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Do spermatozoa have mitochondria
This is something that I have heard/read so many different contradictory claims about over the years.
In high school I was taught that sperm cells have a lot of mitochondria because they need a lot of energy quickly. This made sense to my adolescent mind.
When I was an undergrad, my one microbiology lecturer swore up, down and sideways that they did not have mitochondria. She never gave any reason or evidence, but I had gotten used to the idea that high school info was often out of date and, sometimes, completely incorrect, so I let it slide.
Then I was reading an article for a paper several years back and it said that, not only did sperm cells have mitochondria, but they did not lose them all. That in fact, some were preserved and engaged in genetic recombination with the mitochondria belonging to the ovum (the maternal ones). This contradicts another rule that so many treat as certain, which is that while nuclear DNA is 50% from each parent, mitochondrial DNA is exclusively maternal.
To sum up: Do spermatozoa contain mitochondria or not? And if so, is the recombination I described above likely?

With all certainty yes, they do have mitochondria. What article are you referring to in the second to last paragraph?

I can't remember in the slightest, and I lost my copy with a crashed computer. It was an off-hand comment in a pretty mediocre article. What I was actually researching was a particular gene on the mitochondrial DNA, I was just struck by that statement and the question bothers me every so often.

Wikipedia paternal mitochondrial DNA transmission

The midpiece has a central filamentous core with many mitochondria spiralled around it, used for ATP production for the journey through the female cervix, uterus and uterine tubes. This is a good article explaining more about this topic: http://genetics.thetech.org/ask-a-geneticist/mtdna-comes-only-mom

Thanks. That helped. Who would have thought that what I learned from a high school biology textbook published in the early '80's would be the right answer.


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Flower/Plant Identification
Could anyone please identify this flower/plant found on the semi-shaded banks of a river in East Ireland? It was located near Japanese Knotweed and looks quite similar to this.

That is Himalayan balsam (Impatiens glandulifera).

Tall, stems often reddish. Lvs opposite or in threes, with small red teeth. Fls large, pale to dark pink-purple, with short bent spur; July-Oct. Bare places, especially by streams.

The Wild Flowers of Britain and Northern Europe. Fitter, Fitter, Blamey. 1974. Collins, London.

We have a species of impatiens in the US called Jewelweed. Those seedpods when ripe are fun for kids: they pop suddenly on handling, scattering their seeds. :) The sap is a nice topical anti-itch field remedy for mosquito bites, poison ivy, etc.

Yes, jewelweed is mentioned as an alternative name on the WP page. It is considered to be an invasive weed in the U.K. because it can take over riverside land.

Yes, definitely invasive on this certain riverside.

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Does PCR amplification affect microarray or DNA biosensor results?
I've noticed that PCR amplification is commonly done before analyzing the DNA sample with microarrays or biosensors.
However, won't amplification biases or errors mess up the gene expression profile results you get from a microarray? Secondly, does that mean amplification only allows you to get qualitative information from say an electrochemical biosensor? (rather than actual quantitative information about DNA concentration)

Yes, it does.
That is why you should include positive and negative controls and repeat the experiments multiple time to then average the results.
In general, amplification by PCR is biased by sequence-dependence efficiency. For several reasons (among which GC content, annealing mismatches PCR buffer and the timing and temperatures of the cycling steps) a particular template can be over- or under-estimated.
For example, if one sequence is amplified 10% more than another in one round, it will be 1.1^30 = 17.4 times more abundant after 30 amplification cycles.
Here some literature on the topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292241/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628873/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3129672/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2727727/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433096/
This doesn't mean that you can't get quantitative information. PCR is used to get quantitative results in many fields of research. You "just" have to be sure you are doing it correctly. Be aware that experimental confounders may mess up your results, so be critical when you analyze your own data.

Anytime you have PCR in a protocol, yes, you might mess up the quantification.  So you do as little PCR as you can, so that it stays in the linear range, preserving the different abundances of templates  (qPCR after all is the gold standard for quantifying expression), and you hope that there are minimal PCR biases between templates.

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How much of my ancestry comes from each grandparent?
Three of my grandparents were Eastern European, back at least several generations. I recently discovered that I am less than 25% Eastern European, the rest being Western European and other. How likely is this?

[English is not my native language] I know a girl (say, Natalia) who took a DNA-test at National Geographic, while her half-brother (say, Sam) took one at 23andMe. They were both told that they had one-eighth of Ashkenazi origins. And in fact, they share an Ashkenazi great-grandparent.
So, I conclude that they have one-eighth of this great-grandparent, and the precision was so great that I am inclined to believe that there is a high probability that it is the same for everyone : one-half of each parent, and one-fourth of each grandparent.

On average, 25%, because you have 4 grandparents, and all of your genetic material came from them as a collective. Of course it's possible to be more genetically similar to a particular grandparent by random assortment of chromosomes, but the average will be 25%.
Genetic tests can't tell you what your ancestry is (companies implying this are probably misleading you on purpose). At best, they can tell you how correlated certain features of your genome are with people from a certain geography. Even people who are currently live in Eastern Europe will not test as "100% Eastern European." There is far too much mobility and breeding of populations across geography and far too much variation within populations.

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What is the reason for occurence of introns in eukaryotic mRNA?
After transcription of the Template strand of DNA, in prokaryotes, the translation process begins immediately. But in eukaryotes the mRNA transcript has both non coding (introns) as well as coding (exons) sequences. So they undergo Post Transcriptional processes i.e. Splicing, Capping and Tailing.
From where do non-coding sequences arise in eukaryotic mRNA? I'm guessing its from Heterochromatin (found only in eukaryotes). Is this correct?
Also the process in prokaryotes seems to be hassle-free and simultaneous. But what is the reason for such a complicated process in the more evolved eukaryotes?

No organism is more evolved than any other. That aside, no one knows why introns exist, but we do know that they presently play roles in gene regulation and generating protein isoforms

Please note that you are required to some research of your own before posting here. Not only could you have searched this site to find that your question has been posted before, but you could have searched Wikipedia or the web in general. I see you have not completed the guided tour as you lack the corresponding badge. Please do so if you intend to use this site.

@David My apologies sir for not having done my homework. I wasn't duplicating anyone else's work. Its a genuine thought and i was too overwhelmed by it and posted it immediately. I could have done everything you said. I regret it.

No big deal, just explaining how the site operates. Nobody is accusing you of duplicating anyone's work — that's a standard message generated by the system.

Oh thank you so much sir. I'm totally free of the burden of an accusation:)


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Zygosity and Strands
I am not a biology expert but I have done some homework on understanding alleles, chromosomes, dna in the human genome. Still baffled by a question though:
As I understand it at a particular locus for e.g. if a human has a A on one chromosome and a G on another that individual is considered Heterozygous at that locus because of the difference in the nucleotides (A/G in this case).
However, my question is. What about an individual that has an A on the 3' -> 5' strand (and hence a complement T on the 5'-> 3' strand) on one chromosome but T on the 3'-> 5' (and its complement on the other strand) on the other chromosome. Is this individual considered heterozygos or homozygous?
Basically my question boils down to does the "directionality" of the A-T pairing matter on both chromosomes?
I was thinking it should as only one strand can code for genes which the other doesn't so it should matter whether the A is on the (3'-5') or on the other strand..
Any advice would be great!

As @Nicolai's answer suggests, when you are thinking about coding genes, you should really just think about one strand at a time. Also note that zygosity is normally considered at the gene/allele level, as far as I know, people rarely talk about "zygosity" for a particular base pair, especially because single base changes don't always have an impact on the protein produced. (someone who does more genetics might disagree with me)

Thanks Bryan. I did accept @Nicolai's answer. However, I am not sure I understand what you mean by "Zygosity at a gene/allele level". Per my understanding a gene is just a certain sequence of nucloetides on a strand and allele's are just different "versions" of the same gene present on different chromosomes. So, I thought zygosity has to do with variances in nucleotides on different chromosomes.

crossposted on biostars.org: https://www.biostars.org/p/264076

@Shanbhag Yes, it does, I'm just saying that "allele" and zygosity has whole-gene connotations. If you are talking about alleles for just a single base pair, you are implying that there is no variation in any of the other base pairs. Also, alleles that are actually different at the base pair level but produce no phenotype in any combination might be grouped all as "wild type" alleles. It's just a different level of analysis in most contexts.

@BryanKrause When talking about SNPs zygosity or at least the terms homozygous/heterozygous are usually also used. I guess depending on ones background the connotation of zygosity with genes might differ

The directionality of the strands matters, because genes can be encoded on both strands of a chromosome (each strand can be read in 3'-5' direction by RNA polymerase). Therefore someone with the A-T case you described is also heterozygous.


