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How many generations does it take for the average descendant not to be genetically related to the ancestor?
Parent 1 and 2 have children. Assume infinite, randomly-mating population size. How many generations until the median descendant by lineage of parent 1 has 0 base pairs inherited from parent 1?
I tried calculating this, but it was difficult to model variability in cross-over rates, and my computer is too slow for the Monte-Carlo I made.
Here is my guess:
from math import ceil, log2
import random
import numpy as np

haploid_genome_size_bp = 3300 * 1e6
diploid_genome_size_bp = haploid_genome_size_bp * 2
chromosome_pairs = 23

# Recomb hotspots
hotspot_length = 1500  # Taking the average length of 1-2 kb, in bp
hotspot_interval = 75000  # Taking the average interval of 50-100 kb, in bp
hotspots_per_genome = 30000  # Number of hotspots in the human genome

# Average crossover frequency per hotspot
avg_crossover_per_hotspot = 1 / 1300  # One crossover per 1300 meioses

total_hotspot_length_bp = hotspots_per_genome * hotspot_length

initial_genome_fraction = 1  # Starting with 100% of the genome from Parent 1
generations = 0  # Counter for the number of generations

# Loop to calculate the number of generations required for the descendant to have less than 1 bp from Parent 1
while initial_genome_fraction * diploid_genome_size_bp > 1:
    # Introduce variance in the average number of crossovers per chromosome, for probably needless complication
    # Using a Gaussian distribution centered around the average, with a standard deviation of 0.5
    avg_crossover_per_chromosome = np.random.normal(1.25, 0.5) #this doesn't actually affect the result

    # Total length affected by crossovers in one meiosis event bc hotspots
    total_crossover_length_bp = total_hotspot_length_bp * avg_crossover_per_hotspot * avg_crossover_per_chromosome * chromosome_pairs

    # Calculate the fraction of the genome that is affected by crossovers and recombination in each generation
    fraction_swapped_each_generation = 2 * (total_crossover_length_bp / diploid_genome_size_bp)

    # Update the fraction of the genome from Parent 1 in the descendant
    initial_genome_fraction *= 0.5 * (1 - fraction_swapped_each_generation) + 0.5 * fraction_swapped_each_generation / 2

    generations += 1

print(generations)

Result: 33 generations.
But really, information is lost sooner, since (approximately) non-SNPs won't contribute to information, non-SNPs are shared between individuals. Let's say there's 600 million SNPs, randomly distributed throughout the genome. Let's assume that parent 1 and the entire rest of the population differ at, say, 70% of SNPs (this value doesn't matter much, it's always 29 or 30).
from math import ceil, log2
import random
import numpy as np

total_snps = 600e6
haploid_genome_size_bp = 3300 * 1e6
diploid_genome_size_bp = haploid_genome_size_bp * 2
chromosome_pairs = 23

hotspot_length = 1500
hotspot_interval = 75000
hotspots_per_genome = 30000

avg_crossover_per_hotspot = 1 / 1300

total_hotspot_length_bp = hotspots_per_genome * hotspot_length

initial_snps_fraction = 0.7
generations = 0

while initial_snps_fraction * total_snps > 1:
    avg_crossover_per_chromosome = np.random.normal(1.25, 0.1)
    total_crossover_length_bp = total_hotspot_length_bp * avg_crossover_per_hotspot * avg_crossover_per_chromosome * chromosome_pairs
    fraction_swapped_each_generation = 2 * (total_crossover_length_bp / diploid_genome_size_bp)
    initial_snps_fraction *= 0.5 * (1 - fraction_swapped_each_generation) + 0.5 * fraction_swapped_each_generation / 2
    generations += 1
print(generations)

Result: 29 generations.
It is sensitive to the number of SNPs in existence. If we use 1 million SNPs, we get 15 generations.
Is this right? Can we find a more accurate estimate? My code probably has some mistakes.

My interpretation: assuming a generation time of 25 years, this means if you have an ancestor who lived more than 725 years ago, they are probably (P > 0.5) not genetically related to you in a meaningful way.

If you’re a mother, your mitochondria can go a long way.

@PaulTanenbaum I'm disregarding mtDNA and the Y chromosome, but it wouldn't make much of a difference since only a small fraction of descendants will be paternal/maternal line

Indeed. That’s why I said can.

Graham Coop performed simulations related to this question, based on actual transmission data for each chromosome in humans. He found that after 10 or 11 generations there was >50% chance that any particular ancestor contributed no genetic information to a specific descendant. Fewer than 5% of a person's 14th-generation ancestors will have contributed genetic information to them.

