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Do fruit juices have a diuretic effect & what governs this?
Was just contemplating this.
Juices tend to contain a lot of sugar.

Does the body absorb all the sugar in juices?
If the body does not, that sugar must be excreted by the kidneys alongside water thereby causing a diuresis, right?

NB I realise even if there is a diuretic effect that is outweighed by the large proportion of water in juices. But my question is whether there still is a small diuretic effect

In short: Drinking fruit juice by a healthy person with a normal kidney function do not likely have any significant diuretic effect.
Even if you drink, let's say, 2 liters of 10% fruit juice within 30 minutes, it would likely take about 2 hours for all the juice to be emptied from the stomach into the intestine and absorbed into the blood. Sugar delivered from the intestine will gradually increase blood glucose, but this will be balanced by the glucose taken from the blood by the cells, so, the blood glucose will not likely exceed 11 mmol/L, when glucose can start to move from the blood into the urine and cause diuresis.
I can back up this by the glucose tolerance test in which you drink 1 cup (237 mL) of a drink with ~35% glucose (>3 times as much as in a usual fruit juice). 2 hours after the test, the glucose levels in a healthy person (without diabetes mellitus) will be lower than 7.8 mmol/L, so below the diuretic level (11 mmol/L).


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Which DNA would sperms contain from a transplanted scrotum?
We had a discussion at the coffee break today about transplanting a scrotum.
Let's assume that it's possible.
Would the produced sperms contain the DNA of the donor or the one that got the scrotum transplanted? Can you explain why?

What do you mean by pouch? Testicles? Penis? Marsupial pouch?

Found the correct word (I think). English is not my native language.

Possible duplicate of Is DNA replaced after organ donation?

Johnny: I'm not asking about the organ that was donated, but the sperms produced in it. Aren't they produced using elements from the rest of the body?

So you are really asking for a hypothetical testicle transplant not scrotum, the answer would still more or less be the same as given in "Is DNA replaced after organ donation?". You are not the first to ask this question, if you head over to Reddit, there's an entire thread dedicated to the subject: https://www.reddit.com/r/AskReddit/comments/czaae/if_you_had_a_testicle_transplant_would_your_sperm/
As you can see the answer is the same..

There also is an article in The Verge: https://www.theverge.com/2018/4/26/17286728/penis-scrotum-transplant-surgery-us-veteran-johns-hopkins-testicles-ethics

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Lizard Identification
What is this lizard?

Seen in Hollywood, Florida, on a golf course. It may have been an escaped pet and was approximately 17" long.

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Did the chromosomal fusion within humans affect phenotypical change compared to the separated chromosomes in the other apes?
I just read this article on the evolutionary divergence between humans and chimps, and how the most significant event was when the 24 number of chromosomes in chimps was reduced to 23 in humans due to chromosomal fusion. However, while this even significantly supports the theory of evolution, how does this affect natural selection? What phenotypical changes may have occured between these two groups because of the chromosomal fusion? And what if chromosomal fusion did not occur? Would speciation still occur by other means, e.g. geographic isolation?

A few comments. 1) Is there any reason for using the phrasing while this even significantly supports the theory of evolution, how does this affect natural selection? instead of just asking How did this large mutational event affect the phenotype and the fitness of the carrier? 2) And what if chromosomal fusion did not occur? this type of what "what if the world was different" are impossible to answer on a science website

Would speciation still occur by other means do you have any reason to think that this mutational event lead to reproductive isolation? Between which lineages then (two hominids lineages and among the pan and hominid lineages)?

Ah I see. I'm only eighteen so my question phrasing is still underdeveloped. And I believe reproductive isolation would occur due to post-zygotic barriers such as infertile offspring. The difference in chromosomes number should have an affect on offspring production, either disallowing it, lowering survival chance, or having the offspring infertile. And as for the lineages... I have not studied them haha

Are you claiming that humans with balanced Robertsonian translocations are reproductively isolated?

@swbarnes2 After a quick research, I would say I am claiming that those affected with Robertsonian translocation are reproductively isolated.

And is this claim of yours backed up by evidence?


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Europeans succumbing to diseases they introduced to native Americans
I am reading a non-fiction account of Spanish first contact with native Americans. The Spaniards were shipwrecked, undernourished, malnourished, and dehydrated upon their arrival. Over 75% of them died within a few months. The author writes that after their numbers were thusly reduced, the natives who they were staying with then began to die of "a sickness of the stomach." The natives blamed the Spaniards for killing them.
I am assuming that the illness the natives contracted was introduced by the Spaniards, and that it was one of the ones for which the Europeans had developed a certain level of immunity, meaning that in effect, the natives were correct that the Spaniards were killing them.
The author does not ever specifically say whether any of the Spaniards contracted this fatal stomach illness, so it is possible that all of the Spaniards who died, did so from other causes, such as malnutrition. I am basically trying to find out how likely that is.
My questions are, would the Spaniards' immunity from whatever disease this was help them in the presence of an epidemic such as this, or did their immunity only keep them from contracting it when it was in its latent form? Did their weakened and malnourished state make them more susceptible to a contracting a disease they were carrying, yet were previously immune to?
To put it another way, I'm trying to find out whether it is possible for there to have been a "feedback loop" of some sort when it came to European-introduced diseases.


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how does a dna probe work in DNA fingerprinting?
It says in my textbook ' after hybridisation with VNTR probe,  the autoradiogram gives many bands of different sizes '.  I tried looking on the net and it said there that probe is ' a radioactively labeled ssdna which binds to complementary dna '
My question is,  how do we know that if the DNA we are testing does contain complementary sequences?

You should look up VNTR. Take a look at the wiki page and it will tell you that VNTRs are Variable Number Tandem Repeats, the length of which varies between individuals, making these irreplaceable in DNA fingerprinting and such.
The trick is, all individuals will have it, but the pattern will be different, so you probe such regions which are formed as a stretch of k-mers. And you already know that they will be complementary, because we all carry them.

If you know what genome you are looking at, and your probes are validated for that species, then your sample will have that sequence.

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about the muscle's tension's variables
I'm reading the paper "THE PROBLEM OF THE INTERRELATION OF CO-ORDINATION AND LOCALIZATION", which is written by N. Bernstein.
The paper said
"The degree of tension of a muscle is a function, in the first place, of
its innervational (tetanic and tonic) condition E, and, in the second place,
of its length at a given instant and of the velocity with which this length
changes over time."
I don't know why the tension of a muscle is the function of those values.
If that is just assumption, why the assumption can be established?
Thanks!

In physics, tension is proportional to strain and strain is proportional to change in length per unit length.. so second part seems like a standard result i.e., Hooke's Law

So does the variable E roles like Young's modulus? I understand that the tension is the function of the change of length. But isn't young's modulus constant value? The paper said E also means the degree of excitation. Can you explain me what E can mean?

E in your question is not Young's modulus. It's innervation condition, as you put it, and I've no idea what it is. Young's modulus is indeed constant. Whenever length changes, there'll be a corresponding change in tension so that Young's modulus is constant.

In the paper, E is like the additional force to operate active motion. I didn't know about that because I didn't read that after that content. Thank you for the advise.


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Help identifying a fly by its remains
I recently hiked in a swampy forest in the Yaroslavl region(Eastern Europe) near lake Plesheevo and came across a clearing. Although the area was swampy and verdant, there was a 5 meter wide "bald spot" on the ground which looked like sand. Near that spot there was a lot of buzzing (which I initially mistook for the buzzing of wasps), and soon I found myself covered in these black flies.
The flies clung to my fabric hoodie, at least one tried crawling in my hair, and one tried to find its way into my eye.
I tried shaking them off, but they seemed to be able to cling very firmly to my clothes. (later I discovered that even dead flies were really hard to remove from fabric)
At that point I panicked, quickly retreated, and spent a good 15 minutes extracting every single one of them from myself and my garb.
When I came back, I took a picture of the carcasses of two flies that found their way into my pocket and silently passed away there from unknown causes. Unfortunately, I didn't get to take a picture of a living fly because I was too agitated at the time.

Their length was approximately 0.3 inches and when squashed, they produced yellow spots on my clothes.
I tried identifying them, but didn't have much success. They seem to look like a variety of horse-fly (or a dear-fly), but I think none of them actually bit me. Also, strangely enough, my clothes were sprayed with insect repellent which they seemed to either completely ignore or were actually attracted by.

They look very much like Hippoboscidae. https://en.wikipedia.org/wiki/Hippoboscidae
This family are parasites of birds and mammals, but I am not aware that they are vectors of any diseases to humans. So don't worry. One member of the family is a wingless parasite on sheep (Melophagus ovinus)

Thanks, I think that's it! It seems I was "assaulted" by a spawn of deer flies (for some reason Wikipedia has 2 articles on deer fly, and the one I initially linked was not "the right one"?) The article mentions their bodies are hard to remove once they've attached themselves to the victim (check), they prefer dampness (check), they reproduce on moose and deer (which are numerous in that area), and it can be found in the European part of Russia (check).

The Russian Wikipedia entry also mentions the deer flies can transmit the Lyme disease to humans, albeit somewhat rarily. So it seems to make sense to get checked if bitten after all.

These were NOT deer flies (Tabanidae). That is the problem with common names, that differ across languages. They may have been Deer keds, which are in the family Hippoboscidae.

Interesting, the English Wikipedia page lists both of these names as synonymous for Lipoptena cervi. I guess they're only synonymous in some people's vernacular.

Common names are often used for different species, even in any particular language. The people using the common name are simply not distinguishing the differences, even when organisms given the common name are quite different.


