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Septic Shock: I'll kill myself before you kill me
Most of the deaths caused by extracellular bacteria don't actually result directly form their action. Rather, it results from an overreaction of the immune system to antigens such as LPS and LTA (Superantigens are bacterial toxins with an enormous power in originating immune responses; they are able to activate numerous T cells through a different TCR, which will produce too many pro-inflammatory cytokines, resulting in an excessive reaction by the body and causing self-tissue damage, etc), and it is this excessive reaction of the immune system which ends up killing the organism.
http://www.medicalnewstoday.com/articles/311549.php
http://www.medicalnewstoday.com/articles/305782.php?sr
How come, after all this evolutionary time, we have this self-killing mechanism? Why do T-cells have receptors to such generalized and potent antigens, which will frequently result in self-damage? Is it because at the point of infection that this happens, we would die anyway from it, so it doesn't alter fitness?

Sounds very interesting. Can you please support your claim that Most of the deaths caused by extracellular bacteria [..] results from an overreaction of the immune system to antigens with a reference?

@Remi.b sure, I think it is all very clear here: http://www.medicalnewstoday.com/articles/311549.php
also here: http://www.medicalnewstoday.com/articles/305782.php?sr

@Remi.b this is also interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422540/

the mechanism exists to protect against the spread of infections, the infection cannot utilize the cells to make more copies of themselves if the cells suicide when infected, this is a perfectly normal response to low level infections, sore throats for instance are often caused by this response. Additionally animals that reach the point of septic shock (massive widespread infections) would rarely survive anyway. so the question you should ask is without any form of medical intervention is the individual actually less likely to survive without this response.

@John the question is somewhat that, is there a chance that organisms who died from septic shock would have survived if the immune reaction was less strong? because if yes then it would make sense that we had evolved in that direction.

@John in this case I was talking specifically of extracellular bacteria, which don't grow and reproduce inside host cells, so the death of host cells to prevent that wouln't fit here

Ignore most of my statment, I was thinking of a different antigen response then you are talking about. Although I should mention none of your sources indicate percentages of extra to intracellular infection in sepsis. As for septic shock survival the question is whether MORE would survive, because weakening the immune response is going to get some killed. Almost everything in biology is a cost benefit trade off. this paper has a good description of the benefit of various immune responses during sepsis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422540/

This excerpt is also relevent.  http://www.birmingham.ac.uk/Documents/college-mds/facilities/cis/Essentialimmunology/Chapter1.pdf  "Mice deficient in tumour
necrosis factor are protected fromshock induced by lipopolysaccharide but on the other hand are
more likely to die from overwhelming bacterial sepsis. This illustrates the fine line that the immune
system has to tread between evoking protective immunity and killing the host."

@John yes, but knocking out TNF is an extreme deficiency in the immune system. I was thinking more of something like the organism being able to detect when the immune response is causing too much, potentially fatal host damaged, and then downregulating it a bit

@John yes, the question should then be if having that mechanism would pay off, meaning less individuals would die from weakened immune response than from an excessive one.

which is an entire new system (which could also be exploited) for an exceedingly rare circumstance. Remember the rarer the event the less evolution will be able to prepare for it becasue it is overpowered by more common selective pressures.

@John true, although I doubt apart from modern times that it was of such rarity

Which shows how well the current setup works, consider people prior to the invention antibiotics and germ theory, people routinely lost limbs and survived so the existing system obviously works for preventing sepsis. The only time septic shock comes into play is under circumstances people were unlikely to survive in the first place, severe sepsis. You can see how fast response is more important than a measured response. Preventing severe sepsis would be more important than mitigating it under natural conditions.

@John but not to the point of killing itself. I imagine there must have been a lot of deaths from septic shock caused by, say, a severe urinary infection, whereas if the response were more contained maybe they would have survived

Let us continue this discussion in chat.

The important thing to recognize about the host response to sepsis is that it is actually a generalization of mechanisms used in local infection response by the innate immune system. When an animal has a local infection, such as at a wound site, innate immune cells such as monocytes and macrophages recognize 'generic' bacterial features, such as lipopolysaccharide (LPS). When they recognize these features, they respond by engulfing the pathogen and releasing cytokines that result in local vasodilation and inflammation. In this context, these responses are close to ideal. Vasodilation helps to isolate the area and promotes the recruitment of more immune cells.
These sorts of small infections are very common for all animals (just about every creature cuts itself at least once), including humans, and the absence of this response would result in sepsis (not the immune response, but just sepsis itself) because the infection would not be contained. Control of such local infections is thus 'life-or-death' for all creatures—which is an extremely powerful selective pressure.
The other thing to consider here is when in nature are these local defences overwhelmed such that sepsis, and then septic shock, which is what you are asking about, occurs. The answer is that it does not happen very often. Transient bacteremia is relatively common (it even happens when you brush your teeth, see this paper for example), but overwhelming bacteremia, sepsis, is not very common in healthy individuals. It is generally a condition that affects weakened individuals and those who have already reproduced. We notice it far more now because it is a major cause of death for humans hospitalized for other conditions, as well as older people with pneumonia. Most of the primary causes of sepsis though—major wounds, pneumonia, weakened immune systems—would be death sentences in themselves in the absence of medicine, irrespective of the organism's response to the sepsis.
That is not to say it is completely invisible to selection, for example this paper, and others like it, demonstrate that the immune cells responsible for septic shock are regulated by hypoxia (a major feature of shock). However, it is reasonable to say that any fitness advantage conveyed by a reduction in the intensity of septic shock would be dwarfed by the fitness penalty paid if that reduction also reduced the efficiency of the response to local infections. For this reason, it is likely that septic shock is an evolutionary accident, a trait that exists in part because it is irrevocably linked to a set of highly advantageous traits (those involved in local infection response), rather than a trait that has been extensively selected on by evolution.
Note that this answer is my opinion only. To the best of my knowledge, there is no definitive answer to this question yet, and future research may prove me wrong.

Welcome to Biology.SE! Seems like you are quite familier with how ideal answers are posted here ;) +1 for the effort, and this comment, just to appreciate the nice content in your first answer! :D


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Can intron become exon in alternative splicing?
From this image
We can see several exons that are actually introns in other genes. It's not a really a different gene, it's an alternative splicing of a gene. My background is not biology so is it possible for alternative splicing to behave like this? I only know that alternative splicing is just exon skipping and introns will just stay introns and not become exons. Can someone explain this to me and give any suggestions on which part of biology (or genetics) I need to learn. Thank you.

I'm not sure what you're asking. If a portion of sequence ends up in the mature RNA, it is by definition not an intron.

Hmm, you are right. So, do you think from that picture, it's just exon skipping? What does that kind of gene called? Is it still called isoform? I have a hard time to do RNA-seq analysis for this gene because of overlap position near the end can be mapped to 9 gene.

Just did some brief reading. It seems each form is under the control of its own promoter. This means that A8 will have to splice out the first exons of all other forms (this would be exon skipping). On the other hand, the A1 pre-mRNA doesn't contain any other first exons to begin with. These would be classified as gene isoforms.

Thank you. Can you suggest where you read those explanation? My knowledge in biology is really limited so I need to read many material to improve my knowledge.

http://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=54658

http://www.ncbi.nlm.nih.gov/m/pubmed/16399340/

Thank you so much. So, all of those gene will share 4 exon and just different in the first exon right? Does it mean, if I can count the reads of the first exon, I can estimate to total count of the gene (for example UGT1A1). Because the problem is the result for the last 4 exon is ambigous.

I don't know a lot about the analysis of RNA-seq data, but that sounds plausible to me.

Most of the transcripts you show have different transcription start sites. In other words, this happens because of alternative transcription start sites. So this is not typical alternative slicing. Some genes have different transcriptional start sites, but the case you show has exceptionally many start sites.

If a portion of sequence ends up in the mature RNA, it is by definition not an intron (save for abnormal splicing events and rare intron retention).
Specific to your question, it seems each form is under the control of its own promoter. This means that A8 will have to splice out the first exons of all other forms (this would be exon skipping). On the other hand, the A1 pre-mRNA doesn't contain any other first exons to begin with. These would be classified as gene isoforms

References:
Owens IS, Basu NK, Banerjee R. 2005. UDP-glucuronosyltransferases: gene structures of UGT1 and UGT2 families. Methods Enzymol 400:1-22.
NCBI Gene: UGT1

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What does this mutation notation mean: MAP2K41161fs*12
I received a report that had a mutation notated as: "MAP2K41161fs*12". I'm used to seeing this sort of thing: BRAF(V600E) or BRAF(T1799TA). Can someone tell me how to interpret "MAP2K41161fs*12" ?? Is it a deletion? An insertion? A translocation? Or What?

Can you post a link to the paper? MAP2K is the protein. fs means frame shift and *12 gives the length of the new reading frame (ie the number of codons up to and including new stop codon). Usually before fs they give the first mutated amino acid, so I'm not sure what the number 41161 means (no protein is that long).

Or the protein is MAP2K4 and the number is 1161, but I still don't know what that means since MAP2K4 is 399 aa…

Oh my....duh! Of course I should have figured out that "fs" means frameshift. But I'm used to seeing just the ins or del. I've now looked at a couple of online pages describing this notation, but they refer to the length of the new reading frame (just as you did). This seems like an odd thing to provide...doesn't the new reading frame go on until the next stop codon or complementary indel? And you'd have to provide the terminal event (X or indel) anyway, right? Weird. Anyway, thanks! I can figure out the rest from this hint.

fs means frame shift and *12 gives the length of the new reading frame (ie the number of codons up to and including new stop codon). Usually before fs they give the first mutated amino acid, so I'm not sure what the number 41161 means (but apparently the OP does).