This blog post is part of a series. The first provides some more information about the data and assumptions feeding these simulations.

What is the relevance of the link discussing GWASs?

That was just a link to Graham Coop's blog, where the other posts can be found.

Father/Mother, DNA = D
Child, $\frac{1}{2} \times D$
Grandchild, $\frac{1}{2}\times \frac{1}{2} \times D= \left(\frac{1}{2}\right)^2 \times D$
Great grandchild, $\left(\frac{1}{2}\right)^3 \times D$
One's $n^{th}$ descendant has only $\left(\frac{1}{2}\right)^n$ of one's DNA.
Which generation and later will have only $1\%$ or less of your DNA?
$\left(\frac{1}{2}\right)^n \leq \frac{1}{100}$
$2^n \geq 100$
$n \geq 7$
That is to say, after 7 generations, one's genes are diluted to near homeopathic concentrations.
EDIT
Note that this is a(n) (over)simplfication of how heredity via DNA works. The actual processes are quite complsx.

This is illustrative of a simplified view of the problem, but it doesn't directly answer the OP question which introduces more complex phenomena like recombination. It's a bit more complex than this due to haplotypes, population structure, etc.

@MaximilianPress, I concur. Edited my answer appropriately.

If we assume infinite crossing-over and 600 million SNPs, we'd still be left with 6,000,000 SNPs after only having 1% of the DNA. Interestingly, I think your model basically works similarly to mine, because (1/2)^30 * (600 million) is approximately equal to 0.5. That is, after 29-30 generations, it rounds to 0 SNPs left.

@BigMistake, If our (similar) models are even half as accurate, some things should be impossible, no? Unless ...


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Calculation for underlying genetic value of a phenotype given parents genetic values
What is the most accurate way to calculate a child's genetic predisposition to a phenotype, given both parents' genotypic predispositions?
Assume trait X is 50% heritable and controlled by an arbitrarily large number of SNPs. The trait is normally distributed in the population. Parent 1 is in the 80th percentile of genetic predisposition to trait X. Parent 2 is in the 60th percentile of genetic contribution to trait X. Will the child's predisposition be on average the 70th percentile?
Due to regression to the mean and given 50% heritability, will the best estimate of the child's phenotype be in the 50 + ((70-50)*0.5) = 60th percentile?

Update
OP specifically drew my attention to the use of the genetic prediction, rather than phenotype.
I think that the answer remains more or less the same, except that instead of the actual phenotype distribution, you have the distribution of genetic predictions.
I don't think that quantiles are appropriate for prediction tasks.
Original answer
I believe that the answer is "no" because the percentile is a nonparametric description of the distribution. I believe that the form of your calculation is right, but the values you've plugged in are wrong.
For example, 1.755m is ~50th percentile male human height (from here), 1.78m is ~60th, 1.795m is ~70th, 1.815 is ~80th, and 1.85 is ~90th. Note that the intervals between those quantiles is not regular, so your estimate will be accordingly biased if you act like the quantile matches the value of the heritable trait.
(Sorry about the dumb rounding, I was working from the calculator, which is somewhat imprecise.)
So your midparent estimate for height would be something like 1.755 + (.0425 * .5) = 1.77625m
In other words: use the actual phenotypic measurements (or whatever transformation the heritability estimate comes from), not quantiles.

are you sure? I'm referring to percentile of genetic risk, not the observed phenotype, when I say percentile, until the last step

@BigMistake- ah, I see. I think that my answer remains the same, except that the phenotype in question would have to be whatever the genetic risk value is. It's still a quantile of the underlying distribution, it's just that rather than the phenotype you have a genetic risk measurement. Depending on the structure of the prediction task, there may well be additional biases that require a different form for the prediction, but I can't comment on that.

Does this change if we assume the population genetic predisposition for the phenotype normally distributed? I think in this case, the percentile might yield the same result

@BigMistake not sure that I understand. When you perform a quantile transformation of data (percentile is a 100-quantile transformation), you fundamentally change the shape of the data to a uniform distribution. Normal -> uniform data transformation will not preserve underlying normality, so you will not preserve the moments of the underlying distribution, not even the mean. It will only work if the underlying data is also uniformly distributed. I'd suggest playing with some data to investigate this if it doesn't make sense.