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Effects on body without fitting routine to external time (non 24 hour Circadian clock)
Often I find myself trying to fit my daily routines to factors such as those of the external time, e.g. to light levels outside, and those that others around me live by.
However this often seems inconvenient- often having to round up or round down time spent on certain activities to fit them into my day. Sometimes I find myself tired which affects the quality of my work, but I 'know' it is not necessarily time to sleep due to the outside light levels and the timezone given to me, so I must carry on until some 'reasonable' time is reached.
I was wondering, is there a significant (negative) effect to the following process:
Assuming I need to do nothing which involves direct involvement of others, I attempt a task (inside, controlled temperature with lighting if needed) which I want to attempt until either it is complete, where I then move to the next task, or feel like I must postpone to perform a bodily function (eat, sleep etc.) until these themselves have been satisfied.
Repeat this indefinitely, irrelevant of outside time conditions/ factors, which we assume to be reasonably 'normal'.
(I have an infinite supply of food, water etc. )
Assume work can only be completed with at most minimal tiredness.
I would expect that maybe on average, the times at which humans are to proceed through the tasks match up with the 'normal timings', but I would argue that for myself, this would be caused by quite large fluctuations either side that cancel each other out. (Perhaps at some point I would wake up in the afternoon, another day go to sleep in afternoon).
I would like to know how much of our regular routines is psychologically influenced by others around us compared to how much this is intrinsically in our genetics.
These 'normal' routines seem to make sense for many primates- time of day effects ability to see surroundings, perhaps what food sources are present. But one could argue whether this is as relevant for humans with technology to overcome many of these factors.
I am aware of the Circadian clock, and that it has its own genes, and that it is maintained through certain light stimuli, but I do not know what precise functions it maintains in the body.
So
What would be the physiological/psychological consequences of ignoring the factors of time when completing tasks?
How much of the common human routine is psychological (from being influenced/ made to by others) compared to intrinsic instinct?
Are there any sources/studies conducted on this before?


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Math backbone in biology/genetic
Are there any good books, that shows some advanced models in genetics particularly?
The problem is i don't see any good math model in genetics interactions exept combinatorics. I'd like to know what else math structures and rules are there in genetics.
I'd like create strong math backbone for better understanding genetics, but i can't find any advanced reliable sources for that. Are there any books that could help me?
Thanks a lot.

If population genetics is what interests you (but I don't think it is), then you should have a look at Book recommendation on population/evolutionary genetics? and Mathematical Modelling of Natural Selection.

It would help us to understand exactly what you are looking for if you could link to a specific paper which you would like their work to be reported in the book.

Elements of Evolutionary Genetics; Charlesworth and Charlesworth

I would vote to close as unclear (but I cannot because apparently I already did and then retracted my vote). I do not know exactly what you are looking for. Adding an example of the type of study that you would like to find in your book would help.

Related/ possible duplicate of: A free book/resource for learning genetics? and Which texts are good for beginners to understand evolution on the genetic scope?


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Symmetry of species
I've got a silly question, sorry for that. I know, that we probably have no the right answer and the current answer could be "that's evolution, external conditions". I'd like to speculate, why most of mammals (for ex.) and people especially are symmetric?
I know, that we are not completely symmetrical, but anyway.
Thanks a lot.

When I get back home, I'll try to find a book that I have about this ("Fearful Symmetry: Is God a Geometer?" by Ian Stewart) which tries to address the question of why organisms have the symmetries that they do. If no one else has answered by then, of course...

Not entirely a duplicate or subset of the linked question. -- IF one were to see this question by dshulgin as asking: Why are Chordates still symmetrical? There are two additional considerations not clearly addressed in the linked question. -- 1) Fundamental distinctions in organisms are unlikely to change via Neo-Darwinian Evolution -- 2) Bilateral symmetry is a very good proxy for genetic fitness and therefore a symmetrical member of your species is a better mate selection. -- These two considerations are not relevant to the linked question but do apply to @dshulgin's question here.

There's really two answers to the question.  The first is overall symmetry: mammals, like all tetrapods, are bilaterally symmetric.  This comes from a distant common origin with other bilaterally symmetric organisms.  Organisms which evolved from this common ancestor often have organs in pairs, probably evolving as a re-use of regulatory genes.
The other answer is the high degree of symmetry in external appearance.  While internal organs are roughly symmetric, there is some asymmetry.  However the external appearance of most bilaterally symmetric organisms is highly symmetric.  This suggests a different force at work.  In fact, there is some evidence for sexual selection for bilateral symmetry.  Mate choice is driven by indicators of health, and bilateral symmetry is a common indicator of health.

It is, of course, not just mammals, but nearly all animal life is symmetric. Even plants are usually symmetric in some degree. There are exceptions here and there. For example, one interesting exception is that of the fiddler crab which has one claw larger than another. In general, when a single appendage is present on an animal it is nearly always on the center line of the animal. For example, the horn of a rhinocerous or the central horn on a triceratops, or a human's nose.
The symmetry is generally enforced genetically, not environmentally. For example, if you hold a paper up to your face you will find that the left side of the face is different than the right side, or at least that is the way it is for most people. Thus, once conceived, the two sides of the face grow differently, a phenomena that geneticists call genetic "expression". For example, your fingerprints are "expressed" traits, not genetic traits, and for this reason the fingerprint on your left thumb is different than the fingerprint on your right thumb.
Even genetically, however, many parts of the body are not symmetric. For example, the heart is on the left side of the body, but the liver is on the right.
The evolutionary logic for symmetry probably is because it makes locomotion easier and more effective. If an animal is not symmetric, they may have difficulty moving efficiently.

Although not a biologist, Steven Pinker notes that bilateral symmetry evolved in organisms to allow them to move in a straight line. For a bilaterally symmetrical animal to move, they simply alternate movements between one half of their body and the other. This is true for fish, snakes, insects, mammals, etc.  There are exceptions, for instance, flying and hopping, but those creatures evolved from ancestors that first locomoted by alternating limbs.
If you look at jellyfish, for example, they are radially symmetric, and their manner of locomotion is to swim in a sort of spiraling shape.
Probably after it arose, bilateral symmetry became a sexual selection criteria, because it is costly to perform during growth, as Pinker goes on to explain.


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Were these spiders burried alive by a spider wasp?
I moved a stone plate in the garden in europe, that was stored vertically, leaning against another one.
In the space between the two, I found some soil with small cavities filled with spiders.

Most of the spiders had a (what I think is a) larva attached to their backside. See the white sausage thing in the right half of the image. I noticed that there's what seems to be spider web on the right edge of the cavity.

Some of the spiders showed movement when lightly blowing air onto them. I took some of them out to get more detailed photos. The larva seems to have a white/translucent head attached to the spider body. The internals of the larva appear to be light brown through the translucent body. The larva has a thin white line at the sides of its body.

The least lively of the spiders had a larger larva attached. It has a darker inside and some white dots on its body. It disengaged from its spider and the mouth is visible.

A while ago, I found other spiders in a comparable situation. Having learned that some wasps apparently catch spiders and paralyze them, to be eaten by their larvae, I did some search and found spider wasps
Is the above the work of a spider wasp? I had a look at bugguide - Family Pompilidae - Spider Wasps, but there are no images of their burrows shown.

That's horrific.

Excellent photos. Also look up mud dauber wasp.

I agree, I'd say it is the work of a spider wasp. I'm not familiar with those, so I can't determine what species or genus it might be. But it sure does look similar to some of those stages of the larvae. Very nice pictures! I will try to find out what the white dots on the body of the oldest larva (the last and hungry one) are.

In picture (G) of your link one can see those white dots as well - would be interesting what those are all about - please keep us updated if you find out more.

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How does Cas9 interact with CRISPR?
I read that Cas9 protein along with guided RNA binds at a specific DNA fragment of foreign organism integrated in a host organism DNA. To make the host immune to virus infection Cas9 along with gRNA which is complementary to viral DNA attaches to it host DNA by unbinding it and then cuts the DNA at this site thereby removing the viral DNA. So the host can only remove the virus that enters second time as it makes a complementary RNA from the first virus that has integrated in it and cannot completely remove virus.

Is the process that I am thinking right?
And can we use Cas9 to cut the DNA at any site of our choice?

Are you asking about CRISPR/Cas9 editing systems that you would use in the lab to recombine DNA, or are you actually interested in bacterial adaptive immunity? The Cas9 systems used in a lab setting are engineered, and behave a bit differently to what is found endogenously in bacteria.

We are currently using CRISPR in the lab to modify cells. Like @AMR said, it was modified from the In Vivo immune system to be used in the lab in DNA editing field. The Addgene website features both historical background and an application guide that are very well done. To answer your questions:

The bacteria (S. pyogenes, S. aureus, etc) integrates part of the viral DNA (protospacers) inside its genome, flanked by repeats. When transcribed the RNA derived from this newly combined sequence will direct the Cas9 protein to the viral DNA, which is complementary. Another element required is the PAM (protospacer associated motif) which is on the viral DNA just besides the protospacer. By not being on the bacterial DNA, it ensures that the Cas9 does not cut its own DNA.
The only limitations are the PAM and the off-targets. The PAM is specific for every species (EG S. pyogenes is NGG). Some sequences can be repeated in the genome of an organism, meaning that if you find a sequence that would result in a cut at a desired site, it could still cut elsewhere. That would make the guide sequence a poor choice.


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What order is this butterfly?

I found this butterfly in the rocky mountains of colorado. Its obviously a lepidoptera but I'm not sure what family this butterfly could be. I found it perched on a bush and it is around 40ish mm long. Thank you very much for any answers, making an amature insect collection :3
Edit: I was thinking its a Riodinidae, but It doesnt quite look like it.