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Specific numbers of nucleotides in Okazaki fragments
Okazaki fragments are formed during replication of the lagging DNA strand. What determines the length of these fragments?

possible duplicate of formation of okazaki fragments in lagging strand during replication

@dustin page not found

The length of Okazaki fragments is not necessarily a tight distribution. The lengths are determined by the spacing between adjacent sites where DNA primase has synthesized a short RNA primer on the lagging strand at an active DNA replication fork. In E. coli, as I recall, this occurs on an average of once per 1000 nt.
DNA polymerase holoenzyme then uses that 3'-OH on the RNA primer as a substrate and synthesizes the DNA strand complementary to the Template strand UNTIL it bumps into the next RNA primer.
It is those nicks in the newly synthesized lagging strand, that have a deoxy-3'-OH, and a ribo-5'-phosphate, (that need to be removed and ligated) that mark the boundaries of individual Okazaki fragments.

In chromosomal DNA nucleosomes are spaced by 200 nucleotides.. so, this can be a reason of okazaki fragments limited to just 100-200 nucleotides in eukaryotes? I am confused...

Where did you obtain the number of 100-200 nucleotides? All eukaryotes? DNA replication in eukaryotes probably best characterized in yeast (budding yeast and fission yeast), fruit flies, rats (rat liver biochemistry?), and human cell lines, like HeLa cells.

During replication, DNA is naked: no nucleosomes there. I am not sure but nucleosome formation may be later than ligation of Okazaki fragments.


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Clarification about taxon (plural taxa)
If i am right, then any category placed at any rank in the taxonomical hierarchy is a taxon. For example Panthera, Mammalia, Solanaceae etc. But are general group of organism (casual groups which are not biologically defined like Birds, Cats, Fishes) also regarded as taxa? Please clarify.

Definition of taxon (From ICZN glossary):

A taxonomic unit, whether named or not: i.e. a population, or group of
  populations of organisms which are usually inferred to be
  phylogenetically related and which have characters in common which
  differentiate (q.v.) the unit (e.g. a geographic population, a genus,
  a family, an order) from other such units. A taxon encompasses all
  included taxa of lower rank (q.v.) and individual organisms. The Code
  fully regulates the names of taxa only between and including the ranks
  of superfamily and subspecies.

Birds are called Aves and that is a taxon. Cats come under Felidae. If you are asking - "Is a colloquial/vernacular name considered a taxon". Perhaps the group of organisms can be referred to by a colloquial name when they are not given any scientific name but in this case these taxa are well defined by a standard scientific name (according to the nomenclature codes such as ICBN, ICZN, etc).
So "cat" is not a taxon, but cats fall under the taxon called "Felidae".
In some cases certain groups are not even actual clades. A clade is a monophyletic group i.e. all its members have a common ancestor. The group — reptiles, is not a clade.


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At what rate do chromosomal rearrangements occur?
How often do chromosomal rearrangements occur?

I am interested about these kind of chromosomal rearrangements that are passed on to the descendants, i.e. germ line chromosomal rearrangements. The value I am looking for is similar to the mutation rate but only take into account major mutations such as chromosomal rearrangements.
Supposing there might have some important variance in this rate among species, then I am interested in eukaryotes and particularly in plants. If needed, the answer can be split into the different types of chromosomal rearrangements (robertsonian translocation, other translocations, inversions, ...)

You can have a look at these papers: 1, 2. Gotta go now. will post an answer when I get time.

Just to clarify; you are asking only about larger chromosomal rearrangements (as in translocations, inversions, deletions etc), and not the frequency of also "normal" chromosome crossovers between homologous chronosomes?

Yes, indeed, I am interested in major chromosomal rearrangements and not about normal standard cross-overs.

Do you care particularly about the difference between somatic and germline rearrangements?

I was thinking about germ line rearrangements only. I would necessarily refuse insights about somatic rearrangements though! I edited my question to clarify this point. Thanks for your comment

@WYSIWYG must be really busy...

@RenaissanceProgrammer I was free for quite some time between Sep 2014 and now but nobody reminded me then. I am busy again now :/

Obviously, there won't be a single number for this.
The phenomenon is fairly well understood in yeast. Unfortunately, most studies tend to focus on the rate of formation of specific well-understood rearrangements, and then use that as a baseline. I am having trouble finding a measurement of overall rearrangement rate, although the system is ideal for this.
There has been some work on characterizing rates of rearrangement (and its evolution) across evolutionary history, I don't know if that is directly relevant.
This paper has a decent breakdown of the incidences in humans across different kinds of translocations. For example:

Additional studies (5, 6) followed and the incidence of balanced translocations was ultimately determined to be 1 in 500 in the general population.

Studies using cleavage stage biopsy for reciprocal translocation PGD have reported proportions of unbalanced embryos as high as 82% (57).

There is good reason to expect that it varies significantly across species and across chromosomes. For example, the Drosophila Y is a hotspot.
And (first paper):

Rearrangements involving chromosomes 13 and 14 (der(13;14)(q10;q10)) account for 75% of Robertsonian translocations (12).

For an early paper looking at a large population, you can see here.
Note that most of these human numbers are indicative of population incidence rather than rate of occurrence. Others have attempted to study effects on the translocation rate directly.
The best citation that I found for directly measuring translocation rate is here. However, the data are apparently for somatic translocations and are rather unevenly sampled so I am unsure of how generalizable it is. I looked at WYSIWYG's papers and they might provide some specific examples but they don't seem to address translocation rate directly either.
Take-home, it's hard to directly measure rearrangement rate in humans due to inviability of many/most aneuploidies early after fertilization. Somatic is easier to estimate but may not be representative of rearrangements in the gametes.

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Which plant is this?
I'm curious what plant this is! I found it at 37°52'23.2"N 122°16'55.3"W (north of Oakland, California, USA).

i have at my back yard ,i do not now the name .we have it in Eritrea we call it Chilan smell's good .we use it for holiday decoration.

That's East Indian Fennel. It's a member of the celery family. Every part is edible, including the root and the seeds. It's packed with vitamins, calcium and is used to stop restless leg syndrome, among other ailments. The feathers (leafs) can be used to wrap meat and fish before baking or eaten fresh on a green salad. Once par boiled they lose their licorice taste and can be eaten like steamed spinach. The Italians brought it over in the early 1800s and it flourished. It grows along the freeways of California and other states. I pick large batches of it for my juice extractor and other things. Look up the many medicinal uses of fennel. The flowers look similar to dill.

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answer that actually addresses the question. Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. In particular, you are more likely to get a positive response to an answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. Thank you!

How can you tell the  difference between East Indian Fennel and wild fennel (Foeniculum vulgare)? Is there a difference?

i like it -----

Fennel is native to Europe, so I'm not sure why you would claim this is "East Indian Fennel". If you have any evidence that this is not Foeniculum vulgare please [edit] your post to include that information.

It looks a lot like Queen Anne's Lace, but yellow and with more slender leaves. I believe it's Sweet Fennel (Foeniculum vulgare). It's in the Apiaceae family, which has a lot of edibles: carrots, parsley, fennel, anise, caraway, celery, chervil, cicely, cilantro, cumin, dill, parsnips and more. Black swallowtail butterflies lay their eggs on this, so often you can find a really fine caterpillar on them; bees like the flowers as well.
Apiaceae has 3,700 species spread across 434 genera; it is the 16th-largest family of flowering plants. It has a few poisonous plants, like water hemlock (white flower) and poison hemlock (also white). Wild parsnip has a very similar yellow flower but it's sap is wildly irritating in the medical sense (it will cause pain and blisters); its leaves are very different.

If you crush some of the slender leaves between your fingers, it should smell like fennel (a common spice, e.g. in Italian sausage), or if you aren't familiar with that, a bit licorice-like.

Sweet fennel (left, up to 6 feet tall)        Wild Parsnip (right, 3-5 feet tall)

It does taste like licorice!

@AlwaysConfused if I used this procedure, would I be safe? waiting an hour between each step of (1) lick (2) chew small piece, spit out (3) eat small piece (4) eat large piece. and, like, not continuing if it tastes unpleasant

Briefly asking google about poison-hemlock, it seems like http://www.toxinz.com/Demo/6/UExIMDIyLzEwNGg%3D#secrefID0EJJAI I'd actually be fine if I ate a leaf of it (even if I didn't go to a hospital), I just might get painfully sick for several hours.

Poison hemlock has white flowers, is "leafier" (it's more commonly confused with parsley than with fennel), and doesn't smell or taste like licorice.  I would absolutely bet my life on your picture being of fennel based on the flowers alone.  :)  Another differentiator is that you're more likely to find fennel growing in drier areas (it's pretty common on hillsides and roadsides in the Bay Area) whereas hemlock likes moister conditions (usually near a creek or at least a depression in the terrain -- it grows all over Glen Canyon Park for example).


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What are blood group determinants?
I am trying to understand if they are the same as the blood antigens. The books I have tried to read say something about them being the antigens on the surface of the red blood cell.

In immunology, determinant is another name for epitope (the portion of an antigen recognized by a BCR/Ab or TCR).

Blood group A expresses A antigens and anti-B antibodies etc etc, see the next figure:

Taken from the wikipedia entry on blood groups.


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Are codons that map to the same amino acids interchangeable?
From wikipedia, in the section on the RNA codon table, I see a mapping between codons and amino acids. There, Valine is related to GUU, GUA, GUG, GUC.
Does it mean in the same context that these four codons are interchangeable? Could one replace GUU with GUG?

Yes, those codons can be exchanged to get the same amino acid, but it might affect how much protein is made, see codon usage bias

There are some subtle nuances, as well: http://www.ncbi.nlm.nih.gov/pubmed/11943474

You seem to have read the table a little wrong: T doesn't appear in RNA. Probably you meant GUG, not GUT.