Exactly. Under the assumption that the data is already normally distributed, transforming it into percentiles (now uniformly distributed) doesn't affect the calculation's validity

@BigMistake- still not sure that i understand. If you perform the calculation on the normally distributed data and the uniformly distributed data and compare, you will find 2 different answers. IDK what your goal is here, but getting a different answer sounds bad to me. Not least because your 50th percentile is not the mean! you don't actually know what percentile your mean is. That seems like an issue for making a prediction about the expected value of a phenotype with regression to the mean.

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Sequence homology of cytokeratins
I am reading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7962860/ and do not understand what it means by high sequence homology of cytokeratins in the following text:
"Sequence homology of cytokeratins is very high, but when the proteins are digested into peptides by trypsin they generate many unique peptides. In the amyloid deposits the cytokeratin peptides identified were mostly unique to one protein"
What does high sequence homology of cytokeratins imply about the amyloids?
What is the relationship between the sequence homology of cytokeratins and whether the generated peptides were identified to be mostly unique to one protein or multiple proteins?
Is it harder to remove amyloids that have high sequence homology of cytokeratins?

Going through the quote:

Sequence homology of cytokeratins is very high,

There are many human cytokeratin genes and corresponding proteins, and they have very similar sequences of amino acids.

but when the proteins are digested into peptides by trypsin they generate many unique peptides.

The serine protease trypsin breaks the varieties of cytokeratins into many different polypeptide pieces.  The fact that there are many resulting peptides could be due to the fact that the variety of original cytokeratins in fact have distinguishable differences near the cutting points that trypsin  operates on, despite all the cytokeratins being from a protein family with high residue sequence homology.  (Some of the unique peptides could also be due to there being multiple places in the consensus amino acid sequence of the cytokeratin family at which trypsin cuts the proteins, but the paper does not delve into that detail.)

In the amyloid deposits the cytokeratin peptides identified were mostly unique to one protein.

Given that there are many possible unique peptides resulting from trypsin digestion, it seems somewhat surprising that most of the peptides that show up in the amyloid deposits happened to come from an identifiable single type of cytokeratin.  They are hinting that this particular cytokeratin likely has an important relationship to the process involved in causing the disease (and hence perhaps should be studied more closely than galectin-7, which has previously been thought to be involved).

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text:
Why does calcium homeostasis require more physiology than other electrolytes?
I've been learning about regulation of serum electrolyte concentration. From what I've seen, serum potassium, sodium, H^+ and carbonate levels are managed by aldosterone and angiotensin II. If I've understood correctly it seems that this hormonal feedback system is pretty much all managed from within the kidney itself, reading levels and releasing hormones to control reabsorption/secretion in the nephrons.
Calcium and phosphate homeostasis seems to be quite a bit more complex, with the whole parathyroid gland and part of the function of the thyroid gland dedicated to this via PTH and calcitonin, and also vitamin D. I'm not sure I've fully understood why calcium and phosphate homeostasis needs so much additional complexity compared with sodium and potassium. Maybe this is partly because calcium and phosphate homeostasis involves talking to the bones, but this is not necessary for other electrolytes? Is there another reason?
There are also other important electrolytes such as magnesium, chloride, and sulphate. I haven't seen anything much about how serum levels for these electrolytes are managed. Are there hormonal feedback mechanisms for these electrolytes also?

I'm curious as to why you think hormonal regulation via the parathyroid gland is more complex than hormonal regulation via the adrenal glands (renin splits a liver protein, angiotensin I, a piece of which is split by angiotensin converting enzyme in your lungs and kidneys into angiotensin II. which causes blood vessels to constrict and stimulates the pituitary gland to secrete antidiuretic hormone, which... (etc.) That's not simple to  me. Basically both are hormones released into the blood. As to the others, what were your search terms?

@anongoodnurse well the parathyroid appears to be a whole organ dedicated to calcium homeostasis. The renin angiotensin aldosterone system is also complex, but using some functionality of other organs seems less complex to me than needing a complete new organ. Also it's clear to me how PTH and calcitonin can regulate Ca^2+ within a range, but I didn't see how Na^+ concentration can be decreased, only increased eg. via aldosterone. The question was more about comparison to Mg, SO$_4$ and Cl though.

I don't agree with you about degrees of complexity and "complete new organ(s)", but re. decreasing Na concentration, that's what antidiuretic hormone is for, which is secreted by the pituitary gland (is that a complete new organ?). if your question is about the other ions, evidence of a search is pretty much a requirement on this site. As a common ion, Mg, like other ions, is pretty tightly controlled and a brief search should get you some results.