Not an answer, but couldn't you have taken a picture instead of its life? For all you know, it might be endangered. Or not. But it had a life, and you ended that.

Sorry, I'm collecting an insect collection so I kind of had to kill it, and theres many of these around here so i'm pretty sure it is not endangered. But thanks for the concern

You're very gracious, so thanks for that. Is the insect collection for a school project? I carry a small camera everywhere. It is actually (for me) better to capture a live butterfly in an artful manner than to look at a dead one, but that's me, and I love photography.


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How does the body fight new infections?
I have read that the body contains T-cells and B-cells specific to all antigens in small amounts and that these are activated when the antigen presents in the body. If this is true then why are we not able to fight all types of infection?
If this is not true, how does our body learn to fight new infection or new foreign substances?

Disclaimer: This is mostly like canonical or "textbook" immunology. As with many biological systems, there are caveats to everything and it can't all be covered here. If you have questions outside the scope of this answer, please make another question!
The immune system consists of two subsystems: adaptive and innate immunity. Adaptive immunity as you know consists of T cells and B cells, and fronts much of the resistance to established infections. In fact, without adaptive immunity, you end up with a disease called SCID (severe-combined immunodeficiency), and HIV depletes CD4+ T cells resulting in AIDS. Important no doubt, but adaptive immunity has a process to it which makes it useless against brand new threats to which immunological memory doesn't yet exist. This is where the innate immune system comes in.
So we can either use the mucosal layer in the GI tract or the skin as an example, either way. Of course, the primary defense against foreign threats are such physical barriers as mucus, skin, the ciliary system of the lungs, and so forth. But lets say you get a cut or abrasion and now the skin barrier is compromised and a slew of bacteria enter the tissue. Your tissues contain resident cells such as macrophages (macs) and dendritic cells (DC) which have pattern recognition receptors that either recognize PAMPs or DAMPs. So what's a good PAMP? Lipopolysaccharide (LPS or endotoxin) comes to mind, and is recognized by toll-like receptors on DCs and macs, specifically TLR-4. These cells begin to produce mediators of inflammation such as IL-8 and IL-1ß which attract cells from the blood. The primary innate immune cell in your blood is a neutrophil, a type of phagocyte, which kill bacteria in a variety of ways. You also have a system of plasma (blood) proteins produced in the liver called complement which attempt to coat and directly kill the bacteria, or direct innate cells to targets of interest.
So say the bacteria is in the tissue, the tissue is inflamed, and a dendritic cell engulfs and digests a bacterium. The dendritic cell is what's referred to as an antigen presenting cell or APC, and APCs act to bridge innate and adaptive immune systems. Through an exogenous pathway sort of like this, they break down the bacterial proteins and "present" them on these MHC-II complexes (HLA in human). Macrophages, B cells and T cells may also be APCs. So when the dendritic cell is digesting the bacterial proteins and preparing to present them on MHC complexes, they move out of the tissues into the lymph system by expressing lymph node trafficking receptors such as CCR7 which responds to chemokines secreted by activated endothelium in the lymphatic vessels. The endothelium is activated by the inflammatory signals we talked about earlier. The DC goes to the lymph node where naive T cells and B cells aggregate, circulate in the blood, and re-aggregate.
Naive T cells tend to go back to the lymph node because they too express trafficking receptors such as CCR7 and CD62L that say "follow signals back to the lymph node." So this is where the magic happens. I'm not going to cover adaptive immunity but in short, typically APCs present antigens derived from foreign threats to naive T and B cells in the lymph node, thus activating them. These cells differentiate into a variety of lineages including effector and memory cells. As a note, you first adaptive response against a new threat takes about 2 weeks from start to finish to get antigens to an expanded pool of antigen-specific clones. Memory cells improve the second response by largely forgoing the wall of text above, proceeding directly to clonal expansion and elimination.

Abul Abbas, Andrew H. Lichtman, Shiv Pillai (2014). Cellular and Molecular Immunology (8th ed.). Elsevier. ISBN: 9780323315906.

All understood but I familiar with this system. What I ask is when APCs carry antigens into the lymph node as you said, and they are NOT recognised by T-cells and B-cells, what happens? Assume there is a new strain of bacteria for which there is no particular T-cell or B-cell receptor, then how does the immune system respond?

@Person I can't recall there being a case like that. Typically your lymphocyte repertoire is sufficient to recognize something due to the amount of combinations of possible receptors and epitopes. Otherwise, see SCID or AIDS. To my best knowledge I can imagine the pathogen would either kill the host or your body would attempt an in-situ inflammatory attack. Tissue-resident cells such as resident memory T cells can respond to unrelated threats by recruiting tissue defenses in an IFN-y-dependent manner, for example (1).

These mechanisms heavily damage tissue, however, and present a double-edged sword.

Remember that APCs present hundreds of MHCp-II complexes loaded with different peptide antigens. You have thousands of TCR or BCR combinations, and if I can find the paper, you need as little as 100 MHC molecules to efficiently prime T cells in the lymph node*. The chance that you have an immune repertoire, are not immunocompromised and still don't have the necessary cells is slim.

I see, then why is that there are certain bacterial infections we die from? Considering the body has the T-cells and B-cells particular to the antigen, should the body not able to fight off all infections?

There are a couple good examples. For example, the causative agent of tuberculosis manipulates a number of pathways in innate cells that stunt the ability of adaptive cells to respond (ref). As another example, S. aureus strains can cause agglutination of fibrin with bacteria trapped inside, provoking a continually stronger and more damaging immune response as cells are unable to clear the complexes (see something like type-III hypersensitivity reactions).

In some cases the infection kills you, in others, the now-dysfunctional immune response kills you as a result of the infection.

Yes,it's true.In an overview, our body fights against all these foreign bodies and microbes in order to eliminate them and the threats caused by them.If u analyze deep, what you call antigen is just a protein on the surface of any microbe.Your body cells eg.RBCs, also have antigens on their surface.But your body's immune system doesn't attack them normally.Its because of the recognition of self antigens of our body by the immune system so as to prevent them from being attacked.If your body is attacked by a bacteria that has a new antigen on it that our system has never encountered, the so called antigen presenting cells for eg.,T helper cells, Dendritic cells ,etc. recognize each and every antigen on the microbe surface and present them to developing T and B cells.So the antibodies(the anti-proteins for the antigens) are produced to act against the antigens on the foreign cell surface and render them inactive.These antigen proteins have specific sites called epitopes an which the sites of antibodies ,called paratopes bind.In the set of  disorders called autoimmune disorders the body's immune system attacks some self antigens because of some pathology.For some conditions such as AIDS by HIV the body's immune system is suppressed by initial attack on the T helper cells so that the recognition of antigens is suppressed and the immune system fails.And some microbes have the ability to modify the antigens on their surface.This is the reason for resistance of microbes to drugs.
Reference:Pathologic Basis of disease..-    Robbins and Cotran
----Combining a second answer into one---
It's simple...it has already recognized what are all self and thus any new microbe attacks your body it doesn't need to recognize it earlier...since it is something new the defense system starts working. Naturally when it is not known as self, it's some new invader which is read by the patrolling WBCs and by the effects produced by it( such as inflammation) which draws the attention of other WBCs to the site through some chemical attractants called inflammatory mediators...these attacking happens only when the foreign substance crosses the first line of defense our body has(the so called innate immunity plays an important role in it).WHEN THAT MICROBE IS ALREADY KNOW BY RECOGNIZING THE ANTIGENS PRIOR TO EXPOSURE (i.e. during a second or successive attack) the reactions start immediately i.e. the antibodies already programmed are released immediately along with inflammatory mediators ( which accouts for allergic response).If it is new microbe a recognition process takes place and after that anibodies are produced.HAVING T AND B CELLS FOR ALL POSSIBLE ANTIGENS IS NOT POSSIBLE BECAUSE THE CORRESPONDING T AND B CELLS ARE PRODUCED ONLY AFTER FIRST EXPOSURE and stored as memory cells... during second attack the memory cells are cloned and response is produced.Antigens are just proteins and can be infinitely many(just a single alteration in a protein structure produces a new antigen)...IT DOESN'T NEED TO KNOW WHAT IT DOESN'T KNOW which is not possible if not exposed once... Because of the need  for this first exposure attenuated antigens are given in vaccines so that during the first attack of the corresponding microbe T and B cells readily attack them.

Please add references for your claims and edit spelling and punctuation, at the moment the answer is not intelligible

I understand but what I'm asking is how does the body fight a foreign substance that it has NOT encountered before (with an antigen it does not recognise and simply knows that it is non-self). Does it have T and B cells for all possible antigens?

In my next answer

So you've said ''HAVING T AND B CELLS FOR ALL POSSIBLE ANTIGENS IS NOT POSSIBLE BECAUSE THE CORRESPONDING T AND B CELLS ARE PRODUCED ONLY AFTER FIRST EXPOSURE'', but how does the body produce NEW T and B cells to attack the bacteria?