@LeonAvery - yes - I read it wrong.  thanks for the correction.  Corrected in question.

In Spinal Muscular Atrophy (SMA) a single nucleotide C to T transition mutation occurs in SMN2 gene sequence at 840 that produces the same phenylalanine but it gives rise to some translational enhancer/silencer interactions, so intended final protein lacks exon7, gets unstable and shortlived and patients suffer from lack of motor-neuron functions which lead to paralysis.

I think given that you're just getting started with genetics, you can say that the codons are interchangeable. This is generally true, though not technically correct. Here are a few reasons for why this is the case, though there's probably more:

Specific organisms use specific codons with different frequencies. This is usually related to the tRNA abundance in the cell. Using a codon for which there is relatively less tRNA available would be expected to lead to a decreased protein synthesis rate.
Using different codons can affect mRNA secondary structure, which could affect expression.
Some codons, especially stop codons, can influence translation contextually through a process called recoding. This can include frame-shifting, read-throughs, cleavage or, perhaps most famously, coding for the amino acid selenocysteine and much more. See here.
Different codons can also influence translation contextually through pausing. This affects the rate of protein synthesis as well as its folding. See here.
Changing codons can affect regulatory sequences such as miRNA binding sites. Though these are usually present in the UTRs, they can also occur in the CDS.

Nice answer - I was considering posting another but it would be better if you just added this as another bullet point, as it is not mutually exclusive to your suggestions; this paper describes translational pausing of different lengths for different codons, even for the same amino acid, which affects protein 3D structure as well - so it would appear that codons in the DNA have another layer of information beyond that of simply saying which amino acid to add to the protein next!

In addition, changing the codons could affect silencing or modifications by siRNA, miRNA etc.

A good answer is already provided by @canadianer, but as with many things in biology it is important to keep in mind what organism and/or cell type we are talking about. Because the nuances of the answer to a question about a seemingly universal process sometimes actually depend on whether we want to know about bacteria, or fungi, or mammalian stem cells, etc.
So I think the answer to your question is that synonymous codons are not always interchangeable because of what @canadianer described, but regulation of codon usage is probably more relevant in context of prokaryotes.
For example, for sure availability of a particular synonymous tRNA can be rate limiting in protein synthesis in prokaryotes, but I actually haven't heard of this happening in a eukaryotic system. If there are demonstrated examples, please paste it in the comment..
Also, the secondary structure of the coding part of mRNA is probably less important in eukaryotes, since they have a multitude of ubiquitous RNA-binding proteins that practically coat mRNA (e.g. hnRNP in the nucleus, and probably something similar in the cytoplasm, too)

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What happens to apetite hormones like ghrelin and leptin when a person in coma?
Don't coma individuals feel hungry? If so, how does the brain senses this condition (as coma is caused by neural death or damage) and switches off gene expression of ghrelin and leptin.
Is there any research done on revealing the mechanism by which apetite hormones expression are shut down during brain death???
Thanks


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How are micelles formed from the byproducts of emulsification in fat digestion?
It is known that fat droplets are made into emulsion droplets via the addition of bile salts. It is then said that the emulsion droplets are made into micelles through some sort of lipase, which can be absorbed and transported to different cells through the LDL and HDL pathway.
My question is what is the biochemistry for transforming emulsion droplets into micelles? How does water, lipase, and other factors make these micelles?

I guess - emulsification increases the surface area for the lipases to act and break those bigger droplets into smaller once which can enter the cells directly. http://syromonoed.com/wp-content/uploads/2016/01/Lipid-digestion.jpg

Lipases act on lipids in micelles to break them down into monoglycerides, which can break away from the micelle and be absorbed by epithelial cells. I don't think lipases are necessary for micelle formation.

They are in accordance with the textbook the "mechanism of body function 4th addition"

Fat (triglyceride) enters the small intestine in the form of an emulsion of droplets which are stabilised by surfactants from the diet including proteins and phospholipids.
Bile salts (BS) bind to the surface of these droplets, displacing proteins. The BS-stabilised droplets are the substrate for pancreatic lipase which can adsorb to the BS-stabilised surface and convert the triglycerides to monoglycerides and free fatty acids.
The products of lipolysis then enter micelles that are formed by BS and phosphatidylcholine (PC: also in bile). The prevailing view is that these micelles take the form of discs of bilayer-like structure with BS situated both around the edges protecting the exposed acyl groups, and also embedded within the PC bilayer.
I think that the mechanism by which the products of lipolysis move from BS/PC micelles into enterocytes is not known. However, once they have entered they are re-esterified to form triglycerides which are packaged into chylomicrons (a class of lipoproteins) and exported into the lymphatic system.
Maldonado-Valderrama et al. (2011) The role of bile salts in digestion. Adv Colloid Interface Sci. 165:36-46 doi: 10.1016/j.cis.2010.12.002


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Why are there so many medicinal plants?
Question
Quite a few plant species can be used for medicinal purposes wiki. As an example, Filipendula ulmaria is rich in acetylsalicylic acid (aspirin).
An allele that produces a substance which is beneficial for a predator should not get fixed in the population! Why are there so many drug-like plants?

Thoughts
Here are some (intuitive, unclear or far-fetched, non-exhaustive and non-exclusive) hypotheses I can think of:

Because plants want their seeds to get ingested in order to propagate
Is it because there are so many substances that affect our homeostasy that many plants are toxic and many are healthy just by chance. Containing healthy substances are not adaptations but by-product of evolution.
The substances that are beneficial for us actually evolved to repulse predators. These substances are toxic at high dosage and therefore are efficient against predators that are small or eat a lot of plants (herbivorous). These substances at low dosage might actually have a benefical effect. For example a substance that make blood thicker is very toxic except if you eat just a bit of it while bleeding.
We (primate or whatever taxon you want to consider) evolved in order to get advantage of the surrounding envirronment. Sbstances that were neutral became beneficial. The advantage of being sensitive to various products cause that, by chosing our food source, we can heal. Therefore, by evolving sentivity to various substances, our behaviour can act as a reinforcement to immunity (and other anti-illness system). If this is true, we might expect that the frequency of presence of a plant species affect the probability that out homeostasy get affected when eating it.
Lineage selection. Lineages that produce substances that are active in predators body in a way or another are undergoing many various selection forces because of these substances. Therefore they get a higher speciation rate than other lineages.
Keeping some non-herbivorous species in large population size (by helping them) is the best way to keep herbivorous species in small population (because of territory competition, predators relationships, etc... )

Thks for you answers! I think, you both roughly speaking picked the hyopthesis 3. Let's take again the example of salicilic acid. This acid has an important pharmacological effect but is not directly used by the plant to defense itself. It is nothing more than a hormone (and not sexondary metabolites such as nicotins, proanthocyanidines, menthols, cyanides, etc...).

So why did the Filipendula ulmaria evolve a hormone which has pharmacological effect on human (and all mammals I guess, and maybe even all deuterostome or more)? hypothesis 3 does not provide an explanation for chemicals that are not involved in toxicity.

I think you may be kind of falling in the trap of "if it is there there is a reason"... How many other chemicals are present in the same plant that do not have an action on humans? Just because one specific compound interacts with a protein in humans it does not mean it evolved for that reason. You should consider that s.a. has a very simple aromatic structure, and it is not surprising that it can interact with other proteins than the plants endogenous ones. In any case, when taken in large amounts, s.a. is indeed toxic, so in the specific case, explanation #3 would still stand.

Well, I'm not falling in this trap. It would mean that a combination of the hypotheses 2 and 3 are responsible for the presence of these chemicals.

@Remi.b - Just to clarify, a secondary metabolite is not necessarily used strictly for defense, it is simply a compound that is not detrimental to the plant if not present. For example, some secondary metabolites are pigments, some are hormones, and some involved in structural support (such as lignins, derived from phenolic compounds). On an unrelated note, a "sexondary metabolite" (see your first comment) is presumably a Freudian typo.

@J.AlfredPrufrock Good Point! Thks

Perhaps the question may also be phrased, "Why is it common for plants to produce chemicals that possess pharmacological or toxicological effects in man and animals?", and to that question it is often reasoned that plants, being sessile and otherwise defenceless food sources for predators, produce compounds that affect the physiology of animals in such a way as to make it not beneficial for a predator to consume them, which is close to your 3rd hypothesis. Remember that pharmacological benefit is largely anthropocentric, and relative at that. For instance, a plant compound that lowers blood pressure could be used as treatment of hypertension, but if the plant were to be consumed in its native state in appreciable quantity, it could put the eater into shock, cardiac arrest, etc.
Most pharmacologically active compound from plants comprise a class of compounds known as secondary metabolites: metabolic intermediates that are not appreciably involved with functions of growth, respiration, etc. (often interpreted as evidence for a defence mechanism).
Try this wikipedia article and see what you think: http://en.wikipedia.org/wiki/Plant_defense_against_herbivory
The major classes of secondary metabolites in plants are: terpenes, which are polyisoprenoids, phenolic compounds, including the polyphenolic compounds, which are a popular study in natural products research, and alkaloids (along with other nitrogenous compounds).

+1 for a good answer (and a great username, good to see a scientist who likes poetry :) ).

Nice to see that the wikipedia article cites the Raven and Ehrlich paper (which hypothesizes a coevolution of plant chemical defenses and insect antagonism).

Firstly, most plants or other natural medicinals existed way before we knew about them; it's not that plants mimic drugs, its that drugs mimic plants.
To answer your question succinctly, compounds that we can use for our own medical benefit often do other things, we just adapt them for our own purposes.  Penicillin is probably the best example.  It didn't evolve to allow humans to fight bacteria, it arose in fungi and helped fungi attack bacteria; we just appropriated it.  Similar with plant compounds like taxol (technically fungi again).  Another good example can be found in my recent answer about snake venom.  While a lot of those compounds are toxic to humans, they are very similar or even identical to compounds that in different doses can be beneficial.
Substances like capsaicin (aka spiciness) and caffeine are actually irritants that plants use to prevent predation, but we, in certain uses and doses, go wild for them.  Same for the substances in mustard, ginger, or pepper.  Imagine all the plant or animal chemicals we don't use!