I would argue that sodium, potassium (and H+) regulation is much more complex than calcium (and phosphate) - for the following reasons:

sodium, potassium (and H+) are not just regulated in their own right, their regulation is intertwined with one another, and also affects blood pressure, vascular resistance and plasma osmolality, NOTE: (rough) calculated osmolarity = 2 (Na+) + 2 (K+) + Glucose + Urea
there are arguably more organs involved, and more hormones/chemicals

However, I admit that hormones of calcium homeostasis tend to have multiple functions at different sites (whereas the key players in sodium/potassium regulation broadly tend to do one thing)
FOR REFERENCE:
Renin-angiotensin- aldosterone system (RAAS) includes the following elements:

liver (angiotensinogen) - precursor
lungs (ACE) - enzyme for conversion (AT1>AT2)
kidney (renin) - low renal perfusion > more renin release
adrenal gland (aldosterone) - produced in response to antiotensin II and renin, causes reabsorption of sodium and excretion of potassium

In addition to this, there is:

hypothalamus/posterior pituitary (vasopressin/ADH) - increases water and sodium reabsorption
heart (ANP) - dilate afferent arteriole, inhibit sodium and water reabsorption

Sensor mechanisms:

kidney - afferent arteriole - senses the incoming blood pressure to the glomeruli
hypothalamus - osmoreceptors - sense osmolality and, if low, induce release of vasopressin/ADH
carotid sinus - baroreceptors - sense blood pressure and cause vasoconstriction
heart (as above)

Sources:

Na: gut absorption. Mainly extracellular.
K: gut absorption, release from lysed cells. Mainly intracellular

From a clinical standpoint, there are plenty of reasons why sodium/potassium regulation is important:

hypertension - modern antihypertensives directly act on the above systems (e.g. ACE-inhibitors, diuretics)
hypotension - probably most significant in critical care settings (vasopressors...)
hyponatraemia - can be a life-threatening condition, diagnosing and treating it requires assessment of fluid status (i.e. hypovolaemic / euvolaemic / hypervolaemic), although this does not usually involve targeting the homeostatic systems (the exception would be SIADH)
hypernatraemia - usually due to insufficient water intake or excessive losses
hyperkalaemia - can also be life-threatening (heart is very sensitive to electrolyte imbalance, and particularly to potassium), most often is a result of renal impairment or excessive potassium release (e.g. burns, rhabdomyolysis)
From the list above, it becomes aparent that these systems are at the core of most physiological stresses and many disease states. The challenge is that manipulating one element (e.g. sodium level) can have knock-on effect on other characteristics (e.g. blood pressure).

Calcium

parathyroid - parathyroid hormone - released due to low Ca:

increases renal Ca reabsorption (decreases PO4 reabsorption)
stimulates kidneys to activate vitamin D (calcifediol to calcitriol)
releases calcium from the bone (via osteoclasts)

vitamin D - causes more calcium absorption from the gut
thyroid - calcitonin - released due to high Ca;

stimulates calcium deposition in the bone (via osteoblasts),
inhibits renal calcium reabsorption,
inhibits calcium absorption from the gut

Clinically, these are the typical scenarios for disregulated calcium

hypercalcaemia - hyperparathyroidism, malignancy
hypocalcaemia - hypoparathyroidism (e.g. after thyroid surgery), insufficient (calcium/vit D) intake

In general, for understanding any electrolyte regulation, the key questions are:

what are the sources?
where is it located (intra/extracellular)?
what are the reservoirs (if any)?
how is it removed from the body?

For reference, this is an (incredibly detailed) review of calcium (and phosphate) regulation:
https://www.ncbi.nlm.nih.gov/books/NBK279023/

Thank you, this was really interesting. Part of my question is still open though, which is about how these two mechanisms compare to magnesium, chloride and sulphate regulation. I've spent a while looking and have not been able to pin down an understanding of how Mg levels are regulated, even though I know they have to be tightly controlled and hypo or hyper magneseamia are both critical.


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What is the Latin term for animals which dust bathe?
I have lost track of this term. I am sure that I encountered a Latin word (not a taxonomic word) which applies to all animals which dust bathe.
I fact, I am not even sure how to describe a word like this, cutting across species.

There are some words like pulverulent (adj.), Pulveratores (n.), pulveratrix (n.) (based on Latin  pulver- , pulvis meaning dust, sand, pulver) but OED gives them as obsolete and rare. They are ornithology terms to define birds that use dust bathing as a means of feather maintenance.

