot-candle in the USA? The standard unit of illuminance is the lux. Note that once you know the illuminance on the target, finding out the illuminance at a given distance is quite basic (and is a question of physics/math). I would recommend you restrict your whole question to something like "What illuminance is needed to kill most bacteria with UV-C?".

Close vote retracted and +1.

The wavelength of UV-C most effective at provoking mutagenesis in DNA is 260 nm, which has been shown to kill Cryptosporidium parvum at doses below 10 mJ/sq cm.
http://www.ncbi.nlm.nih.gov/pubmed/12834745
In units of lux, 10^5 lux of sunlight has been shown to kill 99.9% of Aeromonas salmonicida after two hours of exposure.
http://www.sciencedirect.com/science/article/pii/S0043135499001591


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What is the meaning of -//- sign?

Does $-//-$ sign between trpR and P indicate separation of the trpR gene from the operon? Or could the sign mean that the trpR gene may be present adjacent or far away from the operon, both the possibilities?

I think that means they are omitting a large section of DNA in between the trpR and P sections. You see a similar symbol on plot axes when they skip numbers.

Unlike P and O sequences which are literally joined at their ends, the sequences trpR and P are rather distant. The DNA between them is so long, that the limited space of the page prevents a decent proportional representation. So instead of painting a long line of limited-importance strands, the graphic designer choose to omit the part between slashes.
Note that despite the apparent disconnect possibly suggested by the sign -//-, the intervening DNA is continuous. The sequences trpR and P are still on the same chromosome.


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Natural killers cells in insects/ arthropods
I'm wondering if someone knowns anything about Natural Killer cells in insects or other Arthropods. Do they exist or are their any similar cells of the innate immune system that someone knows of?
Thanks a lot!

should be easy to find some information on google for that straightforward question? where else have you tried looking?

I tried google and more specific scientific literature (concerning the immune system of insects, crustacea and drosophila), I find elaborate descriptions of the innate arthropod immune system, but NKcells (or cells that perform similar functions) were never mentioned

NK cells are desinated adaptive immune cells now. There was a discussion on this topic some while ago.


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Which predators only eat some parts of their prey? (Warning — graphic content)

In an small city in middle-east somewhere near a desert, an unknown predator attacks sheeps, goats and chickens. These attacks began a few weeks ago and until now more than 150 sheeps have been attacked. It causes panic and rumors among people and despite official investigations no result has been achieved yet.

Welcome to Biology.SE. Is there a freely available report for these official investigations?

Where in Middle-East do you live? There are different biogeographical regions in the Middle-East.

I remember a show in which (maybe) this case had been investigated (near Mexico probably) and one scientist there showed a dead chupacabra (or what its called) stored in a glass container!

Any predator that cannot eat the entire animal at once.

Scavenger birds also leave carcasses like that since they can't break up the bones and only eat the soft tissue. This produces a hollowed out carcass like that. Although birds will usually eat the tongue and eyes as well.

In the pictures shown above only the soft part of the animals have been eaten. This is common for most predators as these are the easiest parts to eat.
Correct me if I am wrong but the animals seem to not have severe bite marks around the neck. This means the predator was not big. You can pretty much rule out anything around the same size or bigger than the sheep.
To exactly identify what killed them just from a carcass is hard, and even harder over the internet. However, it looks like you are dealing with feral dogs, coyotes or wolves, although with wolves and dogs there would generally be more scarring around the neck of the sheep.
Dogs: I have seen this behavior in dogs. These are normal tame dogs that have discovered the kick of hunting. Where I come form in South Africa the farmers tend to shoot dog packs if they see them on their land. This is because it is a common problem for the packs to attack chickens, sheep or even calves.  They get an immense kick from hunting the sheep but in most cases don't eat it, not like the photos shown at least.
Foxes: Although it may be hard to believe foxes have also been known to kill sheep. However, in your case it is not likely to be foxes. Foxes hunt alone and tend to kill lambs.
Coyotes: Coyote packs have almost identical behavior to dog packs. The difference being that they pick one sheep and kill it quickly. They do not do it 'for the kick' like dogs and rather for the food. Judging from the photos I would say it is possible that this was done by wild Coyotes, if they are found in your area. Coyotes are also not very shy, and will often hunt close to where people live.
Wolves: While possible, I would rule out wolves because of your geographical location. Wolves also tend to be more shy and will stay away from places with lots of people, like a city.
Source:
http://www.omafra.gov.on.ca/english/livestock/sheep/facts/02-029.htm

Please provide some sources to back up your answer.

There is a famous fossil find of a pile of oreodont carcasses in which all but one is missing everything below the waist. the assumption is a predator ate the best parts then either left the rest behind or shoved the rest in a meat locker to eat later.


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How does HPV start?
Not "infect" others. That's common knowledge - sexual activity.
But how does it start? Literally from non-HPV carrier to HPV carrier?

Through sexual activity. Someone has sex with someone who is a carrier and contracts the virus.

Are you trolling me? Because that is not what I'm asking, and I specifically stated that in the first 2 sentences.

I would like to better understand what you're asking; please clarify. As it stands now, though, the comment is correct. How do you think it might happen?

I would like to know how HPV can start in a person. Not infect. I guess one can say that I'm asking about the origin.

There is no such think as spontaneous generation; it can't just "start" in a person. The virus exists, and it comes from someone else. It is spread person to person, penetrative, skin to skin, orally, or, in an infinisimally small number, perhaps from a contaminated instrument. From another carrier is the only known way to acquire it. If you are looking for the origin of the virus, that is a different question altogether, and should be asked as a different question.

I believe what you are asking is the origin of the HPV virus, however currently, there is no real answer to that question. Nor is there an answer to how any virus came to be.
Right now, there are 3 theories as to how viruses originated, all of which can be found in this article from the Nature Journal. The theories are as follows:

The Progressive Hypothesis

This theory suggests a parallel between components of eukaryotic genomes called retrotransposons and viruses. More information can be found in the article enclosed, but basically, retrotransposons, which can be can be "transcribed into RNA, reverse-transcribed into DNA, and then integrated into a new location within the genome" -- just like retroviruses, are hypothesized to be the foundations for the evolution of viruses.
Here is a link to a depiction of a retrotransposons' replication process, with a description. (if you're interested)

The Regressive Hypothesis

The next theory is considered a bit less plausible than the Progressive Hypothesis, but again... no one knows. This hypothesis recognizes that there are some bacteria that have evolved from complex creatures into the parasitic organisms there are currently. This is known as regression. Summarized by this website is a description of this observation as it applies to viruses:

The Regressive Hypothesis: Viruses evolved from more complex free-living organisms that lost genetic material as they adapted to a parasitic approach to reproduction.

The Virus-First Hypothesis

And finally, this theory assumes a world where viruses (or the primitive versions of them) existed even before cells did. This theory states that viruses were once just self-replicating units that, over time, (like many things in our world) got more complicated. This is similar to the Progressive Hypothesis in that it suggests evolution forward and not backward (regression), but it differs in that it suggests that before viruses are/were merely just units even simpler than cells that became more intricate.
Now back to your question, HPV is like any other virus in that there is no known origin for it. However, since the virus has been conceived (no pun intended), it has lived through sexual transmissions and is kept alive like so.