They are produced in Bone marrow along with other blood cells...The process of maturation of Lymphocytes (B and T cells) take place in Bone marrow and Thymus respectively.Hence the name B and T. It is in this process the T cells learn to differentiate self and non self antigens.90% of the T cells fail in this and are naturally killed by apoptosis(Programmed cell death).After they are produced they release corresponding antibodies against the antigens of the invading microbe.The matured Lymphocytes play the roles of recognition and fighting.


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Can a person die from over exposure to rain?
Is it possible to die from being over exposed to rain? For example, if outside for a long amount of time (days) in a continuous storm?
I searched online but didn't find anything immediately. To me, maybe a really long exposure to rain (water) would cause skin tissue issues, which might then have potentially more serious effects on other body organs/systems.

Now that I think about it.... maybe I didn't find anything because it's never happened before... maybe I'm just not good at searching online. but still, can someone answer this question for me,?

Rain per se? No. But when you are wet, your body looses heat more quickly. If it's near freezing, windy, and raining you are in much more danger of developing hypothermia, or low body temperature. If your body temperature falls low enough, you can die. You may hear references to death from exposure, which is shorthand for "exposure to the elements", but the actual problem is hypothermia. If your feet are continuously wet for days and day, you may develop immersion foot, also called trench foot:

Trench foot is a medical condition caused by prolonged exposure of the
  feet to damp, unsanitary, and cold conditions. The use of the word
  trench in the name of this condition is a reference to trench warfare,
  mainly associated with World War I. Affected feet may become numb,
  affected by erythrosis (turning red) or cyanosis (turning blue) as a
  result of poor vascular supply, and feet may begin to have a decaying
  odour due to the possibility of the early stages of necrosis setting
  in. As the condition worsens, feet may also begin to swell. Advanced
  trench foot often involves blisters and open sores, which lead to
  fungal infections; this is sometimes called tropical ulcer (jungle
  rot).


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How effective is it to rinse fruit, lettuce, tomato, ... with water?
The general rule I've seen stated is that to get rid of some nasty bacteria, one should rinse fruit and vegetable under running water before using them, especially if eaten raw.
Most likely the effectiveness of such a measure depends significantly on the details of how this rinsing happens.  So, by how much is the risk of health problems reduced in different cases (e.g. just bath the fruit&vegetable in a water bowl, pass them quickly under running water, bath them and scrub them, keep them for a minute under running water (moving them around and scrubbing them at the same time), ...).
Of course, assuming those fruit&vegetable have already been washed earlier (e.g. before we bought them).

@Charles: This page is the kind of example I mention that gives general rules, but without detailing the actual effect on the probability of getting ill, nor discussing how that probability is affected by the various rules they propose and how we choose to follow them.

@Charles: Could you give me some pointers to those studies?


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Similarity between the human genome and archea genome in deep sea hydrothermal vents?
I'm trying to find some reference that shows what percentage of the human genome is similar to some organism from the domain Archea that lives  near or on deep sea hydrothermal vents.
Can someone points me out in the right direction?

The genomes are so different that it is pretty impossible to make any alignment expect for few very conserved region. I guess that you may be able to align histone genes eventually ribosomes (although they differ a lot). You may want to find these sequences and align them by yourself for training.

@Remi.b         I am curious, but would alignment of these genomes be done by some BLAST like program?

@Ro Siv Yes, exactly.

To achieve whole genome alignment between a genome as large as a human, and as small as an archea organism, is possible, but in the end, you'll have to strain your eyes to see patterns. The archea genome is about 1-5 million bp long, whereas the human genome is about 3.3 billion bp long (that's a thousand times too large).
In practice what this means is that you may or may not have small islands of similarity, in vast regions of emptiness.
Nevertheless, you can align whole genomes using the MUMer tool (http://mummer.sourceforge.net/). The white paper is here
Delcher, Arthur L., et al. "Alignment of whole genomes." Nucleic acids research 27.11 (1999): 2369-2376.
You might also be interested in reading this:
Wei, Liping, et al. "Comparative genomics approaches to study organism similarities and differences." Journal of biomedical informatics 35.2 (2002): 142-150.


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Why I obtain larger bands than expected after minipreparation?
guys!
I made a "home made" minipreparation to obtain my plasmid+insert (totalizing approximately 6Kb). But, when I run a agarose gel, I saw a unique band with 10Kb. Why?

Maybe it was open circular DNA.

Can you please add a gel image?

Have you done this same miniprep with a commercial kit? It may not be related to your homemade procedure. It might also be helpful to know how you were doing your ligation and your homemade miniprep protocol.

If the DNA got damaged in handling it could relax or linearize. That's to say, you have a 6kb vector but it's running about as slowly as the 10kb band in your ladder. You can maximize the supercoiled form by working quickly and gently with the prep.


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Is menopause a design or a degradation?
Does menopause appear to be a designed or an accidental phenomenon?
We might say it is "designed" if there is a biological process that triggers it.  Like menarche, where something genetic says, "Time to ramp up these hormones!"  Or perhaps the ovaries say, "Egg count has dropped below a critical level, time to stop the cycle."
We might say it is "accidental" if it is a byproduct of degeneration like all aging processes, and not the consequence of any particular biological mechanism.

Great question. I’ll try and write up a proper answer later, but it’s widely considered that the menopause is adaption to avoid inter generational conflict in humans.

@user438383 — "Widely considered". I look forward to the evidence. Meanwhile, I would observe that most animals don't survive beyond reproductive age, and that this has been a recent development in H.sapiens.

A third idea is that menopause exists to keep women from competing with their own offspring. It forces them to rechanneled resources in helping their descendants which is an advantage in species with such helpless but high energy demand offspring with such slow maturation rates. A woman at menopause age is unlikely to raise new offspring to maturity in the wild, so there is a evolutionary advantage to rechanneling effort into existing offspring.

Just-so stories are a folklore that we love to tell, but it's important not to get too carried away with belief in them.  To conclude the design or purpose of something, or whether it is accidental, implies a very deep understanding of all the possible paths of evolution, a God's-eye view if you will, that typically evades us.  Even so, predictable statistical effects do guide the course of evolution, so we'll attempt to explain anyway.
That said, I'll name two very sensible ways to explain how menopause came to be - almost surely not the only two.  One is that it is rooted in the social nature of humans, by comparison with cetaceans (especially orcas) which have a similar segment of their population.  If eusocial insects can have most females non-reproductive, it seems easy enough to believe that a lesser non-reproductive population is possible.  Johnstone and Cant, 2010 ask why older rather than younger women assume this role.  They conclude that philopatry of males, rather than females, accounts for the uniqueness of these two groups.  When females disperse and males remain, an older female is more related to young individuals than a younger female, because her sons remain in the area.  If the females are philopatric, the effect is reversed.  (Note that in all human populations, including hunter-gatherers, there is a substantial contribution from postmenopausal women)
The other way I'll mention is simply that arrested oocytes have a shelf life.  Huber and Fieder, 2018 argue for this by comparing the age of reproductive senescence with lifespan.  Their curve levels off a little past the point of human menopause, suggesting it is just hard to keep ovaries going very much longer.
Here's where it's important not to get too caught up in the myth.  A sense of "purpose" would make us argue for one explanation or the other -- but the reality of random evolution means that both can be true.  Oocytes could evolve to surpass current limits of reproductive senescence, and existing patterns of philopatry and social behavior could change.  But for now, this combination of young gametes and social assistance from the elderly seems to work.


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why monocot roots have a wide pith while dicot roots have a narrow pith?
Normally dicot roots have a nartow pith at the center but monocot roots have a wide pith. Is there any specific reason to this?

Welcome to Biology. Could you add a source or reference?


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What are the sizes of the cells that make up human hair?
The question is in the title, but I'll explain why the question arose. I'm curious about the rates that various cells in the body divide, and have found various information relating to this, but nowhere can I find how often the cells divide in hair follicles (only that hair grows about 1 cm per 28 days, and that hair matrix epithelial cells divide very rapidly, which results in chemo patients' hair falling out). I figure that I can calculate a back-of-the envelope answer if I know the average size of hair cells. For example if they are 10 $\mu$m, and hair grows 1 cm per 28 days, then I would estimate that the relevant cell turnover time in the follicle is on the order of 1.5 per hour, assuming that the cellular division leading to the outward growth of the hair proceeds in a serial fashion. This sounds like a roughly plausible estimate, since it is significantly faster than the turnover of other cells in the human body with a high turnover (like stomach or blood neutrophils) which have a turnover of a few days.
In any case I would appreciate any insight, whether the size of hair follicle matrix epithelial cells or the cellular turnover rate in the follicle during the anagen phase.

10uM sounds reasonable, thouhg perhaps a bit low for a keratinocyte when "flattened out". But 1.5 cell divisions / hour sounds way too high. The fastest dividing human cells I'm aware of are activated lymphocytes, which can reach about 10h doubling time. The fastest cancer cell lines are around 15h. Probably there is a larger dividing mass in the follice which then "thins out" into the hair, so that comparing hair growth rate to cell diameter underestimates the doubling time.