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What characteristics do living organisms (like humans or plants) have that viruses don't?
I am not too sure if viruses are considered living organisms.
I learned that living organism:
-Change their size
-Reproduce
-Heal themselves
-Need energy (by eating)
-React to the environment
-Have a lifespan
-Made of at least 1 cell (some exceptions)
Which features that are listed are not in viruses?
If I need to be more clear, please tell me as I'm not very good at explaining.

@DeNovo Hm the answers to those questions are very helpful. I just would like to know which of the characteristics I've posted are the same characteristics in viruses.

Linving organisms have intricate metabolic pathways that viruses donot have viruses stay in equilibrium till they infect host meaning that they they donot exachange matter and energy with surronding when they are outside the body but is a property shown by humans and living organisms.

Hi Udaya, welcome to BIO.SE! In general, we ask/require that answers provide support (typically through reputable sources + images) for their claims. In this way, we can better ensure more accurate responses. Please update your answer with more details and some reputable sources to avoid having your question closed. Thanks!


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Does freezer burn affect only the cells on the surface of food?
Suppose i submerge a banana halfway through in a tray with water. Part of the banana is submerged in water, part of it is on the outside. The water and banana in the tray is being put in the freezer and freeze. Since part of the banana is exposed to air freezer burn is going to take place. How deep does it affect the tissue?
Not a homework question.


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Is this a nest and which wasp species?
A friend found this stuck to his insect screen today.
He said it felt like dust.
This wasp/bee was alive.
Location is Germany.
Is this a nest?
First look:

After peeling it open:

Looks like this is a European wool carder bee (Anthidium manicatum)
More precisely a female, judging by the round end of the abdomen.

Information regarding the nest it was found in:

These bees construct their nests in preexisting cavities, using the trichomes of wooly plants.
Females use their mandibles, which are sharply toothed, to remove trichomes from the stems and leaves of various plants. They then roll up the trichomes into a ball and bring them to a preexisting cavity. Inside the cavity, the bees fashion the trichome ball into cells, where they deposit an egg as well as a provisioning mass consisting of nectar and pollen. Once finished, she seals the entrance to the cavity with a terminal plug, which consists of inorganic and organic materials that she brings to the nest. Source

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What goes into a vaccine placebo, typically and in the specific case of Pfizer's SARS-CoV-2 vaccine trials?
I am curious about what actually goes into a vaccine placebo formulation, given that there were apparently some reactions reported by trial subjects who received the Pfizer SARS-CoV-2 placebo.
From what I've been able to find out online, the actual vaccine contains as principle ingredients (simplified):

mRNA (active ingredient) to make the target antigen (spike protein)
lipids (to protect the mRNA and facilitate its delivery into cells)
salt(s) to adjust pH and match the salinity of blood
sugar to address issues which occur when the vaccine is frozen

An injectable placebo could be as simple as a saline solution... if so, how could reactions be explained? Is it entirely psychosomatic?  Is the Pfizer SARS-CoV-2 trial placebo the complete formulation (or some subset of vaccine components) minus the active (mRNA) ingredient?
The lipids have been implicated in allergic reactions to the actual vaccine; would they have been present in the placebo and account for the placebo reactions?

Simple answer: This vaccine trial compared their trial vaccine against saline.
See the original publication by Biontech and Pfizer in the New England Journal of Medicine linked below. The relevant information can be found in the methods section:

TRIAL PROCEDURES
With the use of an interactive Web-based system, participants in the trial were randomly assigned in a 1:1 ratio to receive 30 μg of BNT162b2 (0.3 ml volume per dose) or saline placebo. Participants received two injections, 21 days apart, of either BNT162b2 or placebo, delivered in the deltoid muscle. Site staff who were responsible for safety evaluation and were unaware of group assignments observed participants for 30 minutes after vaccination for any acute reactions.

As far as I followed up the case of the allergic reactions, two of these have been observed in England. Both people had an epipen injector for such cases by hand, making it possible that they have underlying problems with allergies (as this is not a medical device people usually have at hand), no such cases have been reported from the trial. Allergic reactions are always a small risk with vaccinations which is the reason why this is done in a controlled medical environment.
As for the vaccine reactions in the placebo group, this can be caused by the nocebo effect, where expecting negative effects leads to a more negative reaction. As @BryanKrause mentioned, all possible effects reported in such trials are recorded as possible side effects. This leads to a lot of things being recorded which happened at the same time as the vaccination but have no connection to it.
Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine

In addition to the nocebo/psychogenic effects, I think it's worth mentioning that people experience things classified as "side effects" all the time. People get headaches, diarrhea, sneeze, cough, get stiff limbs. Ordinarily we shrug it off, blame it on last night's meal, how we slept, smells from the neighbor's cooking. But if you just got injected with something that might have been a vaccine, it's natural to attribute it to that thing that's novel.

@BryanKrause Good point. It demonstrates the old "correlation is not causation" very well.


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DNA Sequencing Types & Qualities
I've been searching for a list of the types of DNA sequencing (e.g. Sanger, Next-Generation) and how prone they are to sequencing errors (None, Somewhat, Very), but I haven't been able to find anything.  Here are a few scenarios:

I have a bacterial culture I want to sequence to see if a plasmid was properly transformed.
I want to verify a PCR product.
I want to sequence a large organism's genome.
I want to verify a mutation found in a human tumor (found using exome data)

Given these examples, and any other you use regularly in the lab, can you please give me information on overall platforms (not specific like Illumina, but general like Sanger sequencing) and their error prone-ness?

Don't you think your question is a bit broad? Did you check out reviews on this topic? There are many. See these: http://dx.doi.org/10.1101/gr.168393.113, http://dx.doi.org/10.1186/1471-2105-13-185, https://www.biostars.org/p/2015/

I'll be honest, this seems like an exam question reworded.

@James It's 3 years old, but definitely wasn't an exam question. I was a PhD student and was getting started in bioinformatics & my uni's resources to inform us on this tech was underwhelming. I was trying to figure out what tech I needed for different experiments based on their error rates.

In that case, I think it suffers from needing to be more focussed like @WYSIWYG suggested originally. Essentially this would be more helpful if it was split into 4 questions.

Sequencing does not seem necessary for this... most plasmids contain an antibiotic resistance gene (ex. kanamycin-resistance) that will allow cells that have been appropriately transformed to survive in the presence of kanamycin.
If it's just a PCR product, Sanger sequencing seems the best way to go. It is quite specific and not prone to algorithmic errors as are next-gen sequencers.
Next-gen sequencing would be ideal as you're dealing with the whole-genome. Sanger would prove laborious and low throughput. Any variants of interest you find call always be confirmed through sanger. Illumina sequencers are quite robust at sequence generation at the whole genome level.
This mutation can be verified through sanger sequencing, but you could also conduct targeted re-sequencing of the particular exon (although this seems like over-kill). Since it is a single mutation, I believe the specificity of sanger would be your best bet.


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How does CpG island methylation lead to gene silencing?
I see often the blanket statement that CpG island methylation can lead to gene silencing.  However, I have been unable to find a straightforward explanation of the mechanism by this.
Is it a purely physical block of binding for transcription factors?  Does the methylation create a tertiary structure that is compacting the DNA?  Does it recruit histone modification factors that compact the chromatin?
Please feel free to cite literature so I can go read the papers.

CG methylation has long been associated with gene silencing due to the generally negative correlation between gene promoter methylation and transcription levels.
When CG methylation occurs in the promoter or enhancer region of animals (where these 'CpG islands' tend to be), methylation seems to impede (to some extent) transcription factor (TF) binding.  That is the baseline mechanism for gene repression.  The altered chemical properties of the DNA make it less favorable binding site for its cognate TF.
In some cases, methylation clearly prevents TF binding.  For instance, some TFs bind DNA to block methylation, which facilitates access of another TF or set of TFs to the bound DNA (for instance, this paper by the Schubeler lab about NRF1).  In the case of other TFs, their binding is less reliant on methylation state, possibly due to the strength and breadth of the binding site (for instance this work from the John Stam. lab about CTCF).
Methylation also can affect nucleosome positioning and stability in some contexts; the nucleosome effects are poorly understood currently  because nucleosomes and methylation likely feedback on one another.  See this work from the Zilberman lab for an example.
The role of a higher-order repressive structure forming is arguably not obvious yet; for instance, histone H1 bining does not appear to be heavily influenced by methylation state (although this is somewhat contentious because there is often a positive but weak correlation at repressed elements in the genome between H1 and methylation--for instance just pubmed 'h1 chip' with reviews and read a recent one).  More certain is the relative change in location of methylated promoters within the nucleus to a place of transcriptional 'silence' (inactivity).  These repositioning phenomena are under intense investigation; you can learn more about this by googling for 'nuclear topology and gene repression' or something like that.
hope this helps


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GATK workflow for Cancer
I am just starting to learn to use bioinformatics tools.  My university has a limited and expensive bioinformatics team, so I'm mostly on my own except for big questions.
I am planning to use GATK to run 58 cancer control/normal pairs of Exome sequencing data (Illumina) from FASTQ or BAM file format, through the pipeline, with an output of a VCF & MAF format for analysis.
The current GATK pipeline is used for disease but not cancer, so I was wondering if anyone knew if there should be changes made for cancer.  Here's the current pipeline starting with BAM files:

(Non-GATK) Picard Mark Duplicates or Samtools roundup
Indel Realignment (Realigner TargetCreator + Indel Realigner)
Base Quality Score Reacalibration (Base Recalibrator + PrintReads)
HaplotypeCaller
VQSR (VariantRecalibrator and ApplyRecalibrator in SNP and INDEL mode)
Annotation using Oncotator (?)