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How much ribose do we eat?
I am wondering how much ribose we ingest as food? (Deoxy)Ribose is found in the backbone of DNA and RNA. So, we eat ribose as part of the nucleic acid found in plant and animal foods. While protein, lipid, and sugar content is well analyzed for many staples we consume, I cannot find any numbers on ribose or DNA/RNA. Does anybody know of a reference to shed some light? For example, how many (milli)grams ribose is in a steak or a salad? I'm thinking about this since ribose is a more reactive sugar than glucose. It can thus cause more unhealthy additions (glycations) to other biomolecules when in circulation, so the quantity take up might matter.

PS: Maybe the lack of quantitative data leads people to the false belief that they don't eat DNA on a daily basis? ;-)

Ribose is a sugar. The "-ose" ending gives it away.

Sure, but while there's plenty of information on the weight of glucose, starch, glycogen,.. we eat, I couldn't find any on the mass of ribose consumed.

Note that DNA contains deoxyribose not ribose. I encourage you to [edit] your question to correct that and to add information about why you want to know this — i.e. why you think this is a significant question and appropriate for this site rather than one focused on nutrition. In addition, nutritional information typically describes the total carbohydrate and sugar content — neither of which is equivalent to glucose.

Who cares? Why do you want to know?  What aspect of biology will this illuminate? How would you use an answer, which is presumably related to the percent of tissues that are nucleic acids? Are you assuming the constituents of nucleic acids are absorbed as such in the gut?

Hi David, thanks for the criticism. Do you have data showing that constituents of nucleic acid are not take up and if so to which degree?


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How to measure growth of algae with colorimeter
I am doing an lab for IB Bio and don't know how to use a colorimeter to measure growth in algae. The experiment I am doing will measure the effect of pH on algae growth. The algae will be taken from a fish tank and will include cyanobacteria, diatoms, and algae bloom. I don't know how the transmittance/absorption will relate to growth. I also don't know which wavelength of light to use. Help would be appreciated, thanks!

What is the color of the algae? What is the complementary color of that?

There is/was no lab manual providing you with instructions/recipes/protocols to complete this assignment? You received no instruction or demonstration on how to use the equipment/instruments? There was no lecture material on the theory behind the experiment? That strikes me as rather unusual. What if you electrocute yourself trying to turn on the colorimeter? What if you accidentally ingest one of the solutions or the growing cells? That could potentially be dangerous.

You can measure the turbidity of water using turbidimeters, however, that would not say whether it is caused by algae or something else. Best way, IMO, is to take samples and calculate biomass but there is no straightforward way to do this optically.

The color of the algae is a brownish green.

No, I did not receive any lab manual. We must design it ourselves.

Let's be clear, you are using a colorimeter, not a spectrophotometer?
Can you provide the brand name and model number of this colorimeter?
Have you learned about the Beer-Lambert Law? It states that A = Ecl where
A is the Absorbance
E is the molar extinction coefficient
c is the concentration of the unknown
l is the length of the light path through the sample (the standard path length is 1 cm in spectrophotometers).
The first thing you need to do is measure lambda Max, the wavelength of light that is absorbed the most (or transmitted the least) by your sample. The Beer-Lambert law is linear when A is between approx. 0.1 and 1.0.
So take a dilute solution of the algae and starting at the smallest wave length of light that the device can emit (you can vary the wavelength?). Take readings of the Absorbance and then increase the wavelength by 10 nm. Starting at deep purple, and ending at far red, write down the A values. Plot this data with A on the Y-Axis and wavelength in nm on the X-axis. There should be a distinct maxima in the curve, that is the most sensitive wavelength, and is the one you should use for all your experiments. If the algae is green, then the maxima should be over in the red end of the spectrum (like chlorophyll).
Next you need to make a standard curve that correlates the Absorbance at lambda max with the number of algal cells in the cuvette (the test tube you put in the colorimeter). That means you need an independent method of counting the number of algal cells. If they were bacteria or yeast then you could plate them on agar-filled Petri dishes and count the number of cells per mL (for example). For some cells if you have a high powered microscope and a hemocytometer then you could visually count the number of cells per mL. If neither of these methods are available then you could measure the mass of algal cells by weighing them on a balance.
So by some method you will be able to plot the number of cells in the broth vs. the Absorbance (plot A on the Y-axis).
From this you can empirically determine the molar extinction coefficient of these algal cells.  Then you just need to measure the Absorbance at lambda max on  dilute aliquot of the cell culture and you will have an accurate measurement of the number of cells per mL.
With this assay working then you can inoculate a bunch of identical cultures, that vary by the pH of the growth medium. By removing small aliquots of the cultures at the same time points you will be able to plot the number of cells (on the Y-axis) versus the time they have been growing, and you will see if varying the pH alters the shape or magnitude of these growth curves.


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How do our smell receptors detect and tell apart exhaust or cigarette smoke, or other man-made chemicals?
Somehow we can tell apart exhaust gas and cig smoke, yet neither of those would have existed when we evolved. How is it that we can sense chemical compounds that we've only synthesized recently?

We can also detect the difference between the smell of swimming pools, paint, gasoline.. despite "not evolving with them" - I'm not sure that your question is on topic (it boils down to what are the chemical constituents that give cigarette and exhaust smoke their fragrance, which is a chemistry question). Also I would like to point the human species is continuing to evolve, we didn't evolve to the state modern humans are in and just stop...

This is definitely a chemistry problem, but remember that smoke from burning in itself is going to have many constituents! This would essentially boil down to what does cigarette smoke contain verses car exhaust. Here's an article on exhaust constituents and another on cigarette smoke. There's a lot to sift through, but generally the differences are in the pattern of chemicals that the olfactory receptors can detect.

@Kendall If OP made some small edits, I think this could asking about how our olfactory system can detect particulates that we haven't been exposed to over an evolutionary timescale. Currently I agree that asking which chemicals are similar to ones that we may have been exposed to us over evolutionary timescales is chemistry.

Yes, that's pretty much what I'm interested in - how is it we can sense something that we've only created recently. I'll edit the q. Is there a guide for newbies on how to make sure your q isn't too much on the edge of two disciplines?

It is all small molecule ligand receptor binding. The olfactory receptor has specificity for an epitope on the molecule and a signal is transduced through a G-Protein to create he action potential in the neuron. Different receptors will bind different epitopes on the molecule or molecules for complex odors and generate a signal into the brain that is perceived as a smell. Most compounds that release volatile compounds will have a chemical signature. As we develop, we learn to perceive and assign identity to those signatures as specific things.


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In DNA sequencing, is "mate pairs" synonymous with "paired ends"? If not, how do they differ?
By just looking at Roach et al's paper I get the impression that they are the same thing, and the Wikipedia URL for the former is a redirect to the latter.
However, I suspect they are not exactly the same - for starters, they wouldn't have two different words for the same thing, right?
Can anybody shed some light and suggest some references?
Thanks.

Paired-end is the name of the sequencing approach.
Mates refer to the read pairs that correspond to the same insert, but sequenced from opposite directions.


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How is energy acquired from ATP?
How is energy acquired from ATP (i.e. What is the energy-releasing equation involving ATP plus water)?
I Would be grateful for the answer.

The basic reaction is ATP + H2O --> ADP + Pi + energy
It is the common hydrolysis of ATP, in which the nucleophilic oxygen of water attacks the electrophilic central phosphorus of the last phosphate group, resulting on its separation from the rest of the molecule (which becomes ADP).

In this image: LINK you can see more clearly the steps of the reaction. Keep in mind that the arrow 3 should be pointing to the P and not the O.
To know more about the energy and thermodynamics check this page: http://www.life.illinois.edu/crofts/bioph354/atp_hydrolysis.html
The trick here is the cells being able to utilize that freed energy to their benefit, instead of letting it disperse. This can be done, for example, by adding a phosphate group to a protein, altering its shape and consequentially its function, or by the nucleophilic attack of the first or second phosphate in the ATP molecule of a susceptible electrophilic centre, starting a reaction that could otherwise be energetically unfavourable. If the hydrolysis happens spontaneously in water without coupling it with another reaction, the freed energy will be "wasted" as heat.

very clear and easy to understand now. thank you very much indeed.


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Why can't men produce milk, just like women?
This might seem a bit weird, but why can only women produce milk? Wouldn't it be more beneficial to our species if all humans could produce it? I can't think of any reason only one gender would need it, unless it would somehow be harmful to men.
I know that men can secrete milk in some cases, but why not in general?

The words beneficial to our species very much suggests that you misunderstand evolutionary processes.

Why do you say that, Remi? Traits that are detrimental tend to not be selected for in many ways, while traits that are beneficial increase the likelihood that an organism will pass on those traits to future generations. That is the theory of natural selection in a nutshell.

Evolution does not primarily work for the benefit of the species @DonJulian

related/possible duplicate: Why only female mammals have well developed mammary glands?


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Generate mesh surface from protein structure
What tools are most widely used for generating a mesh surface of a protein from an x-ray crystallographic structure (from the PDB)? Pros and cons would be appreciated.
I'd prefer the output to be a watertight triangle mesh of the protein surface.
Also, I'd like the tool to be scriptable (i.e. no need to open a GUI).
So far, I've been playing with MSMS and EDTSurf. But I was wondering what was standard in research, as well as if there was anything in the standard bioinformatics libraries.