Thanks, that must have been the word I saw, I think.


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What is the precise definition of "cytokine"?
For example, both bone morphogenetic protein 4 and nerve growth factor are paracrine signaling proteins which promote growth of their respective tissues, and both are known to have some effect on the immune system - but BMP4 is considered a cytokine whereas NGF generally isn't. I'm having trouble understanding the criteria by which some nonhormonal signaling proteins are classified as cytokines and some aren't.

Welcome to Stack Exchange Biology. Please read the Help on Asking Questions. You will see that you are expected to show the research you have done to answer a question yourself and why what you have found doesn't answer your question. What have you found in searching for the term? The Wikipedia article refers to it as a "loose term", which is often the case for biological terminology, so rather than a "precise" term the best you can expect might be "common or accepted usage". There are few standards bodies in biology.

@David clearly I've done some degree of research on the topic as I gave very specific examples as well as compared their pertinent characteristics and detailed what about them I found unclear. As I stated, I'm asking a question about what's "generally considered" a cytokine i.e. "common or accepted usage." I was simply assuming there was some line of reasoning in regard to the common classification that I had missed - if you're telling me there is actually no consistency in how it's generally used, that's rather unsatisfying but I'll accept it.

You seem to have a general concept of cytokine that you assume we all share. No. State this and relate it to your examples: It is my understanding that a cytokine is “a molecule that [does such and such]”, to quote [authoritative source]. Consistent with this, X, which [does A] is generally referred to as a cytokine. On this basis I would expect that  Y, which [does B], would also be regarded as a cytokine, but it seems never to be described as such. Why is this? Is there some feature of cytokines that B lacks that is generally assumed but not explicitly stated in the definition above?


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What is the magnification of this microscope image?
I mistakenly forgot to write down the magnification of this lobster egg image.
I do know that each division on the graticule is 20 microns, as I calibrated it using another duplicate graticule: the actual sizes of the graticules are 5mm long with 100 divisions, and I lined it up so that the installed graticule in the eyepiece spanned only 40 of the 100 divisions of the graticule on the base plate. I believe this meant the installed eyepiece graticules divisions represented 20 microns.
I can see that the eye spot on the egg is 29 divisions, so it is 580 microns long.
Is it possible to determine the magnification with this information?

If you know the size (check the literature to see if your calculated size is close to expected for the egg), you generally don't need the magnification - you simply put a scale bar on the image representing sensible units.

Hi @bob1, thanks for your response but i need to report the magnification in this case. Would you know how?

It's impossible to say from an image on the internet - images scale with different display formats/qualities. If you have the original image and can display it at the 1:1 scale, then you can do an approximation. The internets tell me that a lobster egg is ~1/16" or 1.58 mm in diameter, so you could work it out that way.

How about taking another image of another lobster egg (or even the same egg)?  Try to find a setting/magnification where the same zoom of the resultant image with the same image resolution will give you a similar visual representation.


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Is there a detailed model of the resonance of the basilar membrane and excitation patterns of hair cells?
I've read that it's generally understood that deeper parts of the cochlea are sensitized to lower frequencies, and regions closer to the oval window are sensitive to high frequencies. In a sense, a frequency distribution is converted to a spatial distribution along the length of the cochlea.
Is there a precise model that can predict exactly where excitation will occur along the basilar membrane? I.e., can we compute, with relative precision, exactly how to convert between a frequency distribution to a spatial distribution of hair cell excitation?
I'm well aware that a Fourier transform breaks down a sound into constituent frequencies, and if the cochlea were perfectly idealized, that would suffice to take a Fourier transform and then map the result to the basilar membrane. But we're talking about a biological system, which is certainly not ideal. It's not a given that what actually happens is anything like a Fourier transform.
A few things that I'm not sure how to answer are:

The basilar membrane is coupled to itself. If one part of the membrane is vibrating, presumably the adjacent areas are too. How is the vibration isolated into frequencies down to the level of precision that we know humans can distinguish?
The wavelength of sound in water at audible frequencies is much much longer than the length of the entire (unrolled) cochlea. To what extent (and how) are phase differences actually relied on by the mechanism?
The vestibular and basilar canals are coupled at the tip of the cochlea, and there will be a phase difference between them, and this will be involved in the vibration of the basilar membrane. How does is this phase difference involved in the spatial distribution of basilar membrane vibration? (Is there any impedance mismatch at the opening between them?
Will there be wave reflections that matter?)
A pure "Fourier transform" mapping of frequency to length along the cochlea does not explain why harmonically related sounds are also perceived as related by the listener. This phenomenon would be well explained if frequency ω also excited 2ω, 3ω, 4ω, ... modes within the cochlea, so that harmonically-related tones would have very similar patterns of excitation (and thus similar perception). How might this be modeled? Has this been looked at?
I have read that it may be true that hair cells are capable of motion (!?) and may be individually tuned to mechanically resonate at particular frequencies. Is this true? If so, how is this involved in the distribution of hair cell excitation? How much is known about the mechanism/dynamics?