I'd like some verification that this pipeline will output what I need to run my samples on MuTect, MutSig, or some other analysis program.  I appreciate any advice.

I typically deal with the sequence files upstream of this step, or the VCF files downstream--otherwise I would be more comfortable attempting to provide some helpful feedback. At an extremely superficial level, what you have outlined make sense, but I have just never used GATK firsthand (lots of colleagues have and do).  What about posting this verbatim on these two sites: SeqAnswers, and BioStars? I have seen lots of NGS-related Q&A posted there (your question is essentially a very detailed bioinformatics protocol).

MuTect2 was just released into beta as part of GATK 3.5.  It's based on HaplotypeCaller but makes somatic SNV and INDEL calls.  You can find more information about MuTect2 on the GATK blog and ask any additional questions on the forum.
As a note:  IndelQualityRecalibration is not needed with Mutect2, and there is no VQSR available for somatic calls.
MarkDuplicates -> BQSR -> Mutect2 -> Oncotator is a good basic workflow for somatic variant calling.

This post goes over what MuTec requires as input. mark duplicates and indel realignment will probably have to be done on bam file to use it as input. BQSR is optional and does not change the quality too much. HaplotypeCaller is used for germline not somatic variant calling.
If you have followup bioinformatics questions, you might be able to find answers more quickly on biostars or GATK forums

Thank you!  I didn't know that about Haplotype Caller.  The team at my school suggested it.  I will try biostars or GATK forums.


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How can the number of chromosome change during evolution
I found an explanation here, which is basically saying that sometimes the centromeres are duplicated, breaking a chromosome into two halves. But how could this propagate?  I don't think inbreeding is efficient enough for this mutation to become dominant, and it should take a lot of pregnancies for the mutants and the regular ones to produce an healthy offspring. Is the explanation in the link backed by any evidence?
Thank you!
By the way, do we know how many chromosomes did the latest common ancestor of human and chimpanzee have, and when did chimpanzee gain the extra pair of chromosomes (or when did we lose it)?

We cannot have direct evidence as the DNA of common ancestors have either not been found or are degraded to a point where it cannot be analyzed. However when looking at modern genomes we can do syntenic analysis and look at the synteny between chromosomes. Whether you believe it or not, the evidence is within our genome and many other genomes. All you need for it to take hold is an isolated population that is put under selective pressure.

@arax There are two different questions in your post. A post should always be limited to one question. I suggest that you get rid of the second one. You may ask it later.

@arax Speciation due to change in chromosomal number by hybridization between two species, yielding to a third species has typically be quite nicely studied. Would such an example answer your question?

Note btw that a change in chromosomal number is often (not always) associated with a shift in the ecological niche toward more extreme environments. Why is it so? Last time I heard of it, I have been told that nobody really knows why.

Someone asked and then deleted their comment, but to clarify, "direct evidence" in my comment would be intact, sequenceable genomic DNA from a Common Ancestor. Syntenic analysis provides inferential evidence of the events of translocation that have survived in evolution, but without the ability to compare to the actual data of the common ancestor, we can only infer the events.

This article may be useful.  The author goes into several ways that chromosomal rearrangements can go wrong resulting in a change in chromosome number. http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/


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Does the 1:1 sex ratio at birth apply to every human pregnancy or is it a statistical average?
Are there genetic factors that biase the sex ratio of offsprings for each person but average to 1:1 for the entire human population, or does the 1:1 ratio apply to every single fertile person?

The ratio is not 1:1: https://biology.stackexchange.com/questions/27582/why-do-we-have-more-male-infants-born

@kmm The question still stands -- is the ratio a statistical average or applicable to individuals?

The ratio you are referring to is indeed computed aggregating multiple observations and thus it is a "statistical average".
Any individual (or couple, in this case) can have a specific ratio that differs from the average one. Many factors may affect sex ratio, among which sperm/egg viability, chromosomal aberrations, and hormones misbalance are the ones usually affecting the fertility of a couple and they can also bias the sex ratio.
Many other factors can play a role.
Different populations have slightly different sex-ratio and even smoking can skew the sex ratio!

The question is not very well asked but I suppose the OP does not ask whether any given couple can have more offspring of one sex than of the other but rather whether there is genetic variance in the sex-ratio.

@Remi.b I have interpreted the question differently. I will wait for the OP to comment to this answer or to clarify the question. If needed, I will adjust my answer.


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How quantitative is the theory of evolution right now?
We developed complex structures like eyes and brain, whose mechanisms rely on specific species of molecules and relevant chemical reactions. But we did not develop an enhanced night vision, the ability to fly, or a built-in silicon-based integrated circuit.
As I understand, we did not develop the latter set of abilities because they are either not so much needed, cost too much energy to be beneficial, or that they required so many information to be coded into our genome that it would take forever for the mankind to produce sufficient mutations. But could this be quantified? Can we tell if a species will develop a specific character, based on the environment they're in?

By "we", do you mean humans or animals in general?

I don't think so.  You can say, if I throw this fresh water fish into salt water it will have to evolve or die.  You could even say that a population living in a delta where they are exposed to fresh or salt water could possibly develop mechanisms for both.  But you couldn't say with any certainty that they will.  Maybe the species moves further inland as they get better characteristics for fresh water.  I doubt that antibiotic resistance was predicted to occur before we started seeing it in labs.

"But could this be quantified" -- what is "this" in this sentence? What is it that you wonder whether it is quantified or quantifiable? You have to be looking for numbers somewhere, so could you state which numbers you are after? Your last sentence seems less directly related to quantification.

There are some suggestions that evolution is quite predictable, more predictable than many of us think. Richard Dawkins is one proponent. If this is true, there is indeed some elements of predictability in the higher-level results of evolution.

Can we tell if a species will develop a specific character, based on the environment they're in?

This is a major part of what quantitative genetics does. Or more detailedly, quantitative genetics can predict, for a population, changes in a trait given a selection pressure. First of all, for evolution to occur there must be variation in the trait you are making predictions about. Secondly the accuracy of the scale of the predictions matter greatly for the evolutionary model to be tested (eg, "Will body size increase?" vs "Will incisors increase 3mm in 300 generations?").
Several things have to be known to predict the evolution of a given trait:

The number of genetic sites controlling this trait (QTL, or quantitative trait loci). If the all the loci for a trait are known, the nucleotide heterogeneity within the population of those sites can be quantified. The number of genetic loci are important for estimating how often they will change from new mutations.
The effect of each genetic locus on contributing to variation to the trait (additive genetic effects).
The heritability of the genetics controlling this trait, (does the environment contribute to variation in the trait (low heritability) or do genetic differences cause more variation in the trait).
The strength and consistency of selection  (how fit are individuals in that environment along to phenotypic distribution compared to previous generations). Is this trait being selected in isolation, or are other traits which share the same QTL also under selection.
The effective population size.
The rate of migration between this and other populations.

So yes, given the our knowledge of quantitative and population genetic theory, predicting evolution of a given trait is possible. Just as predicting the future is possible with the laws of physics if you know the position of every atom in the universe. It's important to remember that organisms are constellations of 'traits', so predicting the evolution of all traits which make up the individuals within a species could be similar to predicting the futures of several multiverses.

Clarification on the question
The question is a little unclear and I will try to interpret it and answer it. I hope I won't fail to see your goal.
Quantitative vs predictive
There is a big difference between quantitative and predictive. To understand the difference you might want to ask the question on Philosophy.SE.
Quantified vs quantifiable
As @chelonian said in the comments, if you are asking Is evolution quantitative, then you would need to say whether you meant quantified or quantifiable. Almost everything in evolutionary biology (just like in other sciences) is quantifiable but most of it is not quantified as it takes a lot of money and time to do so.
What I think you are trying to ask
Paying attention to the question in your post Can we tell if a species will develop a specific character [..] and assuming that by develop, you meant evolve, then what you meant is Is evolution predictive rather than quantitative.
What I am answering
I will try to answer to the question How good are we to predict future evolution? and just say a few words about how quantitative a science is evolutionary biology.
Evolutionary Biology is a quantitative science
Evolutionary Biology is definitely a quantitative science. It relies a lot on mathematical modelling (incl. statistics and probability theory) and numerical modelling. You might for example want to have a look at Population Genetics and Quantitative Genetics which are at the core of evolutionary Biology.
What are we good at predicting?
Here are a few examples of things we can predict. We can predict how many pairwise differences (or other measures of molecular differentiation) do we expect between two lineages that recently split in a given number of years. We can predict how many mutations of a given fitness effects (whether beneficial or deleterious) do we expect to accumulate over a given period of time in a population. We can make also some predictions about the evolution of multicellularity, sociality, etc. in lineages that are limit-cases (relating again to our ability at a short time only). We can make predictions about the speed of evolution measured in Haldanes or in Darwins (these are units) if we know the genes involved and the heritability of the trait of interest. We can predict the heterozygosity of a structured population. I could cite many other examples. Generally speaking, we have good predictive abilities at short time scale OR for neutral sequences OR for conserved (DNA) regions (strong purifying selection).
In short, we can predict a lot of things but by far not everything yet.
What are we bad at predicting?
I would suggest to decompose the reasons for why predictions can be hard into the following categories. However, I might well forget something and one could argue that my semantic is less helpful some other semantic.

Environment

One issue related to make predictions at long time scale is that the environment changes through time in a way that we are not able to predict accurately enough yet.