PyMOL and Chimera can do that, and both can be script-driven. The PyMOL wiki is full of examples, and probably already has some how-to that would get you started. Chimera also has a complete documentation.


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Is DEET (as in the mosquito repellent), a substituted phenethylamine?
Am I correct to say that N,N-diethyl-meta-toluamide (DEET) is a part of the phenethylamine class? It's structure meets the requirements to be a phenythylamine, however, I was not able to find anywhere on the internet that it is part of the phenethylamine class.

Do you mean phenethylamine? That's the only thing google turn's up. If so, they don't seem to be related (1 less carbon between ring and N, carboxylic-bound N versus amine N)

@Nicolai Sorry I usually type in Word which autocorrects me, but you are correct on the first part. But I'm confused on your second point. How come it passes the requirements to be a substituted phenethylamine (https://en.wikipedia.org/wiki/Substituted_phenethylamine)?

Selegiline is a good example of what I mean, it has a carbon bound N but is part of the PEA class. Why is this then...

Also, technically DEET has a NH group because groups share atoms with the linked group, so writing N-CH3 is the same as writing NH-CH2. There is no difference, unless it crosses over 1 link.

I'm voting to close this question as off-topic because it is not about biology, but is a question about the chemical structure of a proprietary product.

While I feel like this might be a better question for the chemistry SE, lets take a look at the molecular structures:
The basic structure of a phenethylamine (left, modified from here) versus DEET (right, modified from here):

The important chemical differences are:

DEET only has a C-alpha between the nitrogen and the ring, whereas phenethylamines have a C-alpha and a C-beta (see red annotation)
DEET has a carboxylic functional group (an amide bond), whereas phenethylamines have an amino group (see green boxes)

Taken together these differences mean that DEET is not a phenethylamine.

So are you saying that 1-phenethylamine is not part of the phenethylamine class?

https://en.wikipedia.org/wiki/1-Phenylethylamine

Note, I am not talking about b-phenethylamine which is the one you pointed out

@kirill2485 At least based on the different carbon chains of these molecules I wouldn't group them together. I'm not a chemist however, so if you want to now how they categorise this, ask the question at chemistry.SE

I agree with @Nicolai I can't see any reason it would make sense to consider DEET a phenethylamine; it doesn't have an "ethylamine" on it anywhere: that would be 2 carbons followed by a nitrogen. It's an N-substituted amide group (one carbon) on a toluene.


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Plasmid transformation yields only empty vectors
I have to electroporate pMAD cloned with an insert of 7.4 kb in my S. aureus isolate. When I electroporated in RN4220 I had no problems but when I put it in my isolate I just recover few colonies and they have the empty plasmid. Has anyone had this problem?

How do you know they're empty? Are you doing blue-white screening or actually isolating the plasmid?

I ask because if your isolate contains an endogenous beta-galactosidase gene, blue-white screening will not work.

I have the primers to amplifie the region of the multiple cloning sites and it gives me the fragment of an empty plasmid. Also I cut the plasmid with the same enzymes of the cloning and it gives me no fragment of the insert size, only the empty plasmid. When I do the same thing with the plasmids from RN4220, I have the good fragments...

A qualified guess is that either your insert is somehow toxic to the cells or you have a contamination issue with the empty plasmids far outweighing your plasmid with the insert concentration wise.


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I'm trying to figure out what the name of this flower is
This is a flower that grows in my backyard. I really want to know the name so I can read about it and possibly get more.

Rose. (Rosa sp.)

can you give a location and time of year?

It has actually just started blooming again recently and I live In Ga. Let me know if you need more.

That is a rose. At least we have such flowers around my flat and we called them roses for 18 years. See: Rosa Gallica

Welcome to Bio.SE! Please add an image and give some description of the species and provide references to support that the ID is actually correct.


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Is there a defined non-trivial chromosome number distribution for a given kingdom?
I'm pretty aware of the mechanisms for chromosome number evolution in specific groups (e.g. inside a given genus). Nevertheless, looking at a broader scale (e.g. in the Metazoa kingdom), is there a well defined distribution for the frequency of occurrence of chromosome numbers?
For example, are species with small chromosome numbers more frequent than those with large chromosome numbers? If so, is there some sort of scaling relationship between number of species and number of chromosomes?

Page 445 for a start.

Not in my country...


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introduction of system biology to bench biologists
I am trained as a bench biologist and I want to learn about system biology and introduce a system biology type of analysis into my study. Can somebody recommend books and websites about system biology for biologists?

Don't have any good suggestions, but I suspect that the answer will depend critically on how strong your math background is. Can you add a few details about that? i.e., how familiar are you with calculus, differential equations, and linear algebra (matrices)?

"Systems biology" is an incredibly broad category.


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What's the difference between physical (direct) and functional (indirect) protein interaction?
I read that the Protein-Protein interactions one can consider are generally of two types, namely physical and functional, but I cannot get the difference between the two.
I was just thinking that if two proteins are linked in a Protein-Protein interaction network like the ones stored in STRING database, then they are experimentally observed or somehow predicted to physically interact through binding sites to explicitly perform a function, e.g. signal transduction. But as I am reading different sources making the separation between the two kinds of interactions I got a little bit puzzled.
Can you please help me?

What on earth is "I got the PPIs" supposed to  mean? And what is "a PPIN like STRING"? If you are going to post on this site you must take the trouble to define all acronyms (other than DNA etc) and express yourself clearly. Otherwise your question will be thown out as unclear.

PPIN: Protein-Protein Interaction Network,
STRING: one of the largest and more used database related to such networks. I'm sorry for the inconvenience, I thought the acronyms were known. Now the question should be more clear.

Thank you, but definitions belong in questions. Please edit your question.

Done, I hope now it's more understandable.

As I understand it, "physical" and "functional" are just two different ways of analyzing an interaction between proteins.
Proteins can and do interact physically, meaning they can bind in specific ways and sites, and this binding can produce changes in those same proteins (like conformational changes), which alter their properties. This is the purely physical analysis of the protein interaction. The functional analysis begins when we ask the questions "What is the role that this interaction performs in the cell/organism/living system?"; "What effects do these changes in the protein are going to create in the cell/organism/living system?". Often a conformational change in a protein induced by an interaction with another activates or inactivates it. In other words, an interaction can create a conformational change that enables (activation) or disables (inactivation) the protein to catalyze a given reaction, and so the referred interaction plays an important function in regulating the protein's activity. For instance, phagocytes (cells capable of phagocytosis) have in their membranes proteins capable of physically interacting with proteins present in pathogens membranes. They physically bind to them, changing their conformation in the process. This is the physical part of the interaction, it is what happens purely physically (and can be studied more deeply). This conformational change will enable the protein to catalyze a series of reactions inside the phagocytic cell that will ultimately lead to the phagocytosis and destruction of the pathogen. This is the functional analysis of the interaction, it is understanding what is functionally achieved by the interaction, in this case enabling phagocytosis (and can be studied more deeply).


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Plant tissue cultures without Phytohormones?
Is it possible to do tissue cultures without using phytohormones like BAP or NAA. So to just use for instance MS-Media.
Online, I just found that every plant is possible to culture with the right media and growth regulators. But I want to know if it is possible in theory to do tissue cultures without using hormones and if it is what are the disadvantages of that.

No. Tissue culture works like this:

Take cells from your target plant, preferably from totipotent tissues like shoot tips, that can easily become many other tissues.

Place your cell samples into a sterile medium, like an agar plate, then add a growth hormone that transforms the samples into wads of undifferentiated totipotent cells.

Once the cell wads have grown enough, add new hormones that cause them to differentiate into structures like buds and roots, forming new plants.

Remove your new plants from the medium once they have grown large enough.


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Could we detect GMO foods if there were no samples to compare with?
In my understanding, there’s nothing “special” in how a GMO product is composed inside compared to a “natural” product. I mean, still, same principles apply to both: some DNA that controls protein building, and so on.
Now, having read about all existing methods of GMO detection, I still can’t understand how it works: e.g., given two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?
Once you change someone’s DNA, does it contain any signs that it was changed? Or do we need a database of “natural” products’ DNA to compare with in order to be able to detect DNA ones? Or do we need a database of GMO products to compare with?

It seems like you'd have to have some way to distinguish between organisms genetically modified by human action and those genetically modified through natural processes. Plausible, maybe, but not trivial.

This isn't an answer, but there is off-the-wall practical solution:  Grow both foods, and if one of them is bigger, juicer, or (insert other economical improvement here), then that's the GMO one.

@NathanMerrill Is it? How do you know there aren't naturally occurring (if rare) instances of the traits?

@jpmc26 Fair enough: I am assuming that the GMO DNA was mutated from the other one you are given.

@jpmc26 - You're right, that's not a valid test. First, either one could have a gene replaced by either mutation, natural replacement, or human replacement, and second, there's no assurance that the replaced gene makes the plant better in the particular way you're looking at. It might mutate to be less good, or it might mutate to have better disease resistance at the sacrifice of quality root structure.

Check the DNA for a copyright statement.

[G]iven two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

No, you can't distinguish them without knowing a priori the DNA sequence of the wildtype and of the GMO. There is no other mark left within a GMO in the general sense.
Of course, one particular GMO is created with one particular goal in mind. One particular phenotypic effect. If you detect the phenotype of a GMO, then you can recognize it. For example, if you make a GMO tomato that produces a new type of pigment, you can, of course, recognize it by the presence of this pigment! However, there is no general attribute of being GMO that you can recognize. You need to look for something specific that you know about a specific GMO (or specific wildtype).
There are also phenotypic traits that you find (quasi) exclusively in GMO such as Cytoplasmic Male Sterility (CMS) for example. If you find CMS in a plant, then you can be pretty sure it is a GMO. But if you can't find CMS though, you can't be sure it is not a GMO.

given two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

Possibly, assuming they're the same variety, you might get lucky by simply diffing the sequence data. This also assumes the natural variety doesn't change significantly between generations, such that even if the chromosomes have crossed-over (homologous recombination) you could still do pattern matching to realize correlation. Genes/sequences with no correlation at all would then be suspect as novel/introduced.