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Where exactly is pleasure
Question from an outsider: have we been able to pinpoint where exactly the feeling of pleasure comes from?
I know that there are several types of pleasure, I'm talking about the 'liking'. If that involves several separate pleasure centers (which is probably the case), I'm interested in any/all of them.
I am wondering if it is the electrical stimulation part, or maybe the release of some chemicals/hormones (but then, where do they go to produce the feeling?), or maybe a chemical reaction somewhere? How much have we been able to narrow it down? Do we know which part of the chain reaction is actually responsible for the feeling of pleasure?
Is it possible to like without a body, just a "head"? Are there experiment on rats (or people) whose body is completely paralyzed?
Any reference to scientific paper, as well as personal opinions or suggestions as to where I could find this type of information would be greatly appreciated.

Well, I'm glad you're curious, but you must realise that your question is highly complex. You'd certainly have to refer to a research paper for the exact, factual information. All the same, I can tell you a bit about Dopamine (the pleasure hormone) based on recent reading.
Dopamine creates pleasurable feelings when it is released in areas such as the nucleus accumbens and pre-frontal cortex. This happens when positive, or rewarding actions are undertaken. Dopamine release in the nucleus accumbens is so consistently tied with pleasure that neuroscientists refer to the region as the brain's pleasure centre. However, this is not the ONLY pleasure centre.
Now this is all I know. You should probably check out this page for more, in-depth info: http://wings.buffalo.edu/aru/ARUreport01.htm
It's a long read, but I'm sure you'll find something worth your time.

In the central nervous system, dopamine is a neurotransmitter and not a hormone. The 'pleasure signal' idea was an old hypothesis that has since been debunked. It's true that nucleus acumbens activation is linked to pleasure, but the case for PFC isn't clear. It would be more accurate to think of dopamine as modifying brain function in response to reward/reinforcement, but not directly responsible for feelings of pleasure. In fact, it can even be released in response to unpleasant stimuli. But, it has many other roles, like low level motor control.

Of course, dopamine has many functions, apart from being associated with the brain's pleasure system. And as far as PFC is concerned, it has been observed that depressed people have significantly low levels of activity in the PFC. Also, I've read in psychology that when we're joyous, activity in the left Prefrontal Cortex is stimulated, so I guess there is a relation. But yes, how far and to what extent does dopamine influence pleasure system is indeed questionable. All the same, thanks for the update on the debunked hypothesis. Feel free to edit anytime.


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The effect of sugar on rate of yeast Respiration
In my experiment, I am investigating the effect of different types of sugar on the rate of respiration of immobilized yeast (yeast trapped in calcium alginate balls). I am looking at glucose, fructose, sucrose and maltose.
Research leads me to believe that the disaccharides will perform the worst as they require enzymes to breakdown into monosaccharides and so will require more time to digest and this have a slower rate of reaction. In contrast the monosaccharides will work the best for the opposite reason.
Can anyone offer any insights into this hypothesis? Any helpful background theory that would support/discredit this.
Thank you.


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Is it possible to induce protein activation via frequency-specific mechanical waves?
Would it be possible to induce shape changes in specific proteins by providing specific frequencies of mechanical waves in a thermostatically controlled environment such that those proteins may be activated without requiring regular ligand binding?

This should defentily be possible and most likely already exists in the form of touch or pain receptors.
In the case of mechanical nocireceptors, which sense pressure or other mechanical changes in the tissue to signal pain, it's quite likely that there are distinct channel proteins that can correspond to mechanical deformation/pressure/etc, but I couldn't find any specifically known protein.
Most touch receptors seem to be based on bigger structures made up by neurons, so I'm not sure if they have one specific protein that senses mechanical movement, but I also wouldn't exclude that option - especially since almost nothing is known about non-human/mammalian touch receptors.


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Popular science on carcinisation
Carcinisation is described succinctly in a Wikipedia entry. The entry references few scientific publications regarding the subject. But are there any popular scientific articles describing and giving examples of carcinisation in the layman's terms?

GoogleScholar > Carcinisation


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UK - What type of spider is this?

Location: East Anglia, UK.
Approximate size (including legs at full span; like in the image): about 3cm.

It appears to be a Noble False Widow Steatoda nobilis

From http://britishspiders.org.uk/wiki2015/index.php?title=File:Steatoda_nobilis.jpg
It apparently is thought to be introduced to the UK, and there are some reports that the bite has caused some issues for some people.
https://en.wikipedia.org/wiki/Steatoda_nobilis

I had suspected as much but I wanted to see if someone else would come to the same conclusion. In fact the spider in the image you have provided is pretty much a carbon copy of the one I have shown (although mine had a smaller abdomen). I have caught ~5 of these spiders this year so far; all of which have reasonably small abdomens compared to what I would expect on a false widow; I'm assuming that makes them males? I have caught one with a very large abdomen which was unmistakeably a False Widow Spider, but that was 2 years ago.


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Why are there not two trees of life?
Life on earth started an estimated 3.8 billion years ago, very soon (in geological time) after the earth’s surface cooled to become solid and the first oceans formed. Nowadays, we believe that all living things can trace their ancestors back through a multi-branched tree of life, to this first living thing.
How do we square this rapid appearance of life, with the fact that it only seems to have developed once? In other words, we didn’t have life starting up in 10 different places on earth, giving rise to 10 different trees of life, why did we see only one?
In a variation on Richard Dawkins’ Selfish Gene, is it possible to think about a Selfish Tree?
Once the first tree of life arrived, it set about changing the atmosphere and environment generally, multiplying the number and range of species to fill every available niche (eg cold, hot, land, river, ocean, acid, alkali, large, small) in order to leave no space or circumstance for a second tree of life to spring into being.

@David - Maybe it's a pun? I think it's a pretty good pun. Trees do change the atmosphere without the assistance of anthropormophic nonsense...

Have you found a convincing argument in these two and a half years ?

Molecular phylogenetics, among other lines of evidence, strongly suggests that all extant life shares a universal common ancestor. However, this analysis is confounded by horizontal gene transfer. The following hypothetical figure, for example, explains how genetic phylogeny (right side of the image, this is what we are able to observe) may not represent true evolutionary relationships (left side of the image, this is what we are trying to infer) in the presence of horizontal gene transfer (represented by an arrow):
Martins L de O, Posada D. 2013. Proving universal common ancestry with similar sequences. Trends Evol Biol 4(1):e5.

While this problem can potentially be overcome by considering many genes, this becomes more difficult the further back in time you go, and impossible if you consider primitive life (such as an RNA world), about which we know very little. Assuming multiple origins of life, horizontal transfer of heritable information soon after their generation could be possible, as well as undetectable today. This creates a rather tangled tree, as visualized below:
Smets BF, Barkay T. 2005. Horizontal gene transfer: perspectives at a crossroads of scientific disciplines. Nat Rev Microbiol 3(9):675-678.

It is also possible that life originated multiple times on Earth, but only one "tree" survived to the present. In this scenario, there are multiple trees of life with many extinct and only one extant.
To sum up, the answer to your question is not known.

Definitely this. I'd expect that at the beginning of life informaron exchange was very permissive and fluid, with a lot of environmental DNA caught up by the protocells.

@LinuxBlanket That’s my intuition as well, but it seems unknowable.

What we know is that there's a single (more or less) genetic code, so even in the case of multiple origin of life, one code has dominated the "life scene". Do you know something about the evolution of tRNA?

@LinuxBlanket Yes, something, but certainly less than I should. Why?

The emergence of life out of matter is a very rare event.
The chance of having such event occurring more than once in a small time-frame is very little.
If the time-frame is large enough, then "New Life" could emerge again. However, in that case, the new emerging living organisms would be extremely disadvantaged by the presence of the "Old Life", already evolved to efficiently compete for energy sources etc.
Any new, barely functional, primordial life form cannot outperform the already existing ones, thus it would undergo extinction pretty soon. And that is why we ended up with a single tree of life on this planet.
Some links for further reading:
http://www.science20.com/stars_planets_life/calculating_odds_life_could_begin_chance
http://www.science20.com/news_releases/the_mathematical_probability_of_life_on_other_earth_like_planets
https://www.sciencedaily.com/releases/2018/01/180108090109.htm
https://www.scientificamerican.com/article/universal-common-ancestor/
https://www.nature.com/articles/nature09014
https://link.springer.com/article/10.1007%2Fs00239-010-9407-2
https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2896%2900631-X
https://www.sciencedirect.com/science/article/pii/S0022519318300419?via%3Dihub

"Any new, barely functional, primordial life form can not outperform the already existing ones, thus it would undergo extinction pretty soon. And that is why we ended up with a single tree of life on this planet." - I don't see how this is "by chance."

"The chance of having such an event occurring more than once in a small timeframe is very little." So, having two trees of life is unlikely, not impossible. Thus, it's still a matter of chances.

By that definition, just about everything and anything is by chance. I think your answer would be better if you left out the first line, and moved your last paragraph up top.

Mmm... Agree  I'll change my answer

Do you have a reference that clearly state the life originated only once? It actually feels more likely to me that there has been a number of abiogenesis events with creation of life-life creatures (but really at this level we come to the difficulties of defining what is 'life') but only one lineage made it over more than a few years and quite convincingly, one one lineage made it to today.