Noise

I am not here talking about measurement error or sampling error (these are concept of statistics you may want to check if you don't know them), I am talking about the stochastic process that are inherent to biological systems such as the randomness of mutation processes and genetic drift.

Genotype-phenotype map

We have too little understanding of molecular genetics in order to be able to predict how different specific mutation would affect the phenotype. As a consequence, we today still have very little predictive power about the evolution of a phenotypic trait that is currently totally inexistent.

Complex systems

For example: demography affects evolution which affects the social environments, which affects demography which affects pattern of species competitions which affects the evolution of another species which affects its demography which affects the evolution of a third species which affects the demography of our first species, etc... These kind of complex systems are often mathematically not tractable.

Parameters

We often don't know the exact parameters of the lineage we are interested in. There is a lot of measures to take to be able to make predictions and we often don't have the money (or the time) to make all these measurements (assuming we are able to accurately measure them). For this reason, we are often relatively good to make predictions for a few model organisms but pretty bad for the vast majority of species.

I apologize for my total lack of reference but it would take hours to search references for every claim
Applications of evolutionary biology
There are not a lot of applications of evolutionary biology for the moment but still there are some proving its predictive power. These applications include

medicine and epidemiology (incl. evolution of resistance)
artificial selection and other technics mainly to improve crops nut not only
Various search algorithm such as genetic algorithm

General Advice
The best way to learn about evolution and to answer your own questions (or help you to ask more accurate questions) is to actually take a short course. Understanding Evolution by UC Berkeley is probably a good place to start.


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What is the reason for having an extra recognition site for a restriction enzyme?
Can the size of a supercoiled plasmid DNA be determined by using standard DNA size fragment electrophoresed in parallel? 2. An unknown DNA molecule was cleaved using several restriction enzymes individually and in various combinations. The DNA fragment sizes were determined by agarose gel electrophoresis and the restriction enzyme recognition sites were mapped. Subsequently, the DNA was sequenced and an extra recognition site was found for one of the enzymes. However, all the other mapping data was consistent, within experimental errors, with sequence data. What are the simplest explanations for this discrepancy? Assume the DNA sequence had no errors.
My answer:
the  extra enzyme recognition site was cut-off with the fragment due to partial digest that occurred because of insufficient enzyme was added or the rxn was stopped after a very short time.
Am i wrong? my logic here was such that they only found the extra recognition site after they sequenced the DNA thus it was not available during the rxn and thus it was either cut off unevenly in one of the fragments OR it could have had the complementary sequence to it that was methylated that hid it.
Detailed answers are appreciated!!

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.

you mean if say i had ECOR1___HindIII___ECOR1 the extra recognition site would be neglected?

Yes, exactly. Although I was envisioning, for example, 2 EcoRI sites separated by between 0-50 bp of plasmid DNA. Depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because they run off the bottom of the gel, or because they don't resolve). Similarly, depending on the size of the adjacent fragments in the various digests, and the assay's limit on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".

thanks perry, could you copy your answer and post it under answers? I would love to list you as a the correct anwer owner

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.
For example, if there were 2 EcoRI sites separated by between 0-50 bp of plasmid DNA, then depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because small fragments run off the bottom of the gel, or because they don't resolve well unless the gel contains a higher percentage of agarose or acrylamide).
Similarly, depending on the size of the adjacent fragments in the various digests, and this assay's limitations on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".


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genetic complementation problem
I've attached the picture of the problem.
SO, based on the information I managed to assemble two large cistrons. (if the combination of two mutants yield (-) mutations are on the same chromosome)
A)so my cistrons are:
1)(1,4,5,6,7,9)
2)(2,3,4,7,8,10)
Note: somehow 4 and 7 is present in both cistrons
B) they ask us what mutation could cause two different cistrons have the same mutants
I was thinking maybe an insertion? i just dont get how it's even possible since if they have the same mutants doesnt it mean they overlap and thus are on the same chromosome??
I would appreciate if you could explain me what type mutation could cause it and check if I did the complementation correctly

bacteriophage T4 has a single chromosome (approx. 200 kb in length). The chromosomes are terminally redundant,  so the genetic map is circular, even though the physical map is linear (as I recall).
A mutation in E. coli (or its viruses) that affects two adjacent protein-coding genes is said to be 'polar'. This indicates that the two genes in question form part of an operon. A strong loss-of-function mutation in the promoter for the operon will typically affect the expression of all the genes in the operon. In your example there are two cistrons, or genes, in the rII locus of T4.

It is possible that the data for this question are taken directly from the published literature. I suggest you search PubMed for papers by Seymour Benzer, from the 1950s.

Sorry Perry, I just don't understand what you mean. So you're saying this problem can't be solved or the mutation on operon is the cause?

I was trying to say that these two cistrons form an operon in the phage genome, and that by knocking out the promoter for that operon you would reduce the expression from each cistron. Another way to say this is that there are two genes bedside each other on the chromosome. The upstream gene has a promoter and the downstream gene does not have its own promoter. The downstream gene uses the upstream gene's promoter. this means that the mRNA from that promoter will be polycistronic and contain 2 open reading frames. Breaking one promoter kills the expression of 2 genes.

So how can this mutation be called then? 1 promoter per 2 cistrons? I've never encountered anything like this in my class before

On second thought, the answer they probably want is that 4 and 7 are deletions, or deficiencies, that remove some part of both genes. That is going to be a simpler explanation than the operon with two cistrons.


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E.coli division and its DNA replication
E.coli divides in 20 minutes and its DNA replicates in 38 minutes .Kindly explain.


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What program was used to create this visualization of a neighbor-joining tree?
I know there are many programs out there to visualize neighbor-joining trees in phylogenetics. I have a tree in Newick format. Does anyone recognize the features of this image as coming from a particular visualization program? I have tried several that may have produced this but with no success yet.
Note: I have to visually compare a new method's NJ tree with the result shown here, so that is why I really want to know exactly what program was used. This is not a question about software recommendation or opinions. Thanks!

Honestly this looks like something someone put together by hand in illustrator (or a similar program)

Can't you just ask the author?


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Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?
Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics, and why don't hospital acquired infections exist elsewhere ?
The infections that are caused in hospitals are usually a result of bacteria that are resistant to multiple antibiotics making them difficult to treat, but why are the bacteria resistant to all these antibiotics?
I realize that a lot of antibiotics are used in hospitals but the question that comes to my head whenever I read this is "So?".
To make my misconception clearer, I will use MRSA as an example .
I mean , for the Staphylococcus aureus bacterium to become resistant , the antibiotic has to be used on it , so how can the antibiotics used to treat different infections in difference people act as a selection pressure for  Staphylococcus aureus ( the Bacteria that causes MRSA )?

Hospital plumbing a 'vast, resilient reservoir' of superbugs. I'll make this an answer at some point...

Hospitals have certain features:

They are full of people immunocompromised in some way (old, exposed tissue, on steriods etc.)
They are full of people with pathogens
They are full of doctors who will give antibiotics to people with pathogenic infections

This is a perfect breeding ground for drug resistance in pathogens, with lots of pathogens, lots of places for them to grow (patients) and quite a lot of exposure to antibiotics.  You use Staphylococcus aureus as an example, and it is a good one.  We all have some of it on us, but it is not generally exposed to antibiotics so it does not develop resistance, and we do not generally have large areas of exposed flesh that would cause it to be pathogenic.  In hospital this is not the case, so we get it causing trouble and developing resistance.
These things do occur outside of hospitals, but it does not tend to be as common or frequent.


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What happens in a brain of a person suffering with apathy?
According to this article

Apathy is a profound loss of motivation not attributed to decreased
  level of consciousness, cognitive impairment, or emotional distress.
  Apathy refers to a set of behavioral, emotional, and cognitive
  features such reduced interest and participation of activities of
  daily life. Another prime characteristic is lack of initiative or an
  absence of responsiveness to stimuli as demonstrated by a lack of self
  initiated action.

Could you describe what happens in a brain (on the level
of neuroreceptors) of a person suffering with a lack of
motivation (or apathy)? And how does it look in the healthy
brain?

Could you explain why you think a lack of motivation is not healthy?  And why there should be some physical difference?  I'd think it'd be like asking whether there's a difference in your computer when it's playing computer games vs running a computational modelling program...

@jamesqf apathy is a disease, similar to depression, but there are differences

Why do you think this?

Plus 1 from me. You donated time and effort from the apathy and created a bounty. Also interesting to me.

Starting your comment, first, apathy in itself is not a disease; it's not categorized as such by any medical or psychiatric organization. It is part of the symptoms of some disorders, including depression, schizophrenia and Alzheimer's.
Furthermore, apathy is not a simple symptom, but rather a constellation. That also makes it more difficult to address its brain correlates. From a review,  Moretti & Signori (2016):

Apathy is an uncertain nosographical entity, which includes reduced motivation, abulia, decreased empathy, and lack of emotional involvement; it is an important and heavy-burden clinical condition which strongly impacts in everyday life events, affects the common daily living abilities, reduced the inner goal directed behavior, and gives the heaviest burden on caregivers. Is a quite common comorbidity of many neurological disease. [...] As a general observation, the occurrence of apathy is connected to damage of prefrontal cortex (PFC) and basal ganglia; “emotional affective” apathy may be related to the orbitomedial PFC and ventral striatum; “cognitive apathy” may be associated with dysfunction of lateral PFC and dorsal caudate nuclei; deficit of “autoactivation” may be due to bilateral lesions of the internal portion of globus pallidus, bilateral paramedian thalamic lesions, or the dorsomedial portion of PFC. On the other hand, apathy severity has been connected to neurofibrillary tangles density in the anterior cingulate gyrus and to gray matter atrophy in the anterior cingulate (ACC) and in the left medial frontal cortex, confirmed by functional imaging studies. These neural networks are linked to projects, judjing and planning, execution and selection common actions, and through the basolateral amygdala and nucleus accumbens projects to the frontostriatal and to the dorsolateral prefrontal cortex. Therefore, an alteration of these circuitry caused a lack of insight, a reduction of decision-making strategies, and a reduced speedness in action decision, major responsible for apathy. Emergent role concerns also the parietal cortex, with its direct action motivation control.