No.  Furthermore, the line "once you change someone's DNA" contains a wealth of misconceptions.
Once you have your potato/tomato/whatever, the DNA does not change during the life of that individual specimen.  The genetic modifications change the seed before the individual specimen grows, and do not change the individual specimen during its life.
As far as genetic modifications go anyway, each seed inherently has different DNA from its parents.  "Normal" breeding has given us a diversity of plants and animals which are so massively different from the originals as to be virtually unrecognisable as the same species in many cases.  (If you didn't know better, would you think a dachshund and a husky were the same species?)  And whilst we might think of it as "normal" today, when the techniques around selective breeding were first developed, they in turn were seen as highly unnatural, particularly the practise of breeding an individual with a parent or sibling.
This still relies on normal rates of DNA mutation within the same species.  More interestingly though, DNA can also be picked up from other sources.  This is identical to how scientists insert or replace genetic material for GMO - indeed, GM techniques to carry this out were founded on understanding how this takes place in nature.
This is where objection to GMO falls down.  Sure, the result may or may not be healthy.  However you are already using/eating/breathing pollen from individual specimens which have carried out gene transfers with other species.  The difference between the natural version and what happens in the lab is only the same as the difference between natural breeding and selective breeding - it's simply that someone is deliberately choosing which attributes to pass on to the next generation, using tools which already exist within the organism's DNA.

It would depend on whether you knew the markers they used to identify the transformed organisms.
When I (briefly) did Genetic Engineering back in the mid eighties we would add antibiotic resistance genes as well as the gene we wanted to insert.  The combination would then be incubated with the vector (e.g. bacteria) and the transformed bacteria could be filtered out by growing them on antibiotic laced plates.  Then you'd grow up a transformed bacteria and insert it into the target organism.
So, the presence of bacterial antibiotic resistance genes in your hypothetical potato could be an indication but not a guarantee of human modification.


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Pedigree Analysis
I was doing some pedigree work and couldn't figure out why my answer is wrong. This chart is supposed to be an autosomal Dominant method of inheritance, but I am finding an autosomal recessive pattern that fits? If anyone can point out my mistake, that would be appreciated. I have labelled my attempt above each member, where aa = disease phenotype and Aa or AA is a normal phenotype. The disease pattern describes Marfan syndrome (autosomal dominant). Any help or pointers would be appreciated.
I decided not to label the pt who has a *'s family, because there are several possibilities that don't affect the answer.
Edit: I also found an autosomal dominant pattern that fits, but the issue is with the autosomal recessive pattern, so I am only posting that one.

Is it reasonable to assume that everybody that enters/"marries into" this family tree happens to be a carrier for the same recessive trait?

I do not see any "error" in the logic of your pedigree.
However, pedigree analysis is not a logic puzzle; it's a practical tool. There are additional logical solutions you have not come up with. For example, every affected individual in this tree could result from a de novo somatic mutation with no inheritance at all. Or the phenotype could be not genetic at all: the observed pedigree pattern might well apply to "people who have been in a serious car accident". Or, it could be a polygenic trait that is not easily tracked in pedigrees even if there is some underlying inheritance.
You're expected to have some additional assumptions that are met to even bother undertaking a pedigree analysis, and one of those likely assumptions is that the disease is rare. That is, it's rare enough to rule out more ordinary polygenic traits and make you think there's a single gene involved. In that case, it is not reasonable to assume that everyone entering the pedigree from outside (e.g. marrying in/breeding in) happens to be a carrier of the disease.
It looks like that's what was necessary to make this tree work: besides the initial aa/Aa pairing at the top, there are 4 other individuals that come from outside and pair with someone who is a descendent of that pairing (there are actually 5 in a sense, if you include both of *'s parents, but we can reduce it to just * and count them as #4). You've marked all 4 of these as heterozygous carriers for this pedigree to work. It would be extremely unlikely for this to happen with a rare disease.
See also the concept of Occam's razor.

Bryan already answered in a very exhaustive and elegant way. The fact is that most textbooks and teachers, when dealing with recessive traits, assume they are severe diseases, for which it is reasonable to expect that they are rare in the population. This will also make the recessive allele rare in the population, and the likelihood that 4 married-in all carry the disease allele is so low to be neglectable.


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What other cognitive behaviors in bees, outside of navigation, are affect by neonicotinoids
It is conclusive that neonicotinoids alter navigation in bees when locating food sources. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091364
But if so, shouldn't cognition also be affected? And if it is affected, then wouldn't the effect on the hive be even more pronounced due to inaccurate bee dances and an overall delay/inability in finding food source? Shouldn't this be conclusive in explaining neonicotinoids to be a contributor to colony collapse disorder?

It is assumed that this effect of locomotive behavior IS an effect on cognition (1-4). Navigation requires snapshot memory, learning, and attention (2-4). You asked if this effect of neonicotinoids on cognition manifests itself through other vital behaviors. The short answer, yes. Specifically neonicotinoids are shown to effect mating, queen behavior, and foraging short and long distance (5-7). It is suggestive that neonicotinoids are a contributing factor in collapsing colonies with both meta analysis and direct evidence of effects on behavior (5-8). I think you are more questioning why people have not done anything about this issue or more definitive in their action against colony collapse. That is more of a political issue. Since the pesticide does not have as many human health effects at levels that cause bee collapse, the policies to resolve this issue are not as clear. EPA has discussed making restrictions regarding use the use of neonicotinoids, but they will still be used. However, they have actually been banned in France due to these effects. Hope that answered your question!
Sources

Honey Bee Behaviors  doi:10.1016/S1364-6613(00)01601-6
Bee Navigation and Memory          doi:10.1006/anbe.1997.0574
Learning and Memory in Bees doi: 1146/annurev.ne.19.030196.002115
Behavioral Neuroscience ISBN: 978-0-87893-092-0
Bees, neonicotinoids, and Dance Behavior Effects doi: 10.1242/jeb.068718
Bees, neonicotinoids, and Foraging Behavior Effects  DOI: 10.1046/j.1365-2435.2000.00443.x
Queen and Colony Effects   DOI: 10.1126/science.1215025
Colony Collapse meta study DOI: 10.1007/s10646-010-0566-0

Can you please add DOI or Pubmed links if possible?

Sure thing! I'll add the DOI at the end of each citation.


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Reseach on feeling pain of other people
I'm more of a tech than bio kind of guy, but I have read and learned a lot alongside of my girlfriend's education. Which is very interesting!!
Currently I want to investigate : people claiming to feel another persons pain when they are touching them.
I cannot seem to Find any papers about it. I guess I'm using the wrong search terms.
Or does nobody research about it ?

I believe what you are referring to is called 'sympathetic pain,'and the reason you can't find any papers on the subject is because it is not really a well studied concept. That is primarily due to the lack of robustness in the sensation and idiosyncratic nature of the phenomenon. Personally, I'm not too familiar with the concept beyond placebo treatment of patients with such pains.
HOWEVER, I will explain the different types of pains briefly, their biology, and where the pain you have described fits roughly. There are three categories of pain (scientists sometimes argue four, but for our sake let's say three): nociceptive, inflammatory, and neuropathic. Nociceptive pain is the immediate pain reaction you get when you sense something harmful. It's that jerking sensation you get when you touch something hot or you feel something hazardous coming your way. This pain comes from peripheral nerves that link your senses of touch or perception directly to your spinal chord for an immediate knee jerk reaction. Thus, there is no central nervous system (or brain) processing of the pain, just a reaction. You end up feeling the pain more intensely later once the moment has passed. Then inflammatory pain is the pain you get when you cut or bruise yourself, have allergies, stuffy nose, etc. It is the more common and treatable types of pain and is easy to detect. It comes with redness, swelling, and sensitivity to the general area. Biologically your body is stimulating this pain because your inflammatory system is trying to attack any invasive particles or repair damaged sections of the body. There has been much research done in this type of pain (see sources) and is treatable with non-steroidal anti inflammatory drugs (NSAIDs) such as aspirin, Tylenol, etc.
The last type of pain, which is the sympathetic pain falls into, is called neuropathic pain. This pain is more abstract and is often described as constant and idiosyncratic (non standard intervals). In research it is often modeled by inducing diabetes and doing damage to the nerves to cause constant pain signals to the brain. However, the method is controversial in both practice and in efficiency of modeling. This because there are often many different biological ways to induce cognitive pain and it is primarily central nervous system based (aka in the brain), whereas this type of pain is specifically induced by nerve damage (hence neuropathic). This type of pain is often tested using cognitive based test parameters to see if a drug can relieve some of the mental struggles either caused by the pain or causing the pain. There are also such cells called "mirror neurons" that fire when you sense (visual, audio, touch) something and then cause a similar behavior or sensation to occur within the person. It is possible that seeing or feeling someone else's pain causes these mirror neurons to fire for certain people, perhaps due to associate learning or a memory that person has that reminds them of pain they once had. I've attached some literature on the subject for your leisure, but it is a poorly understood science that we are trying to grasp in modern research. Hopefully that answered your question!
Sources

The Principles of Neuroscience by: Kandel, Schwartz, Jessel, Siegelbaum, and Hudspeth (most indepth source)
Pyschopharmacology by Meyer and Quezer
From Mice to Men: Jacqueline Crawley
Pathology Based Pain
Inflammatory Pain Review
Neuropathic Pain Review
Mirror Neurons

thanks for your extensive answer, it was really helpfull. But I more looking into feeling pain without you are able to see/hear somebody only touch them, is there any info available about that ?