@Remi.b I didn't read that claim in this answer anywhere. I think it could be added that there could have been, and likely were, many events that you could consider as building toward some emergence of life, but once something fairly organized took hold it would have had too much advantage to be supplanted.

@BryanKrause The answer starts with The emergence of life out of matter is a very rare event which I took as suggestive that it is sufficiently rare that it only happened once but I agree that I might be doing a little bit of a stretch here.

@Remi.b I am looking for proper references to add. In general, I agree with you. It is a speculative answer since we don't have the evidence of any life-form differnet from the one we know. To my understanding, if the emergence of life would have been "commonly spread" then we should have evidence of it. Of course a "life-form" can exist for a shost time and then go extinct without leaving traces. But then again, that means that the emergence of a "strong enough form of life" is rare, and the most probable scenario is to have only one form of it taking over at the beginning.

I only read one of your links (the Nature article.) It doesn't support your answer the way you think it might.

@anongoodnurse It's just to start thinking about it. The basic idea is: taken separately, each event, like the emergence of a single chemical network, it's fairly common. If you mix "some random ingredients" you will get some reaction. If you apply selective pressure and reproduction, you will get improvements in the reaction rate. However, the chain of event that needs to happen to get a protocell is really long. The probability of each step, summed up, makes the emergence of life a pretty rare event.

Yes, I would agree that the emergence of complex life is a rare event, but I would disagree about simple life forms. If conditions were perfect for it to happen once, why not a hundred times? A thousand times? A million times?

This also explains why, experimentally, we can produce DNA/RNA peptides and membranes starting from simple chemical compounds quite easily, but we cant easily reach a higher level of complexity. To mix all together and get a protocell out of it is orders of magnitude more difficult. Indeed we are not yet able to produce a living protocell out of matter.

@anongoodnurse Indeed it could have happened. But then why don't we see the discendants of those hundreads of thousands emerged life forms? Probably they never kick off. As far I can tell, only one form of life managed to make it. A DNA/RNA-based protocell. Al the rest that was in the primordial pound, didn't make it, so ultimately, I do not consider it life. Of course it is matter of definition. If you consider some chemical system able to reproduce for a week and then disappear life, then I accept your point of view. But I consider such cases "failed starts" instead.

@alec_djinn "...I do not consider it life." Nonsense. I'm not talking about amino acid soup. I'm talking about life. Life is life, and the definition changes with new discoveries.

...all living things can trace their ancestors back through a multi-branched tree of life, to this first living thing.

I don't know exactly how anyone can claim that life arose on this planet only once. For all I (maybe 'we') know, it may have arisen a number of times, but only the most well-suited survived/adapted on this planet in its then-conditions long enough to begin a record of the type we now call the 'tree' of life (complex/eukaryotic organisms). You can't 'know' what you don't know. You can theorize, but you can't know.
Scientists make new discoveries all the time. There was a time (lasting millennia) when men of science* believed that life (in the form of a mud fish, for example) came from non-living matter (a mud puddle, in this case.) When that idea became laughable, the microscope was invented, and people still believed that microscopic life (bacteria, for example) arose from the proper conditions (a hay infusion, in this case.) It wasn't until Pasteur climbed the Alps with his experiment that spontaneous generation was finally put to rest.
At one point, we thought Homo sapiens were the only humans. We didn't know bacteria could live in the stomach, or in a lake full of arsenic.
How do we know what to look for when we talk of "life" if it's not life as we know it? We need to keep studying, keep thinking, keep our minds open about 'life' to find out more about it, like how many times it is likely to have arisen.
*I'd like to think that women of science knew better but were simply ignored.

I'm sorry, I think I don't get your point. Are you proposing that living forms of a second tree of life may still live on earth without us knowing?

I wouldn't say trees. Tiny shrubs or smaller, though, yes, past and present. Do you find that difficult to fathom?

I think you may need to state it more clearly, then :) also, see my comment on Samid's answer for my objections to this (albeit fascinating) hypothesis.

I don't really see the point. Sure, what you're saying is true in general about science: there is always more to discover, and there is room to be wrong about previous theories that were thought to explain certain phenomena. However, this is true in general and not specifically related to this question. The original question could simply then be rephrased as 'Why is there only evidence for a single tree of life?' This answer doesn't really address that. Also, the quip about gender is honestly totally out of place and should just be removed.

There's a serious answer here: the first paragraph (I'd ignore the rest).  We have no evidence of any history life on this planet before colonial or multicellular organisms formed clumps large enough to fossilize (and even then the evidence is unclear and debatable).  There could have been several microscopic replicating (living) systems that formed before the one we see today formed.  If they existed, they apparently died out, unsurprisingly without leaving macroscopic evidence of their existence visible today.

@Eff You are entitled to your opinion, as am I. Write an answer if you don't like mine. Crick is brilliant, Watson is an idiot, and Rosalind Franklin was dismissed. As to my answer's relevance to the question, again, write your own answer. I believe mine answers the question, and I'm not alone in science to believe what I do.

"There was a time (lasting millennia) when men of science believed that life  came from non-living matter."  I'd argue that the current prevailing opinion still looks for that mud puddle that life came from.  We've just pushed that mud puddle back roughly 4 billion years, and we call it an ocean now.  How far we have come from those barbaric days =)

It is entirely possible it did arise multiple times and we are the results, one of the nicer aspects of nucleotides is they can combine, it is possible different independently derived gene lines combined in the early stages. In our best guesses about what the most primitive forms of life would be like it is fairly easy to combine them. We simply don't know enough about exactly how the earliest life was structures to say with any certainty one way or the other. it could even be yes and no with life that was not compatible with this cooperation being driven to extinction by the cooperating ones. But as others have pointed out the window for this to occur is small, once the first form of life evolved the ability to breakdown larger molecules for raw material newly evolved life would be doomed, as would earlier ancestors of this "predatory" line. Life would literally clean up the traces of its early origins.

What is "life?"
It turns out to be a surprisingly tricky question.  Even descriptive lists like the one on Wikipedia  fall just a hair short of actually being a definition.  Through the years life has been famously easy to intuit and understand, and famously hard to analyze and pin down.  Whole branches of philosophy deal with that question.
This creates an uncomfortable challenge in answering questions like this one.  It's possible to define "life" in such a way that, if we were to look into the past with a magical crystal ball, we might find existed "outside of our tree."  I might then say "no, that's not how I define life," and pick some minor detail which exists in our tree but not in this "second tree" and add that to my definition.  Because there's one one overarching agreed upon definition with clear crisp edges, there wont be one clear agreement.
What we can say about the past is that the observed facts regarding the origin of life are consistent with the theory that life sprang up once, and only once.  That is intentionally shy of the wording you used.  I, personally, have problems with science using phrases which overstep the bounds of what it can actually prove, so I prefer to use more restrictive phrasings when the going gets tough.  For 99.9% of the time, "life originated once" is a sufficiently clear phrasing.  For the 0.1%, like this question, it's nice to rely on more precise wording. (and I'm open to any suggestions on more precise wordings in the comments)
I will note that we do find things that occurred more than once in the evolutionary tree.  It is currently believed that wings and flight evolved four separate times: insects, birds, bats, and pterosaurs.  To use the more precise phrasing, the observations in the fossil and genetic records are consistent with the hypothesis that they evolved four times, and rather contradictory with the hypothesis that they evolved just once.
That's not to say that's direct evidence in relation to your question, but I think it does point out the fact that scientists do indeed look for something happening more than once.  It would be an interesting result for them.  To date, nobody has been able to make a solid argument to show that life did indeed evolve twice.  Thus, a "second tree of life" gets relegated to the same dusty corner as Russel's Teapot.

If we look for life based solely on characteristics we've observed from the tree of life, then we will only find life forms connected to that tree. What I mean is, our current understanding of life revolves around cell theory, therefore whenever scientists go out to look for new life, they look for characteristics related to the cell.
May be another life form or tree exists that isn't derived from the cell. Food for thought.

But I think we can agree that the tree of known life, let's call it like that, has wildly outperformed the second one, at least in term of "visible" organisms in most terrestrial and aquatic niches. Also, features of life (birth, death and reproduction) aren't that subtle, I think we would be able to spot them if we came across them. What do you think?

@Samid "solely on characteristics, we've observed from the tree of life" what do you mean with this? We started distinguishing life from matter way before any tree-of-life concept was defined. Only when we started digging into the cellular and molecular biology of the various organisms on this planet we recognized their common origin. If we would have found organisms working with different chemistry, far from DNA and proteins, then we would have adjusted the tree-of-life accordingly. But up to now, all the living creatures we have examined have shown strong similarity at many different levels.


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What are these balls in meshopyll cells? [Plant biology]
Anybody knows what are these small balls? The picture was collected with a confocal fluorescence microscope. These balls have a green epifluorescence and they are in mesophyll cells of rice leaves.


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To have a drug travel to a specific place in the body can you just coat the drug in extracellular signals recognized by target cells?
In a lecture of mine the professor was talking about the issue faced in regards to drug therapy when it comes to targeting lung cells in cystic fibrosis. It was said that if unless the drug gets targeted just for the lungs it could simply travel randomly throughout the body and thus not effectively treat the disease. My question is if cells internalize extracellular signals and travel/respond accordingly why can we simply not coat a drug for cystic fibrosis in extracellular signals that specifically bind to lung cell surface receptors?