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help with mushrooms identification
I know that mushrooms identification is a difficult process. but I would like to ask for help in the identification of this one.
It growth over the grass in a backyard on Toronto, Canada.

If you still have access to the mushrooms, it would be helpful to know the spore color. In case you're unfamiliar with how to find this out, you can take a 'spore print.' Remove the cap from the stem, place it on a piece of paper (or preferably aluminum foil), cover it with an upside-down glass, and wait at least 8 hours. The cap will deposit spores on the paper, and you will be able to see the color.

Amazing picture, by the way. These are very photogenic.

Added the spore print. Thank you for the instructions.

Brilliant. I would call that black from the picture, but do you see any tones in it?

This is most likely a member of the genus Panaeolus, based on the black spore print (distinguishing from Psilocybe and Conocybe), growth in grass (distinguishing from Psathyrella and Naematoloma), small stature and thin stem, bell-shaped cap, brown cap and gills, and lack of a ring on the stalk (David Arora, Mushrooms Demystified). The gills in the photo appear mottled to me, which is a diagnostic feature.
Unfortunately, species in this genus are especially difficult to identify. Michael Kuo writes on Mushroomexpert.com:

Beyond a few "easy" species, identification in Panaeolus requires microscopic examination, a good interlibrary loan desk, and the ability to read French and German.

Panaeolus foenisecii is a common member of this genus with macroscopic characteristics that match your specimens (see Mushroomexpert.com and MykoWeb for detailed descriptions). The cap in this species changes color when waterlogged, which would be worth noting if you see it again. However, I am unsure of this ID without microscopic observation.

Panaeolus foenisecii. Image: Michael Kuo, Mushroomexpert.Com.


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Is there an equivalent to a refresh rate for the brain and consciousness?
Computers have a clock rate that synchronizes their processors. In spite of tempting analogies, the brain is clearly not simply an organic computer. It is constantly changing, rewiring and pruning its pathways, awash in changing nutrients, hormones and other chemicals in a manner that dwarfs any computer ever built.
But is there a biological equivalent to a refresh or clock rate in the brain that organizes perception, cognition and reaction? Is there a timing signal that creates the fleeting now of our consciousness? Or are the various sensory inputs, internal processing, memory storage and accessing, cognition, and signal output only loosely coordinated?

First of all you should understand how exactly a brain works. Brain is modular- there are some signals that are continuously fired whereas others are situational. The "clock rate" would apply only to continuously oscillating circuits. It is fine to draw analogies but as it is written, your question appears quite broad. Please read up some basics on how brain and neurons work and narrow down your question to a specific issue.


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Are identical twins clones?
Identical twins have the same genetic make up but they differ in development so are they in a way clones?

I don't see the point of your question. Seems like an unnecessary debate on the semantics. Lets say if we clone you, it is not really necessary that your clone will behave like you. There can be developmental differences too. Will that make the clone of you actually "not a clone" of you? In any case, in professional references people hardly use the word "clone" to mean genetically identical. The usage of the term "cloning" in molecular biology and developmental biology is restricted to certain procedures.

I'm voting to close this question as off-topic because OP basically asks what a clone is. Too trivial imo.

Are identical twins clones?
A clone is an individual that is genetically identical to another (see wikipedia > cloning). As you said, identical twins (better called monozygotic twins) are genetically identical to one another and therefore an identical twin is a clone indeed.
The role of the environment
Be careful, to not think of clone (incl. monozygotic twin) as individuals that look exactly alike or behave exactly alike. Even for traits that are highly heritable, environmental variation is causing a lot of phenotypic variation and two monozygotic twins do not encounter the exact same environment and can eventually grow up to be very different people. Note that the two blastulas will differ a little bit in concentration of proteins, fats, developmental factors and other things. Such small differences can have important impact on the development of the fetus.
See this post on heritability to have a better understanding of the underlying environmental variation explaining phenotypic variation in populations.
But they are clone for life, right?
Well, it depends on the exact definition of clone but it is important to understand that the expression of genes varies a lot in response to the environment. See for example wikipedia > epigenetics. Also genes may change slightly as we age (see Can genes change as we age?).

The same wikipedia article you quote clearly states that twins are not clones (see my edited answer)

The article says Human cloning is the creation of a genetically identical copy of a human [..]  It does not refer to the natural conception and delivery of identical twins This claim is about the expression human cloning and not about what a clone is.

What is wrong with using the definition for human cloning? The question clearly refers to humans. However, even if you would like to be picky: I think to such a general question, the more generally used and clear definition given by merriam webster applies much better than stretching the technical definition normally used for bacteria and apply it to humans.

As I understand it, the term human cloning refers to a set of processes to create clones. Generally, this set of processes does not include monozygotic twins. This does not mean that identical twins are not clones of each other. A clone is generally defined as an organism that is genetically identical to another one. In this regard, two monozygotic twins are clones. Does it make sense?

What you seem to say is that we define a clone not only based on its genetics but also by the process by which it has been created. Note however, that such definitions yield to possible issues such as the definition of a parent cell.

It would be great IMO, if one of us could offer an answer who draws to the issue behind the definition of clone (and eventually cloning) and how this relate to monozygotic twin. It will be important to make clear that, monozygotic twins, just like clones, are genetically identical.

I picked up on your suggestion and tried to expand my answer to encompass the different definitions of cloning.

Simple answer: No.
Merriam webster defines a clone as follows:

a plant or animal that is grown from one cell of its parent and that has exactly the same genes as its parent.

Identical twins have identical genes to their sibling not their parent. The reason behind this is that this definition of cloning refers to the artificial biotechnical method of creating genetically identical offspring. While identical twins are a naturally occurring phenomenon caused by a splitting of the embryo during early development.
Edit:
Long answer: It depends entirely on how you define a clone.
On one hand there is the original (biological science) definition (used in Remi's answer) which is mostly applied to bacteria: In that definition, clones are distinct organisms with identical DNA information. In that definition, identical twins are indeed clones, since they share the same DNA information.
On the other hand there is the definition from Merriam Webser (quoted above) which is the nowadays more commonly used definition outside the scientific community (also depicted in popular movies like Star Wars). That definition refers to the technical process of "human cloning" which is defined in the The wikipedia article that Remi quoted:

Human cloning is the creation of a genetically identical copy of a human. The term is generally used to refer to artificial human cloning, which is the reproduction of human cells and tissues. It does not refer to the natural conception and delivery of identical twins.

According to that definition, identical twins clearly are not clones and they would probably be offended to be called such.


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DNA Sequencing - Sanger termination method: What effects will more ddNTPs in solution have on the resolution on agarose gel via electrophoresis?
Say instead of a small amount of ddNTPs, you add a significant percent of ddNTPs to dNTPs. I was thinking this would reduce the resolution for larger fragments due to more ddNTPs terminating elongation earlier on.
I am doing a project on Sanger Sequencing and was wondering this, thank you. (Any suggestions would be appreciated)

You are correct. The greater the ratio of ddNTPs to dNTPs, the more frequently ddNTPs will terminate the reaction, resulting in shorter mean fragment size. However, Sanger sequencing is not done with agarose gels. The result visualizing a Sanger reaction on agarose, using more ddNTPs would result in a smear closer to the bottom. For actually visualizing the sequences on acrylamide, or with capillaries, increasing the ddNTPs would reduce the resolution of longer fragments. It is a balance you need to optimize.


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Does cancer cells come from same process as evolution?
Here is how I understand it:
DNA replication is not 100% perfect and error can happen, this error can be good(evolution) or bad(cancer properties).
But its not the only source of cancer cells - DNA can be damaged by environment, and in rare cases it can receive cancer properties.
Am I correct?

Welcome to Biology.SE. I think this is a duplicate but I could not find the other post for the moment.

Yes, you are about correct. A cancer is an evolutionary process. There are selection pressures both at the multicellular levels and at the cell level. Note that the dichotomy are associated terms this error can be good(evolution) or bad(cancer properties) suggests some misunderstanding about what evolution is about.

@Remi.b this is not a duplicate of that. I do seem to remember another dupe...


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The extinction of the passenger pigeon
During the time when the passenger pigeon was hunted down to only captives in the zoo, how could the zoo not maintain a small population and keep the species alive? Why did the population slowly die out? I thought a bird can successfully raise multiple young, given the near perfect conditions in captivity in which the people there are trying to keep them alive?
Just a question I ramdomly thought of, so answers would be appreciated!
Edit: this is not a duplicate. Birds can have multiple young. That will increase the population success rate.

Too small of a population to maintain I believe.


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mRNA extraction from mice ears.
I am trying to extract RNA from mice ears and for some reason I don't have RNA when I perform the electrophoresis. I directly cut the ears and I put it in a tube with a bead and trizol. then I place it on ice and I use a mash machine for tissue lysis for 8 minutes and 4 ºC. After that, I perform RNA isolation according with a protocol using chloroform, isopropanol and ethanol.
I think the problem could be the extraction. Do you have any suggestions?
Thanks.