Not specifically. The closest thing to that type of research I know about are the mirror neurons cited above.

thanks again, that a pity there is not alot of information about this topic. why not conduct research in this area ? Seems to me it can give new insight in how the brain/body of a human works if you don;t test it you never will know.
But what i want to do is the next, measure and experimenting with people who claim they can feel it with an openbci and look at the brain responses. seems interesting to me ?

It is harder to test. There is a great deal of bias and a HUGE degree of variation, which can hide any significant findings. If you feel I have sufficiently answered your question feel free to mark it as answered so people can mark and reference it. :)

i know but thats the challange, do you have any information about how to setup a good experimental approach to this ? So do not overlook very obvious mistakes i could make :)

There are several good reference books for designing a proper neuroscience experiment. I think you will want to focus on social biases and really make sure to note things like demographics, gender, age, ect. in or to control for any confounding effects. Good reference books are "Behavioral Neuroscience: A practical approach" by Sahgal.

thank you so much for the information ! I'm going to read it

The OP might be asking about what is called mirror touch synaesthesia
Like all synaesthesia [also spelled synesthesia] this is a new area of research. I have synaesthesia but I don't have this kind. Most researchers study "grapheme synaeshesia" grapheme because that is easier to make into empirical results.
Dr Anina Rich studies synaesthesia. She might have papers about it. Dr Anina Rich


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What causes swelling after impact?
Why does the head swell after getting hit by something hard? What is the liquid that forms after impact?

When physical damage to the cells occur a biological process called inflammation occurs. When inflammation occurs, white blood cells are rushed to the area in order to fight off any bacteria or harmful waste leakage from damaging the cells further. In order to get the white blood cells to the site of damage faster, the body induces a process called vasodialation where the arteries are expanded and blood is rushed to the site. This causes the site of injury to swell and redden, two signs of inflammation. The white puss that forms comes from the white blood cells. The white blood cells release chemicals that kill of bacteria and waste in the area and forms a white pus that will eventually harden or break through the skin to be exerted. If the site of impact begins swelling within a matter of hours, it is likely acute inflammation is occurring and the body is rushing blood to the site. However, if swelling occurs on a more rapid time scale it is more likely that this fluid is from the damage of the impact itself and the cells and capillaries are leaking blood and extracellular fluids (What is Swelling?).
In short, when you bump your head your body is trying to fight off further injury and infection by inducing the inflammatory response. It is also leaking fluids due to the impact and may result in rapid swelling at site of impact. The symptoms you discuss are due to inflammation and are a normal process of your body's defense mechanism. Hope this helps!

I'm not sure you're correct (at least I'd appreciate seeing evidence for your assertions.) Inflammation takes time. The bump that appears after hitting one's head takes moments to minutes. I think this is much more likely to be simple extravasation of serum from damaged cells and capillaries, etc.

Thanks for the rebuttal. The question offered no information when regards to time scale, but vasodilation and rush of blood to the site of impact can occur within a matter of hours (http://www.nationwidechildrens.org/swelling-bodys-reaction-to-injury). If swelling occurs on a shorter time frame, @anongoodnurse 10  is correct in saying it is likely due to the peripheral damage to the capillaries and cellular structure. Thanks for the input, I will be updating my answer!


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What is a sex-biased gene?
How do you define a male-biased gene and a female-biased gene as they are found in the abstract of this article.

perhaps by strong difference in expression between two sexes.

WYSIWYG yes, that's what I was thinking too. Let's wait and see if someone can make sure of this.

In the linked paper, the authors discuss this as sex-based gene expression that evolved by sex-specific selection. The expression is not limited to one sex (which are sex-limited genes). Sex-biased genes are expressed by both sexes, but differently between sexes.


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Why does ATP contain ribose rather than deoxyribose?
I read in a textbook that ATP is made from ribose and not deoxyribose. Originally, I thought that the pentose sugar didn’t have functional importance.
Is there a functional reason why the ATP used in metabolism has to be made from ribose?

I have edited your question, in particular changing the reference to ATP being used in respiration to being used in metabolism, and making it clear that your concern is the lack of a functional role of the sugar ring in ATP hydrolysis. If this is not what you meant, do revert the question, clarifying.

Can I ask for a clarification of your question. Are you asking why dATP does not function in contemporary energy metabolism, whereas rATP does? (i.e. why the enzymes will not use it). Or are you asking why organisms evolved to use rATP rather than dATP?

Mainly why rATP is used in metabolism and dATP is not, I assume it may be to do with the fact dATP is used in DNA but I was wondering if there was a specific biochemical reason

Short answer:
The pentose ring does not participate chemically in the energy transfer reactions involving hydrolysis of ATP to ADP.
Enzymes that catalyse these reactions would tend to be specific for ATP (rather than dATP) because they bind the whole molecule and this would most likely include the 2'-OH of the ribose ring. dATP would therefore bind less well or not at all. (There may also be an advantage for evolving such specifity so that dATP could not compete for the active sites.)
The reason that evolution produced ATP as the energy transfer molecule rather than dATP is purely a matter for speculation. One might argue that it is an extra energy expense to reduce the ribose ring, although I prefer a more mundane answer. That is that if one assume RNA genomes (and enzymes) predated DNA genomes evolutionarily, then molecules involved in energy metabolism that contain ribose — not just ATP, but NAD and coenzyme A — arose at that time. When the genomes switched to DNA there was no selective advantage in changing ATP (and NAD) as well, and such an advantage would have been required as the enzyme systems that used these small molecules would by then have been already established.


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α-β Interfaces of Hemoglobin
I am trying to learn the interactions that hold the hemoglobin tetramer together, and the conformational changes induced at various allosteric sites. So far, what I know is this:
The tetramer can exist in relaxed state (R-state), or tense state (T-state).
The R-state favors oxygen binding, while the T-state favors oxygen release.
At the C-terminus (a histidine residue) and the 40th residue (aspartate) of the β-chains, and the 146th residue (histidine) of the α-chain, there are two salt bridges. When red blood cells are present in tissues (with a pH of 7.2), the formation of both bridges are favored. When both bridges are formed, the T-state is favored.
The second residues of the β-chains are also a histidine. (This is near the N-terminus). This residue participates in an ionic bond with 2,3-BPG. At the 82nd position, there is a lysine residue that also participates in this bond. (This is a little over half-way down the amino-acid sequence). By binding 2,3-BPG, the T-state is favored.
On the binding of oxygen to a heme-group, the iron atom moves to the center of the protoporphyrin ring. Attached to the iron atom is yet another histidine. This histidine is attatched to an α-helix that is attached to the terminal-carboxyl of the α-chain. By moving the α-helix, a conformational change is induced in the other subunits to shift the structure to the R-state.
What residues of which subunits are the α-carboxyl termini in close spatial relation to, and how does this movement induce the R-state? And which residues hold each dimer together, and how do they affect the R- or T-states?


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Is human mtDNA unique in its single origin?
Other than Humans, is there another primate who has a traceable “original Eve mtDNA”?

can you give some more background information on what your talking about? Can you define "original Eve mtDNA"?

I was referring to Prof. Sykes book the Seven Daughter of Eve referred to by another as Original Eve mtDNA!  My question was simple, is there a comparable circumstance in other primates?

You can trace back any piece of DNA (from any life form) to a single ancestor called LUCA (Last Universal Common Ancestor), so the short answer is 'yes'. But be careful in your interpretation.
If you look backward in time, you can see that lineages merge (siblings merge first, then cousins merge, etc...) and you necessarily end up with a single individual. In absence of recombination (which is the case for mtDNA), you can always trace back a piece of DNA this way and always find a single ancestor. The age of this common ancestor depends mainly on the population size and demographic history of the lineage. Typically, in a panmictic diploid population of constant size $N$, the expected time to the MRCA (Most Recent Common Ancestor) of the population is $2N$ generations.
So yes, you can find an "original Eve mtDNA" in any species. But please by "original" don't think this ancestor must have represented any novelty or anything of interest and do not make the mistake to think that before this ancestor no one had mtDNA.
The second paragraph is an extremely vulgarized explanation of coalescent theory. You should have a look at an intro to coalescent theory (wikipedia article here) but you might well need an intro to evolutionary biology first. Understanding Evolution might be a good way to go.

Good answer. +1 Maybe, to further clarify things for the OP, one could add three things about what the 'original Eve mtDNA' carrier was not. (i) She was not the only female alive at that time. (ii) She was not the ancestor of all genes in the gene pool. (iii) She was not necessarily a member of the species.

Very important add-up to avoid misconception. Thank you

I was referring to Prof. Sykes book the Seven Daughter of Eve referred to by another as Original Eve mtDNA!  My question was simple, is there a comparable circumstance in other primates?

And I was thinking the answer was pretty easy as well. Please let us know what is unclear to you in my answer. Side note: please do not post the same comment twice.

Thanks, I am not academically trained.  What had confused me was that Prof. Sykes and others, currently seem to find this "Clan Mothers" evidence surprising.  However, if this is common in all life...my curiosity is satisfied.

I never heard of the concept of "Clan Mothers". If you want to question Sykes's claim you'll need to give more info about the concept he's using (give us some background) and probably quote him. You might need an intro level in evolutionary biology though before being able to do so (if you don't yet).

Sorry, I have asked my question poorly and confused it with the genealogy term. “The clan mothers were not the only people alive at the time, of course, but they were the only ones to have direct maternal descendants living right through to the present day. . They show how everyone alive on the planet today can trace their maternal ancestry back to just one woman.
Sykes wrote, and maps the migrations of the worlds populations  haplogroups.
My question is, how would this compare to chimpanzee populations?  Do all species inherently have an common core sequence in their mtDNA?