Yes you can, in principle, coat the drug particle with ligands such that it will be targeted to specific cell types. This is being considered and actively worked upon for development of targeted drug delivery. However, you should also bear in mind that doing these kinds of coatings would be costly and it would greatly increase the cost of the drug.
At least, in the case of cystic fibrosis or any other disease of the lungs, an easy method of restricting the drug to lungs would be by taking the drug in the form of aerosol, using inhalers.

Mechanism of inhalers.   Picture source: http://www.globalasthmareport.org/management/inhalers.php


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Why does a cell produce a lot of p53 protein only to later degrade it?
It is known that the half life of p53 is short and so does that play a role in the amount of energy the cell would need to expend to degrade all the p53? By that does the fact that the half life of p53 is so short does that just allow for the cell to not have to expend very much energy to degrade the p53 so in a way the cell doesn't "mind" having to degrade the p53 since it wouldn't take a lot of effort?

Transcription, splicing, translation, and protein degradation all require significant amounts of energy for the cell.

This answer is not reserved for the example you cite but for all proteins/RNAs which have high turnover. So your question generalizes to
What is the advantage of having high turnover? or in other words, What is the advantage of regulation via degradation?

Fast responsiveness. If your protein/RNA has a low turnover then it would take a lot of time for it to clear up from the cytoplasm even after the activating signal is gone. Enhancing the degradation will make the response fast. Cell cycle proteins such as p53 have to clear up as soon as the cell progresses to the next phase.
In certain cases an additional degradation control makes the regulation more efficient. If the "regulated" gene happens to be in turn an activator of many downstream genes, then efficient control actually helps in saving the cellular resources. I can't cite any literature for it but I have observed this in one of my unpublished research work using mathematical models.


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Why is Bcl2 a good target for cancer therapy?
Bcl2 is a family of proteins that are involved in the inhibition of apoptosis in cells. My question is that what makes this anti-apoptotic protein useful in cancer therapies as opposed to focusing on pro-apoptotic proteins? Are Bcl2 proteins simply easier to work with as opposed to the pro-apoptotic proteins? Or Bcl2 proteins have some sort of other characteristic that has allowed them for be the target for cancer therapies?

I don't have time for a full answer now, but the very quick explanation is that by inhibiting Bcl2 activity, you promote apoptosis. Bcl2 proteins are inhibitors, and by inhibiting the inhibitor you activate whatever process you're looking at.

Bcl2 is an anti-apoptosis protein, meaning that by inhibiting Bcl2 you will inhibit its anti-apoptotic effects. In other words, by inhibiting Bcl2 you actually induce apoptosis in cancer cells. This is one of those concepts in biology that can be hard to follow... that is, "by inhibiting an inhibitor you cause activation".
Cancer cells in particular seem to be resistant to the endogenous pathways in the cell leading to apoptosis, and the reasons for this phenomena are an area of active research. There are two major pathways of apoptosis within the cell, the extrinsic pathway the involves caspase proteins and the intrinsic pathway that involves Bcl2 and a number of other proteins associated with the mitochondria.
Bcl2 is part of a family of proteins that are involved in the intrinsic pathway of apoptosis - for a great and recent review see this recent review... or search on PubMed for a number of recent review articles.
Interestingly, cancer cells have a particular type of mitochondrial dysfunction that may be related to Bcl2, which is still incompletely understood. Cancer cells somehow inhibit the intrinsic apoptotic pathway, which involves the mitochondria. Additionally, cancer cells decrease aerobic metabolism by the mitochondria and preferentially use anaerobic metabolic processes instead - called the "Warburg Effect" by individuals in the metabolism and cancer fields. This was originally described by Otto Warburg almost 100 years ago - i.e. that cancer cells preferentially use anaerobic metabolism - but why this occurs is still unknown to present day.


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de novo assembly applications
Hey I hope this question supposed to be in this forum.
I'm not from the biology community, I'm from the data security community so im not familiar with the words you might use for answers
I need to use an algorithm that very similar to the de novo assembly algorithm.
I'll try to explain myself better I've some sequences of '1' and '0' all of them are pieces of one big sequence.
I've seen some applications that work with this algorithm such as SPAdes tadpole and Geneious but i couldn't make any of them to work for me except the Geneious because it was the simplest.
Geneious is not good for me because i need something that i can use by command line in the terminal
what application do you recommand me to use that i give input the sequences and the output will be the big sequence.
BTW, in the Geneious I've used a FASTA file for my sequence where my '0' and '1' translated to 'C' and 'D'
Thank you very much wait for your answers :))

You can try Velvet, but you'll likely end up with thousands of contigs unless your expected reference genome is pretty simple. This question hits many of the difficulties with de novo assembly. I'm also not sure what you mean by this:

BTW, in the Geneious I've used a FASTA file for my sequence where my '0' and '1' translated to 'C' and 'D'

Are you trying to use this for a purpose other than actual genome assembly? You say you're from the data security field, so it's unclear what's your end goal. If you only have a binary sequence, you better have a really long read length and hope there aren't too many repeats or you'll really have issues finding a consensus sequence.


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Is disease transmisson through milk consumption or meat consumption considered direct or indirect transmission route?
From an epidemiological point of view, is consumption of raw milk or meat considered as indirect or direct transmission ? Let's take the example of bovine TB. Is consumption of unpasteurized milk considered as direct or indirect ? IMO since milk is a tissue (liquid tissue but still), it is part of the cow, then how could you go more direct than eating the infected animal ?

Direct transmission is through direct contact with the infected person with no intermediary or vector. The Ebola virus and AIDs virus are examples. Indirect would be malaria spread through mosquitos, plague via rats, etc. The common cold spread through droplets in the air could seem indirect, but because of the proximity required, the CDC website lists it under direct. The CDC will provide reliable information for a lot of questions regarding infectious disease.


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How do mosquitoes react to blood feeding on a highly ethanol intoxicated host?
Considering that a mosquito can consume up to five times its body weight in blood during a single meal (Encyclopedia of the Arctic, M.Nuttal), and considering a very strong alcoholic intoxication of about 3g of ethanol /l of blood, what could be the effect on the mosquito of such a "binge blood feeding" ?
Blood with a 3g/l ethanol concentration corresponds to a a beverage with 3/789 (ethanol density) = 0.38 % of alcohol.
Brought to a human level, it is as if a 80 kg man would drink 400 kg of blood, which would have a volume of 400/1.06 (human blood density) so 377 L. Within these 377 L, 1.43 L is pure alcohol. Weight of that alcohol would be 1.13 Kg.
In mammals, blood weight represents about 1/13 of the total body weight, therefore in our example for a 80 kg man about 6.15 kg, hence 5.8 L.
So since alcohol is readily absorbed through the gastrointestinal wall, this would quite quickly lead, based on the "unfed" weight, to about 195 g of ethanol / L of blood. Ethanol lethal dose in human is commonly reported to range between 8 and 14 g / L. So with that dose you're dead about 15 times.
So I am perfectly aware that I am asking about mosquito and not humans, and that i am not taking into account several other parameters, but the demonstration was just displayed to prevent answers like "naaaaah no way dilution is way too high", so please elaborate your answers and comments and don't hesitate to provide references.
On another level those comments would be useful to clarify many animal models used on studying vector borne diseases involving the blood feeding of the vector on anesthetized animals.

The body weight of the mosquito is 10 gr, so it wont drink too much "alcohol" for the 50 gr of blood that it drinks.


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Could the EDTA coating of tubes kill blood fed mosquitoes?
Problem is as follows: culex pipiens fed with freeze-thawed cattle blood sampled in 9ml EDTA tubes enjoy their meal and thrive. Same population fed with freeze-thawed human blood sampled in 4 ml EDTA tubes die. 4ml tubes are overall quite less filled, hence hypothesis is remaining EDTA is more concentrated possibly leading to the death of the mosquitoes. Is this something plausible?
Thank you !

Have you tried using other sample tubes? For example heparin or citrate coated?

Not yet, i'd like to solve that mystery of cattle versus human blood

Put them in the same sized tubes?


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Hammerhead worm

Which Bipalium is this worm? It has no tripe. Nor head collar. It is dark brown as can be seen in the image. This worm is right now in Mauritius. Please help me recognise this Hammerhead worm. Thanks

I am not completely sure, but I think that this is a Hammerhead that comes from Asia: the Humbertum Covidum. It is a new, invasive species, hence the name. I am not sure because the Humbertum Covidum tends to be "Fatter", and your Hammerhead is longer. Another reason why I am not sure about this is that the Humbertum Covidum is a Asiatic species, which is very rare in Mauritius. However, I think this is the most accurate response, and I hope this helped!


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Do similar adaptations result in similiar genetic code?
Sometimes organisms within the same species evolve similar adaptations to similar living conditions without interbreeding.
Let's say we have two human populations which need to adapt to a colder climate, albeit one lives on the Northern hemisphere whilst the other one on the Southern hemisphere. Both populations develop hairy skin. Would the gene encoding the hairiness of the skin look similarly in both populations? Would this gene be at the same locus at the same chromosome in both populations?