Do you see a pellet when you precipitate the RNA?

yes I saw a quite big pellet, but when I do the electrophoresis using a positive control, I suposse to see either two bands or a smears if it is degraded and it doesn't appear anything like that.

Let us know the composition, buffers, running conditions (voltage etc.) of your gel.

that's not the problem, since I use the samples to do a qPCR, I have used taqman, SYBRgreen, two different machines and I dont get amplification, but I do get in a previous sample used as positive control.  So the problem is I don't have RNA in my samples. (the gel it was just to check if I have RNA and it also works with a positive control but not with my samples)

@Bio What were the A₂₆₀/A₂₈₀ and A₂₆₀/A₂₃₀ ratios? The problem could be the beads as well. Were the beads sterilized properly and kept in RNAse free conditions (in DEPC water)?

The RNA may have denatured during extraction if there is no absorbance reading after PCR. Did you produce the control sample or is it supplied?


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house keeping gene variation under treatment
I am injecting BCG in mice ears to measure the local inflamation response in the infection side, one ear in the same mouse is kept as control by injecting PBS, in the other one, BCG is injected. When I do a qPCR the house keeping gene comes out later in the BCG ears compared to PBS control (even I measure RNA and DNA concentrations to have the same amount of materia). Does it means I have less amount of material in the PBS injected ear? or could it be the expression of the house-keeping gene is afected by BCG infection? Any other ideas?
Thanks

What house keeping gene are you using as a control?

I tried 3, Gapdh, bactin and hprt, and always appears the same problem, the ears infected with BCG all the house keeping genes is shown to appear at less cycles compares to the ears injected with PBS.


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why and how multi allele gets reported during variant calling in vcf?
This might be a very basic question for many here. With the basic understanding of inheritance, eventhough there is a possibility of multiple genotypes due to multi alleles, the resulting genotype can only have two alleles(paternal and maternal) that way after variant calling, an allele at one position can be homozygous or heterozygous. So there can be max of two alleles, but why do we see multiple alleles at a given position in VCF. I am trying to understand the science behind this. Please help out. Thanks!
chr5    127640782   .   AG  A,AA    .   .   .   GT:AD:DP    1/2:0,28,409:437

Can you please clarify what you mean by multiple alleles at a given position in VCF.? Maybe, you could show an extract of a VCF file to show us what you mean. Are you surprised that in the population there can be more than 2 alleles at a given site?

In your example the 4th column contains the reference allel on the given position. It is not said, that your sample has this. The 5th column contains all alternative alleles found on the given position.
Which alleles are present in your sample is given in the last column by 1/2. This means you have one allel with the first value in the 5th column and one allele with the second value given in the 5th column. You see, that your sample has exactly alleles, but none of them is the reference. This would be indicated by a 0.

A vcf can contain multiple columns representing allele data for multiple samples.  I also see no reason why you could not represent a tetraploid sample's data in a vcf.  One might also have a mix of organisms i one sampe, like a mixed population of bacteria.  If you could get your SNP caller to call a tri-allelic SNP, the vcf format can handle it.

The other possibility I can imagine is that the format is designed to accommodate heterogeneity between individual cells in a sample, and inevitable sequencing errors.
If you sequence a sample from an organism which (mostly) has two alleles at a locus (e.g. A and G), there may still be individual cells which have a C or T at that locus, and there may also be sequencing errors introducing a C or T in reads which were actually an A or G.  The VCF format would then still be able to represent the low-probability calls, in addition to the higher-probability ones.


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What type of animal is this?
There was a leaking fire hydrant across a sidewalk. On the other side was a lake. The fire hydrant water was streaming across the sidewalk.
I saw it swimming in the sidewalk away from the side of the lake to the fire hydrant.
What is it?

Could you give us some idea of scale, it's about 18 cm long on my computer screen, I'm sure that's not right.

Welcome to Biology.SE. Identifications questions should include: 1) the location (e.g. country and region — the more specific the better) where you observed this organism; 2) the species-identification tag; and 3) an estimate of the size of the organism. Click on or hover over the 'species-identification' tag for details. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

Likely a dragonfly larva, but I don't know the specific type. They live in water and eat anything they catch like small fish.

This is incorrect. It's a mole cricket

They live in water ?

They do not. They live underground. Likely flooded out of its underground hole and seen seeking drier ground. (Alternatively, it could have already been aboveground and just gotten caught in the deluge).

I must agree with you , but I made a close guess.

Second: This is not a dragon fly instar.


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Please help identify the species of a possible butterfly
I took picture of this weird butterfly. It landed when I was drying my clothes. But it didn't even move when I try to shake it off. After I took a lot of pictures, I tried to shake it outside.
It might not be clear in the picture, but there is a bit of pink on its 2 wings near the body in the next to last picture.
Location: Asia (Southern part, Vietnam), and this butterfly is in the countryside.
Climate: hot, humid, it is currently Raining season, night is cool, day time is not too hot.
This might even be a type of moth?

Definitely a moth, probably hawkmoth. Very beautiful

Please [edit] your post to include an estimate of the size of this insect — that information can be very helpful for identifications. Also, are mango's grown nearby — adding that information is now very relevant given bob1's answer.

I googled the name, and yes it match up perfectly. I released the moth already, so can't put it with a ruler, but it is around the palm of your hand. Yes, there are plenty of mango trees around my place, sorry I didn't think about adding the surrounding tree type for better reference.

I'm no expert - just like browsing pictures, so totally open to other suggestions.
I think this is the Mango Hawkmoth/Sphinx moth (Amplypterus panopus), which is a fairly widespread moth of SE Asia, including Vietnam and Thailand.
You can see the pink of the underwings (terminology?) here and you can see the big lines across the wings. If you imagine the wings folded so that they lie across the body, you can see the nice horizontal stripes and dark head seen in your photos.


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I saw these strange bee in my garden, and they drag little insect and/or caterpillar to their nest

I saw these strange bee in my garden, and they drag little insect and/or caterpillar to their nest. What are they?
When I catch them by gloves, their body is extremely hard. I notice since a few of my normal honey bee are found dead on the ground. I am in tropical region, is this a type of Asia Hornet? I haven't seen US hornet, so I can't compare, but I felt like these bee are much smaller than the American Hornet for some reason. These bee are either smaller or same size as our Asia honey bee.
Is there anyway I can find the nest? I saw a bunch of small insect near where I saw 1 Asian giant hornet (I am assuming this is a hornet, I will exterminate them regardless, just want to verify if this is indeed Asia Giant Hornet - though this is quite small to be call giant). Is it plausible that where they gather the insect is where their nest is?

Welcome to Biology.SE. Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this essential information — also try searching online for "Asian Giant Hornet". ——— Finally, please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

In addition, your question isn't really clear — I'm assuming that what you really want to know is the identity of this insect. If so, please remove the irrelevant parts of your post. Note that "is this dangerous" isn't a good question for this site — it depends on many factors. Is the question: Is this dangerous to humans or some other organism(s)? If to humans, we don't answer personal medical questions and what constitutes "danger"? Anything with mouthparts can bite and that type of insect could be able to sting. Does the person in question have an allergy?

if you don't have another photo take another picture of that plate with a ruler paid across it, preferably from a similar angle. but yes location will be important.  I also suggest googling "parasitic wasp". behavior wise it seems like a fit.

where are you located?


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Why is protein cyclisation desirable?
There are a number of methods to "cyclize" an existing peptide:

Disulphide bond as described in Disulfide Bond Mimetics: Strategies and Challenges by Gori et al.
"Linchpin" based (linker chemistry) as described in Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al.

Why would the "cyclization" of a protein be a desirable goal?

As described in the abstract of Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al., protein cyclization improves:

resistance to proteolytic degradation and conformational stability. The latter property leads to an increase in binding potency and increased bioavailability due to increased permeation through biological membranes.

In simpler terms, a protein that is cyclized is less likely to:

Fold into an unhelpful shape.
Be broken up by an enzyme.

Thus, they are more likely to:

Act as better binders for a given target
Make it across a cell membrane


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ID request - larvae on potato plants
Several of these were on my potato plants in Washington state, USA. This one about 7mm in length, some were a bit larger. They were moving in an inchworm-like fashion, but only by touch - I don't think they have eyes.

This specimen was photographed after placing in isopropyl alcohol, which changed the color (it was almost white while alive) and the shape somewhat.

This larvae doesn't seem to match the common pests of potatoes. It is possible this larvae has been infected by a fungi and so is distorted in shape and colour.

@SergiiDymchenko — In the future please [edit] your post rather than putting important information into comments. Not everyone will read comments and they are also ephemeral, so they should only be used to discuss how to improve a post. Thanks!

One notorious pest of potato plants are cutworms. Unfortunately due to the the discoloration of the species I am not able to identify for sure which species of cutworm it is.
Cutworms attack a wide host of plants (more info here). According to that same website, the main ways to avoid the damage these larvae can cause are to:

Remove all plant residue from soil after harvest or at least two weeks before planting...

... plastic or foil collars fitted around plant stems to cover the bottom 3 inches above the soil line and extending a couple of inches into the soil can prevent larvae severing plants; hand-pick larvae after dark; spread diatomaceous earth around the base of the plants (this creates a sharp barrier that will cut the insects if they try and crawl over it); apply appropriate insecticides to infested areas of garden or field if not growing organically

These larvae come from a large variety of insects so don't associate them too quickly with one insect or another (many websites associate them with moths but that is not always necessarily accurate).
Here's a source that elaborates a bit more on how to treat them plus another source for how to use pesticides in a garden safely (if no other option is convenient).