Well, yes this quote will be true for any piece of non-recombining DNA in any lineage (which includes mtDNA in chimps). The answer still hold. You should really read about coalescent theory to get a better understanding of this general subject.


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Why choose strawberries for DNA extraction?
The NileRed video What is DNA and what does it taste like? | Edible Chem shows the extraction of a surprisingly large amount of DNA from some strawberries. At 02:22 the narrator says:

What I think is really cool, is that it’s actually possible to isolate DNA from pretty much any living thing. For this video though, I’ve decided to get it from strawberries, because it’s one of the easiest sources.

I'm wondering if DNA is inherently easier to extract from strawberries than other fruits, vegetables, or other foods in general, or if for some reason there is more DNA (or DNA plus other molecules bound to it) it in strawberries than other foods to begin with.

As he is mentioning later in the video a "major reason" why he used strawberries, is that it's easy to crush them. In order to extract DNA from the tissue you need to damage the cells. We used tomatoes once, but with a blender. Works just as well..

@Frieke I was hoping for something more profound ;-( I am vaguely aware that some plants have absurdly huge genomes, and I was hoping that there was some amazing factoid about the strawberry genome being particularly huge.

There's more than one reason behind the use of strawberries:

They are octoploid (8n), so they have eight copies of each chromosome per cell, i.e., there is a
lot of DNA to isolate per unit of volume;
Ripe strawberries contain enzymes (pectinases and cellulases) that help to break down cell walls and aid in the release of the DNA;
They are easy to pulverize;
They are cheap, readily available, and their use is not restricted by ethical constraints.

Note that the genome (i.e., 1n) of strawberries is not particularly big, i.e., around 700 Mbp; for comparison, humans have more than 6 Gbp. Given that human are 2n, the total amount of DNA per strawberry cell is about half that in a human cell.
Source
- University of Washington - this pdf file

Octoploid? Holy granola! I had a hunch the choice of strawberries wasn't completely random. (reminds me of Did the Cheela on Dragon's Egg have twelve-stranded "DNA"?) I'll ponder further what "(2n = 8x= 56)" means in the morning, but I'm guessing it means there are seven distinct chromosomes. Does the 700 Mbp refer to one set of seven, or 8x7=56 chromosomes together?

@uhoh I have added the n issue; good point.

Thanks! fyi, going down the ploidy rabbit hole I've just asked How do we know for sure that Morus nigra (black mulberry) is tetratetracontaploidic (has 44 copies of each of its seven chromosomes)?


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Debug Fresno; why are the released mosquitos said to be sterile?
I saw in the news that Verily Life Sciences will participate in an experimental release of sterile male aedes aegypti mosquitos in Fresno, California. Aedes aegypti is considered an invasive species in California, and can be a vector for human disease including dengue fever, zika, and chikungunya (according to the video). See the Verily blog Debug Fresno, our first U.S. field study and/or the attached YouTube video Introducing Debug Fresno.
The released male mosquitos will carry a bacterium called wolbachia, which when transferred to the female during mating will prevent eggs laid by the female from hatching. Wobachia presence, parasitism and mutualism with insects is widespread, and Wikipedia's article on it even includes a section on applications to human-related infections.
Question: Are the males said to be sterile because of the bacteria which results in nonviable eggs, or are they also incidentally sterile in addition to being vectors for the wolbachia bacteria (and eggs were presumably fertilized by other matings)?

I haven't read too much into it, but I think both is correct. The males are sterile and they make the females subsequently sterile.

@CMosychuk that would be my guess too. Since the males don't carry anything genetically that would reduce the population, releasing fertile males would be counterproductive. But I don't know if one can call otherwise fertile males sterile because they carry the bacteria, so I think the use of "sterile" here does not refer to the impact of the bacteria on the eggs.

different, but in the news First-ever US release of genetically modified mosquitoes begins in Florida Keys

I've just asked: Why do OX5034 GM mosquitos require the presence of tetracycline to survive? What does the drug do in this case?

Males are effective sterilization vectors
You can think of male mosquitos as fertile only in theory. Any mating of these mosquitos will generate no offspring whatsoever, so they are effective sterile and they spread this characteristic to females.
The bacteria makes they sterile in the end, the same way any disease in others cases.


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How is the side-polarity of the myosin filament in myofibril maintained?
If myosin molecules are the properly oriented relative to their position in the myosin filaments, the sarcomere is not functional. But how is the orientation of the myosin molecules determined? Why is there a symmetry in the arrangement of myosin molecules in the myosin filament? And are there any diseases associated with the improper arrangement of myosin molecules?

There are a lot of other proteins like titin and dystrophin to name few which maintain the sarcomeric structure. But got no clue of anything specific. Its important to know that it's not just the actin and myosin floating in the muscles as textbook diagrams show.


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Does the VR headsets make us focus extremely close?
Firstly, if I ask this question in Ask Different or Super User, the users there may say this is related to a biology or physics.
The background is: we were in general told that: don't read a book too close, or don't watch the TV too close, because it will make our eyes focus with a really short focal length, and that means our eye muscle has to make the biological lens in our eyes to be extremely convex shaped.  As a result, we can easily develop myopia this way.
Does this apply to VR headsets, such as Apple's Vision Pro, or Meta's Quest 3? In these cases, the "display" is like one or two centimeters or fractions of an inch away from our eyes.
So in that case, does that make our focal length to be extremely short and therefore, injure our eyes in the long term?

The VR headset is presenting two different images to each eye, so strictly speaking, the eyes are not looking at the same object (as in a book or TV).
This idea has been used in non electronic devices (Stereoscope) for a long time to see pictures in 3D.
So the eyes are not actually focusing at the VR device screen but further away.

I don't think it works this way:  Mom says: hey Peter, don't watch TV so close, like 2 feet away. Peter says: Mom, don't worry, I am closing one eye to watch the TV 2 feet away, so it is not using two eyes and so it doesn't matter

@heracho its about distance to the screen from the eye

So, your question is more about this phenomena? : https://en.wikipedia.org/wiki/Vergence-accommodation_conflict

The display may be two centimetres away, but there are lenses between the display and the eyes, and they project the image to make it look like it is much further way. This is necessary, because most people cannot focus properly on an object that is only 2 cm away, and it would cause the eye strain or fatigue that you mention.
It's a bit like looking through prescription glasses. Lens are very close to our eyes, but it is not the lenses that we focus on. We focus on where the light rays coming through the lenses appear to be coming from.


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What is Growth and how can we define it to be a defining property of life?
I was reading a book and it said that internal/intrinsic growth is defining property of life and not extrinsic growth as saying accumulation of dust on a book makes it a bit bigger, even if it is by a few mm but since it's just a deposition of material and it can be removed, so it's not living. Now, if we see intrinsic growth then I had a doubt. Say we took a piece of log and dipped it into the water. Then the log will also grow in size and this growth is from inside, but the log of wood isn't living. So, I was in doubt that how can I define growth for a living.

There has been a lot of debate on this topic actually and there is no universally agreed upon definition of life. Almost any point that you raise can be refuted with a non-living counter example. Therefore, I think that this question will most likely accumulate answers that are primarily based on opinions rather than facts.
However, if you just refer to growth in living systems it almost always means replication (of cells/genetic material).

All rudimentary definitions of life I've ever come across include growth as only one of many properties. I doubt a log of wood also conducts reproduction, homeostasis, or metabolism (to list a few other features). Similarly, a computer virus reproduces, thermostats self-regulate, and abiotic chemicals may 'metabolise', but somehow these don't confound us. I think the questioner can't proverbially see the wood for the trees :-)

Actually this question came in my mind when I encountered a question that said whether plasma membrane is living or not.My mind instantly drifted towards coacervates prepared by some scientists in order to explain that how 1st form of life would have originated. Then I thought that if I prepare a phospholipid bilayer and add all sorts of protein and stuff in it,can I call it living? Will it show growth? If not then what is life and what is living. How do we define growth in a way that it can best explain life.

If you are just asking what does growth mean in the context of living systems then it almost always means replication of a unit: cell or genetic material (cell division, DNA replication etc).
Note that increase in cell volume or the inter-cellular space (accretionary growth) also happen in living systems and they are also considered growth. However, at a gross level these processes are indistinguishable from what is happening to wood that is dipped in water.
So growing is not an exclusive feature of living systems but still one of the defining features.


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Patterns of craniofacial topology
There are animals which are not directly related but have similar craniofacial topology.
For example: koala, donkey, mouse, turtle, parrot all have features seemingly belonging to same topology, especially by baby species.
Mostly it is features like bridge, bridge to eye socket position, nostrils, upper jaw.
Here is a sketch of what I see as a pattern:

Pronounced bridge, eye sockets on the same centerline with the bridge base. Nostrils and upper jaw center area.
Interesting is that there are other "groups" of species that also seem to have their own pattern.
E.g. cats and owls.
It appears to me that there are several basic patterns that can be observed through many species, and thus
species can be classified in such way.
Are there studies of craniofacial topologies that have connections with patterns and such classifications?

Can you be more clear about what you mean? Similar compared to what?

If it's not a coincidence (which is correct) and you don't think evolution is the cause, what do you think is the reason mammals (kind of) look alike? (Personally, deer and koalas don't resemble each other very much to me, but if you mean, hair, bilateral symmetry, eyes, noses, ears, upper and lower jaws, etc., then yes, I agree.)

You may be interested in Paedomorphosis

@BryanKrause some clarifications are added

I'm still not really clear what you think these species have in common that other related species do not.

The morphogenesis of craniofacial structures is a rather elaborately controlled process at both the molecular and mechanical levels. There are a variety of papers on the subject that you might consult. While not an expert, I suspect that this question is too broad to adequately answer all at once.

@BryanKrause that would require comparing at least two types and adding more images. I'll add it later.