Do similar adaptations result in similiar genetic code?

It can be the case but it is not necessarily the case. You sure can have the same mutation happening and raising in frequency in two independent lineages but you may well also have different mutations leading to similar adaptations in different lineages.
Example
As you talk about humans, let's take an example from humans. The ability to digest lactose (milk) at adult age has evolve several times independently. I just copy-pasted from this answer of mine

Gene LCT
Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.
Expression of LCT
In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.
Today, the inability to digest lactose at all ages in humans is called lactose intolerance.
Three independent mutations
Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different [SNPs][6] (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.

In this example we can know that the ability to digest lactose at adult age evolved at least 3 times independently. It is quite hard to tell whether it had evolved more than three times. It is indeed possible that the mutation G/C-14010 had occurred in two independent lineage but it would be hard to disentangle them today if the two lineages are not clearly geographically isolated (and in humans, very few populations are really isolated from the others).

That's exactly what I suspected, just wanted to make sure. Thank you for your answer, I really like that you included a real-world example I can stick my nose deeper into :D


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Interbreedability between current humans and his ancestors
I want to know the first point of time in the past when genomes have diverged so far from modern human genomes so that they both (human and ancestors) are not interbreeadable anymore and can be seen as separate species.

Does pre-zygotic isolation count?

Related (but definitely not a duplicate): How could humans have interbred with Neanderthals if we're a different species?

"Does pre-zygotic isolation count?" I don't think so ;-).

Short answer
Considering only post-zygotic isolation and based on below discussion, I would tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA for safety.
Long answer
Concept of species
The post How could humans have interbred with Neanderthals if we're a different species? makes a good introduction to the difficulties behind the concept of species.
Pre-zygotic isolation
Anatomically speaking, it is probably possible to get a spermatozoid cell from a 20th century man start fusing with a Homo abilis ovule (and vice-versa). The potential pre-zygotic isolation will rather be caused by aesthetic appearance.
To the risk of sounding posh, I would say that Homo abilis hairy face does not exactly fall within my standards! I suspect it will be the same for many of us, humans of the 20th century. It is hard to really know how much time one needs to go back to consider that we don't disgust each other enough to refuse mating together. There are a few reasons why this is hard

Reconstruction (esp. facial reconstruction) is often too inaccurate to really allow to tell how ugly their faces were.
It is going to be super hard to tell what they would just about our faces today! I bet they'd laugh at our ridiculously small jaws!
It is hard to fully separate the environment from the person. In middle-age (in Europe at least) people would bath a few times in a life-time. Again I would consider this not in my standards!

But let's focus on post-zygotic isolation.
Post-zygotic isolation
Humanzee

The humanzee (Homo sapiens sapiens × Pan) (also known as the chuman or manpanzee) is a hypothetical chimpanzee/human hybrid. An unsuccessful attempt to breed such a hybrid was made by Ilya Ivanovich Ivanov in the 1920s. There have been occasional reports of human-chimpanzee hybridization, notably regarding a performing chimp named Oliver during the 1970s, but none of them have been confirmed. Similarly, the possibility of a chimpanzee–gorilla hybrid, known as a koolakamba, also remains unsubstantiated.

There is no evidence of humanzee but it is important to realize that the idea of such hybrid is not fully unthinkable. Human and chimpanzee share a common ancestor about 6 millions years. So, if a humanzee is consider eventually possible, I would quite definitely consider that a H. abilis (~1 MYA) or H.erectus (~2 MYA) and 20th century human could well interbreed if we were to live at the same time.
Sumatrans and bornean orangutans can hybridize (Malinson, 1984) despite that their lineages have split about 1.3 MYA!
So putting all of that together and follwing some vague intuition, I would personally tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA (MRCA with gorillas). But really, it is a rather vague intuition.
See also CrashCourse > How to Make A Humanzee

Ok. I posted this question in a german q&a website. They also came up with estimations of about 500000 to 7 Million years.


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What are embryophytes? And how are they characterized?
What does it mean when it's said that plants are embryophytes?
What are the specific characteristics that help determine that?

The name derives from their innovative characteristic of nurturing the young embryo sporophyte during the early stages of its multicellular development within the tissues of the parent gametophyte.
source
https://www.revolvy.com/main/index.php?s=Embryophytes&item_type=topic
Similar definitions are in the New World Encyclopedia and Merriam Webster Dictionary.


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Monohybrid Cross
There are two types of pea plants according to Mendel:
1)Tall(TT or Tt)
2)Dwarf(tt)
But I have a doubt! Is there a heterogeneous dwarf pea plant(tT)? When there can exist a heterogeneous tall pea plant, there must exist a heterogeneous dwarf pea plant also! This doubt is troubling me very much! Please clear my doubt!

Why there must exist a heterogeneous dwarf pea plant also. I don't understand why you think it must be the case.
Under this simple genetic model, there is no environmental variance and T is dominant over t (t is therefore recessive) and therefore the heterozygotes Tt have the same phenotype than the homozygote TT. There is no Tt individuals that have the same phenotype as tt.
If t was dominant, then Tt individuals would have the same phenotype as tt individuals. If T and t were perfectly additive, then Tt individuals would have a phenotype half way between the TT and the tt phenotypes (Tt would be of average height).
Please note, that very few real life cases are that easy. There is often interaction between many loci and there is often (if not always) environmental influence on the phenotype.


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Does the right ventricle affect blood pressure in pulmonary veins?
Now, I know there are multiple things that push the blood through the entire pulmonary circulation like the contraction of arterial muscular walls... But what I want to know is whether the right ventricle pumps the blood even through the pulmonary veins, or whether its effect stops at the arteries.
This may not be of significance to be honest, but I got into a debate with a friend over this and thought people here would end this debate :)


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Bug identification: rectangular green and copper creature
I've found a very strange-looking creature on the street of a local park (Russia, Urals). It was 2-3 cm long,  almost rectangular, with green and copper colors, running somewhere with low speed. I've never seen anything like it before. Here's a picture (sorry for the quality):

Does anybody know what this is?

I tried zooming in on this picture and wasn't able to; that having been said, from what I can see you have a mating pair of whatever these are (I do know the order, and think I know the family, but I am having a tough time locating a web-based resource that will help in a deeper identification).

@ArthurJFrost This is an interesting option. I think they would move more chaotically if they were mating (and this thing crossed a road on my eyes), but I'm no expert.

@ArthurJFrost you are correct, I see legs at both ends.

Some sort of Pentatomidae, but that's as close as I can get with this photo.


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Do bacteria develop a resistance to antimicrobial peptides at the same rate as against "regular" antibiotics?
From what I understand, antimicrobial peptides are roughly grouped into three structural sets, with large variations present between different groups as well as within the groups. Their anti-microbial properties tend to be through slightly different avenues than traditional antibiotics as well, since they can effect cell wall structure and some intracellular targets.
I have been told that antimicrobial peptides are thus able to be effective against as larger spectrum of organisms and that said organisms develop a resistance more slowly.
I do not understand why either of these cases is true, since any antibiotic sharing the same target should have the same effectiveness. Also, evolutionary pressure is what drives resistance, so why should that be reduced against antimicrobial peptides?


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How do plants benefit from their seeds being buried?
Common planting advice, when starting many plants from seed, is to bury the seed some small distance under the soil.  It seems like most plants (at least members of class Dicotyledonae) will grow a root, lift the seed casing out above the surface, then the cotyledons push off the seed coat.
My question then is: why is it recommended to put the seeds below ground at all?  It would seem that dirt only serves to interfere with the first stages of growth.
I can guess at a few reasons:

To keep moisture around the seed
To make sure the root hits dirt no matter which way the seed is oriented
To prevent predators from eating the seed
To keep the seed in place

Absent these reasons, is there any reason to have soil sitting on top of a seed?

Excellent question!
The main reason why us humans bury seeds seems to be to keep seed-eaters from finding them, though any historical evidence that could conclusively prove why we started doing that is probably lost to time, since we discovered agriculture before we began writing things down. Beyond that, you've rightly identified a number of advantages to burying seeds.
First, it may be helpful to note that no physical substrate is even necessary for plant nutrition. We can actually grow plants in mid-air, but for the fact that we would still need something to keep them still. Seeds will germinate if you simply spray nutrients at them - see aeroponics. This is because plants take in what would be soil nutrients via cation exchange and diffusion, as opposed to more a more active process like phagocytosis. By surrounding the seed with nutrient rich substrate, we inadvertently improved germination by exposing more of their surface area to nutrients.
As far as soil seeking behavior goes, Thomas Knight demonstrated that plants can actually find the ground by following gravity. He did this by sticking seeds onto a rotating disc to simulate gravity in another direction and germinating them there. The seeds responded by growing roots away from the center and sprouting stalk towards the center.
Of course, burying seeds too deep means that they may run out of energy before they can break the surface. However, it seems that many varieties of seed have a better chance of germinating in darkness.
Resources

On the Direction of the Radicle and Germen during the Vegetation of Seeds
A Reversible Photoreaction Controlling Seed Germination

Ahhh I hadn't thought about light coming into play