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I found this tiny transparent creature in my aquarium - what is it?

Please help me identify this 1-2 mm nearly transparent animal which I found in my salt water aquarium.

Can you give some kind of indication of size, is it a freshwater or salt aquarium?

Can you say also if it's moving or not, is there any sign of a rudimentary (presumably transparent) shell? (I'm thinking freshwater limpet, but the symmetry may not be right).

Hi.. It may be in 1 Or 2 mm and i just 2days back only bought the aquarium and filled with salted tap water.. It's moving and it's walking with it's legs by walls only.

It's very transparent like water..

Oh, those things are legs, that's a whole different thing. Now I'm thinking some kind of arthropod, perhaps a parasite, will look into it.

I thought it might be a turtle or crab

I moved it small glass jar today morning only. Can I put it ian that har for some days.. Do you have any idea approximately how many days it will takes to find out what it would be...

with a good picture i could tell you what it is right now,please take a better picture by turning off the light in the room so only the water in the tank is lit and be sure to focus the camera properly.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; and 3) an estimate of the size of the organism. Please [edit] your post to include this essential information as comments are ephemeral and so should only be used to communicate about the post. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

Initial thought was a Triops species. But your specimen is too small for that. Likely some kind of crustacean.

i had that with my tropical fish, i found 2-3 it wasn't too much of a contagion though it was not good.

Now THAT is a fish louse in the Argulidae family. They are bloodsucking parasites that attach themselves to fish with those round suckers near their head and feed with needle-like mouthparts. Needless to say, I'd advise you to find and eliminate as many as you can, as they'll be harming your fish with their bites.

Time to him read on all the fish parasites that affect common goldfish and tropical fish and see what to be wary of.


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Is this some kind of crane fly?
I found this insect inside my house in Austria and it looked like some kind of wasp-moth to me. It is quite large with about 3 cm in lenght (excluding legs).
I looked up various images of crane flies here but couldn't find one that resembled the one I photographed, especially with those antennas and wasp-like imitation of the lower back.
Can someone help me identifying this insect and also tell me if it can bite or sting?

Looks like something in Ctenophora (true crane flies), potentially Ctenophora ornata? They're found in Europe and appear to have similar wing and body coloring, as well as the large antennae:

Image from Wikimedia commons, by Jean-Marc Liotier
I don't believe crane flies sting, but I am not an entomologist, so I defer to the experts on that point (and the species ID as well).

No, they definately cannot sting, since they are flies (i’ve no stinger). Crane flies cannot bite either, so harmless and the coloration is only for show and mimicry.


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What part, roughly, of the carbon in a plant comes from the soil? As opposed to the atmosphere?
C4 plants contain a slightly higher percentage of carbon-13 than C3 plants. Is this because of carbon obtained from the soil or the atmosphere?
I have read that plants using different chemical pathways, such as millet and wheat, incorporate distinctive proportions of stable carbon isotopes from the SOIL.
Do C4 plants need more carbon-13, or does that process just happen to result in accumulation of more carbon-13?

Always good to cite things you've read.

Does this answer your question? How do plants absorb CO2?

Only a small fraction of plant carbon is soil-derived: e.g. from Majlesi et al 2019:

although the majority of plant C was obtained from atmosphere by photosynthesis, a significant portion (up to 3–5%) of C in plant roots was derived from old soil

(in an experiment with Scots pine and reed canary grass).
As laid out by this review of C4 photosynthesis (Kellogg 2013), the primary reason for differential isotopic make-up of C3 and C4 plants is that the biochemical pathways they use fractionate isotopes differently — not because the plants' requirements are different.

Because of the very different
affinities of Rubisco and PEP
carboxylase for CO$_2$ , C$_3$ and C$_4$ plants
differ in the carbon isotopes that they
assimilate. While most atmospheric
CO$_2$is made up of ${}^{12}$C, a small fraction
includes ${}^{13}$C. Rubisco has a fairly high
$K_m$ and hence low affinity for CO$_2$, and preferentially fixes ${}^{12}$C. The ratio of ${}^{13}$C
to ${}^{12}$C ($\delta^{13}$C) in a C$_3$ plant is thus much
lower than the ratio in the atmosphere;
the carbon in structural and storage
carbohydrates contains much less
${}^{13}$C. PEP carboxylase has a lower
$K_m$ for CO$_2$ than Rubisco and hence
a higher affinity; as a consequence it
discriminates much less against ${}^{13}$C
than Rubisco does, so that the $\delta^{13}$C
is appreciably closer to atmospheric.

Kellogg, Elizabeth A. 2013. “C4 Photosynthesis.” Current Biology 23 (14): R594–99. https://doi.org/10.1016/j.cub.2013.04.066.
Majlesi, Soroush, Jukka Juutilainen, Anne Kasurinen, Promise Mpamah, Tatiana Trubnikova, Markku Oinonen, Pertti Martikainen, and Christina Biasi. “Uptake of Soil-Derived Carbon into Plants: Implications for Disposal of Nuclear Waste.” Environmental Science & Technology 53, no. 8 (April 16, 2019): 4198–4205. https://doi.org/10.1021/acs.est.8b06089.


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probe amplification in MLPA
I'm reading an article about MLPA (Multiplex ligation-dependent probe amplification) and I got stuck on this sentence:

The advantage of splitting the probe into two parts is that only the ligated oligonucleotides, but not the unbound probe oligonucleotides, are amplified.

The principle I don't understand is why won't the unligated oligonucleotides be amplified? As is my current understanding of the PCR, the primers should normally anneal and produce fragments which would end at the end of an oligonucleotide (at the "ligation site" - so they would be shorter, but they should be there), am I wrong?

Please [edit] your question and add a citation to the paper you are reading so we may see the sentence in context.

It's the wikipedia article which is linked to MLPA word.

I work for MRC-Holland, the developer of MLPA, and what Kacper explains is indeed the case. Any RPO (right probe oligo) that is not ligated is also amplified in the MLPA reaction, as the reverse primer can bind to the primer binding site of the RPO. HOWEVER, since this unligated RPO oligo LACKS the binding site for the (fluoresently labelled) forward primer, the amplification ends here. LIGATED probes, in contrast, contain the binding site for BOTH primers, and hence are amplified exponentially. Furthermore, the fluorescent label is only incorporated in the amplicons that results from ligated probes.

I suppose unligated oligonucleotide would also be "amplified" but on much lesser scale(?only one part of probe?). For instance after 6th run of PCR you would get 2^6=64 amplicons of ligated probe but only 6 for one unligated part(?second starter is designed to anneal to second part of antisense oligonucletide of probe?). After 30 runs there is massive diference that allow you to only detect properly ligated probe. I'm not sure if I'm right but this is how I understood it.
Peace:)

Why is the down-vote please? I find this pretty reasonable. À propos, thanks for the answer.


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How can I propagate a community of anaerobic bacteria sampled from mud in a bog?
I'm doing research on anaerobic bacteria. In the fall I took mud samples from a bog and have been working with them but I didn't take enough. Now winter has rolled around (Im in Canada) and all the bogs are frozen over. I need more material to work with — is it possible to make a mud mixture myself and carry over the bacteria?  If so could anyone help me out with the mixture ratios? Is contamination a concern here (I would assume not)? And how long would the propagation take?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. I've made edits to your question that I think make it a better fit for this site — please check to make sure I haven't broken anything! We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, could you use a Winogradsky column? Thanks!

I suggest getting an augur or whatever it used to make ice holes for fishing , and cut  down into the bog and get more samples.


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Poly-G tails in NovaSeq Paired-end sequencing from museum samples
I'm currently working with DNA samples originating from museum specimens, this means they have been stored in formaldehyde for the last 50-100 years.
The DNA I'm analysing has been sequenced by Illumina NovaSeq 6000 with paired-end sequencing.
As far as I'm aware NovaSeq uses two-colour chemistry, where Green is T, red is C, yellow (green + red) is A, and no green, no red is G. Over time and increase in sequencing cycles the green and red signal will become weaker, resulting in mistaken categorization of the nucleotides as G in the tails of reads.
This poly-G pattern is however only observed in the 3' end of the 2nd read in the pairs, which I find a bit weird.
Is this an expected pattern (only in the 2nd read in a pair) from NovaSeq or could this possibly also have something to do with my samples being stored in formaldehyde for the last 100 years, thus degrading or affecting the DNA?

Have you tried sequencing some fresh sample to see if the same pattern appears?

unfortunately im not the one performing the sequencing, im doing the bioinformatic analysis. But yes some newer samples has been sequenced, however this has been done with Illumina Hiseq4000 and these samples does not show the same pattern with Poly-G. But the Hiseq uses a four colour scheme.

of course ideally the newer samples would also have been done with NovaSeq, to determine if it is the sequencing or the sample ages.

Is this from a single sequencing run or multiple sequencing runs? I would suspect that something got jacked on the sequencer if I saw that in my data. Did you monitor the sequencing run? What do the quality scores look like? Have you run FASTQC or FASTP? I would recommend investigating all of those things.


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What is this? Is it harmful?
Anyone find out what this is? Looks like A Caterpillar with a home it made from surrounding items, this was found in VA in the moutians on our home.! It went back inside its home after attempting to touch it with my phone. It's the size of an adult female pinky.♀

That appears to be what is known as a bagworm:

According to the University of Maryland extension Home & Garden Information Center, they can cause significant damage to ornamental plants especially conifers.


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Fossil identification
I recently found a fossil which I am unable to identify. I believe it's a sea creature, but I don't know what kind. my best guess is some kind of shell or a porpita.
I appreciate any help.
this is the image of the fossil.

The features of this fossil that I can describe are :
1- It seems to be circular
2- A pattern of lines which spread from the center
3- It does not seem to be curved (like a shell) — it looks flat
4- Dimensions are about 1.2 cm by 1.2 cm (circular)
5- This fossil was found in Iran/khouzestan
Another thing to mention is that where I found this fossil, I found other sea creature fossils like starfish and shells.

Welcome to the site. Can you please edit into your question the dimensions of the fossil and where in the world the specimen comes from? These will greatly increase your chance of getting an answer.

Thank you so much for your guide. I edited the question and added dims and location of discovery. @bob1

your question is a better fit over at https://earthscience.stackexchange.com/ but you need to provide more information like a more exact location and if possible what other fossils can be found in the area,this is to find what geological time it is from.

without more information, best guess would be a natural cast of a fish vertebra.

Mah Es there is also https://www.reddit.com/r/fossilid/

I think that this is a cast of a limpet shell, not the shell itself. That is, not the fossil itself, but the imprint left behind when the fossil is formed. There should be another half to this imprint that consists of the fossil itself.
Limpets look like this:

 Image attribution: Tango22, CC BY-SA 3.0 https://creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
You can see the pattern of radial ridges and a serrated/pointed edge to the shell. In the imprint you can see the radial ridges as dark lines and the serrated edge in the bottom of the image. If it were the true fossil, not the imprint, the inside of the shell would be smooth rather than ridged (see image in linked Wikipedia page in first paragraph on Limpets).
Limpets are members of the Gastropoda class of organisms, which includes quite a diverse range of animals, and many of the things commonly called limpets are not particularly closely related to each-other. Which species of limpet the fossil might be I have no idea, but you could look into species found in the Caspian Sea and Persian Gulf or other nearby sea.


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At what age does the mouse skull stop growing?
Unless otherwise mandated, neuroscientific research on mice is done with ~7-week old animals. There is a sort-of mantra that at this age their skulls stop growing.
However, recently, I noticed a rather robust difference in how I have to place ~4-month old mice in a scanner versus 7-week old ones. I am pretty sure this is due to skull size, since I am fixing all my animals relative to the ear canal, and there should be no fat/hair accumulation in the inner ear. Also, if there would be, I am quite certain I would feel it.
This made me try to look up the source of the 7-week recommendation, but up until now I found nothing. Do you know whether it is correct that the mouse skull "stops growing" at 7 weeks of age, and if so, what studies support this observation?

Apparently there's a really nice paper with some very informative figures on Cranial Base and Craniofacial Development in Mice. They measure the distance between key landmarks of the cranium over a period of 112 days.
The paper does not specifically look for landmarks that allow a good positioning of the brain relative to the ear canal, but from their data on Cranial Base length, one may conclude that:

The position of the brain relative to the ear canal is highly variable during the first 28 postnatal days.
The position of the brain relative to the ear canal, along with most measures pertaining to the neurocranium become more stable after about 56 days of age.
There are small but significant changes in the neurocranium between 56 and 112 days of age. The position of the brain relative to the ear canal could for instance become around 0.5 mm more rostral between 56 and 112 days of age.

My observation indicates the same tendency, though I would say the shift in position was greater (perhaps 2mm) - but since they did not choose the ear canal proper as a landmark, it is difficult to compare.

This doesn't fully answer the question, but for those mouse skull sutures that do fuse, fusion is complete by about 45 days of age, according to Studies in cranial suture biology: IV. Temporal sequence of posterior frontal cranial suture fusion in the mouse.  That suggests that most cranial expansion is more or less complete by about 6 weeks of age.  I think there is still the potential for remodeling of the skull, especially bone thickness and so on, but since your interest is on the internal size of the cavity, this may help address it.


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Albino pedigree question
https://www.proprofs.com/quiz-school/playquiz/?title=pedigrees-quiz is a link to the website containing this question.

I'm not sure how you came up with your table, but I encourage you to start over.
Among other things it appears to me that you've made an unwarranted assumption about the unaffected sister's genotype.

I suggest you start by making a Punnett square for the albino's parents and think about what that means for unaffected sister.

Next think about what must be true for the unaffected sister to have an albino child with the unrelated non-albino man.
• Once, you've calculated the probability of that situation you're one step away from your answer.

Finally, given the situation in (2) what is the probability that the couple will have an albino child?


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How exactly do mutations cause genetic variation in bilaterians?
I am trying to understand how mutations cause genetic variance, and I'm stuck on one issue that I'm going to try my best to explain.
(I am specifically talking about mutations that cause a phenotypical change). The question is focused on organisms with a distinct germ-line.
My issue is with trying to understand where mutations need to occur to cause variation. For example, does the mutation need to occur in the DNA of either the specific sperm or the specific egg that gave rise to you?
The body of an organism obviously has a vast, vast number of cells. If a mutation occurred in just one of these cells, then surely it wouldn't have any phenotypical effect. Even as an infant or an embryo, if a mutation occurs in just one of your many cells, that is unlikely to cause any phenotypical changes (phenotypical variance) as your body develops. So, is the only way for a mutation to have a phenotypical effect is for it to occur in the gametes that produced you? That way, all of your DNA would inherit the mutation, since all of your DNA would be replicated from the DNA of the sperm and egg.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, I encourage you to think about cancer — are you sure you want to claim that "if a mutation occurs in just one of your many cells, that is unlikely to cause any phenotypical changes (phenotypical variance) as your body develops"?

I actually think this a reasonable question because, although the answer may appear obvious (and the poster argues for it on the basis of logic) my own impression is that it seems to be rarely emphasised in texts. So I can understand the poster wondering why.

The phrase you should look for to understand this is "germline mutation".  Also look up "germ cells", which are handled with kid gloves, so to speak, to avoid mutation as much as possible.

@David — I still feel like the question is under-researched (and that the logic in what is now the final paragraph is dubious). However, in light of Bryan's answer and your feeling that it is of value, I have withdrawn my close vote and made edits. If you have a chance I'd appreciate your checking to make sure I've actually improved the question ...

For example, does the mutation need to occur in the DNA of either the specific sperm or the specific egg that gave rise to you?

To give rise to heritable genetic variation in the sense that it's a mutation that exists in all of your cells and is transmitted (with some probability) to your offspring, yes, it must come from the gametes, with the caveat that it need not occur specifically in the gamete, but in any of the cells giving rise to that gamete in either parent. I suppose it could also occur in the fertilized egg cell, and mutations shortly thereafter may produce a chimera where a substantial fraction, but not all cells carry that mutation, but as mutations are most common during cell division I think it's okay to simplify a bit and presume the source is the gametes for most heritable mutations.
Estimates of how many of these mutations exist per human fertilized egg (relative to their parent genomes) vary, but you can assume that each human has something on the order of dozens in coding regions that their parents lack, plus others in other areas of the genome. A whole human organism has far, far more mutations, and these cause issues with aging and cancer in their cells, but these are not typically heritable.
The number of mutations per replication depends on genome size and also the stringency of that organism's replication machinery. In general, complex eukaryotes have stronger systems for correcting replication errors, so you can expect bacteria to have higher rates of mutation. Some related reading:
Correlation between genome size and mutation rate?
How much variation in mutation rate in there in the human genome?
Bacterial division and mutation rate
Mutation rate in viruses
Veltman, J. A., & Brunner, H. G. (2012). De novo mutations in human genetic disease. Nature Reviews Genetics, 13(8), 565-575.

Each generation (per individual), approximately 74 de novo single-nucleotide variants (SNVs), three novel indels (small insertions or deletions) and 0.02 larger copy number variants (CNVs) arise in our genome

Ségurel, L., Wyman, M. J., & Przeworski, M. (2014). Determinants of mutation rate variation in the human germline. Annu Rev Genomics Hum Genet, 15(1), 47-70.


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Are these pineapple seeds starting to germinate?
What is this? Is it the structure from where pineapple seeds grow? The photo is a slice of fruit.

Welcome to Biology.SE. Never seen anything like that inside a pineapple, but it vaguely resembles an inflorescence (grouping of flowers). However it isn't clearly like what is expected for a bromeliad. I'm skeptical that you can get an answer here with this picture. Did you keep this structure and is there any chance you get clearer pictures — ideally using an SLR camera with a macro lens, but borrowing different models of cell-phones might also help (assuming that is what you used). Alternatively, do you have access to an institution with botanists on staff and a dissection microscope?

@tyersome sorry I didn’t keep it. But I understand the limitations of what I’m asking based on this photo only.

Is it the structure from where pineapple seeds grow?
Yes, these are pineapple ovules, which if properly fertilized would develop into seeds.* The structure they're attached to is the placenta, which is found inside a chamber called the locule. In pineapples, three locules together form an ovary. Pineapples are interesting in that the whole fruit is made up of dozens of ovaries all grouped together, each one with a flower facing the outside of the fruit.
See this blog post for a good explanation of what's going on.
Are these pineapple seeds starting to germinate?
No, these have not been fertilized. To germinate the ovule would need to be fertilized, mature into a seed, and then be planted in the right environment for the embryo to continue development.

*Commercial pineapples don't generally produce seeds because pineapples require genetically distinct pollen for fertilization. Commercial pineapples are propagated from cuttings because it's faster and more reliable than trying to obtain seeds.

Awesome answer, thanks! This pineapple did have seeds.