What are the best models/research about this question?

Too many questions in one post here.

Ni, G. Modelling Cochlear Mechanics (2014) looks like a nice review to begin with. Also, searching for "biophysics of cochlea" will give you many results.


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How to convert Kilo Units (KU) to mg?
Im searching for AChE (Acetylcholinesterase) and on sigma-aldrich it is showing 2 KU or 2000U/mg of protein and on MedChemExpress it is showing 50mg then how can we calcute how much will be the drug in the Sigma product

Would be easier to help if you provide the links to these pages. Sigma should also mention the actual quantity (ug) near where the price is. I assume that's what you are looking for?

There is no conversion from Units to mg. units are a measurement of enzyme activity, generally reported normalized to mass as units/mg

Have a look at the sigma product  - it should have the mass or the number of units. Simple conversion from mass to units using the provided info.


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Unknown insect in southern Kansas
My wife and I just moved to Southern Kansas and are still learning the local fauna could anyone please tell us what type of insect this is.

This is a male Metric Paper Wasp (Polistes metricus).
Bugguide is an an authoritative source for arthropods in North America and describes these as:

Very dark--abdomen is black... thorax dark reddish-brown with black
lines. Tibiae and tarsi are yellow (1). Males, like those of most
Polistes species (exception being P. annularis), have a yellow face,
while females have a reddish-brown face.

https://bugguide.net/node/view/60264
We see here that the abdomen, thorax and leg segment colours all match-up. The yellow seen at the top of the face is enough to separate it as a male.
Looking at iNaturalist for vespoid wasps in Kansas, we see that the most commonly observed wasp is this species.

Further, looking at the other species there in Kansas for similarly-coloured wasps, there are a few dark ones with reddish colouring but they would have red or yellow stripes in the abdomen, not all-black as this species has.
https://www.inaturalist.org/observations?place_id=25&taxon_id=48740&view=species
Bugguide has an extensive gallery of photos of this species, and I found one other with no wings:
https://bugguide.net/node/view/987823/bgimage
This is the only photo I found in the >1000 photos I browsed in Bugguide and iNaturalist of this species that shows a specimen with no wings. So it is probably not a natural occurrence for these wasps to lose their wings (like from some natural predator or mating or feasting ritual or anything) -  from the crumpled-look of the wings in the photo, my best guess is that these wings have been melted.


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ddT-tailed TA cloning, and the fate of a double nicked plasmid in E. coli
In an undergraduate lab class on TA cloning, it was explained that ddNTPs are used as the substrate for terminal transferase when making the T overhangs of the vector. I was told this was to ensure that the overhang is only 1 bp long.
However, they also say that after the insert binds to the vector, the remaining 4 nicks are ligated. I was immediately confused, because due to the missing 3' hydroxyl groups (consequence of using ddNTP), a phosphodiester bond could not form in 2/4 of the nicks. I may be mistaken, but the oxygen from the 3' hydroxyl is integrated into the bond, so the nick cannot be ligated if it is just a 3' hydrogen. Some people said that ddNTP cannot be polymerised on, but can be ligated.
T.A. Holton and M.W.Graham, 1990 partially answered my question. They confirmed that 2/4 of the nicks cannot be ligated if ddNTP is used (see image).
I have several questions about this

Suppose the insert (striped) encoded a protein, can it be transcribed even if the nicks are there?
What would happen to the nicks during DNA replication?
Would the nicked plasmid be repaired somehow? Is there a mechanism that can recognize and fix the ddNTP nick?
This is a paper from 1990, does modern TA cloning (say, NEB T4 TA cloning protocl) still use ddNTP? If not, how do they assure that the overhang is only 1 bp long?

As for (1), I think perhaps in theory it can be transcribed, as the promoter side of the insert is not nicked, and RNA pol does not need to traverse a nick to access the insert. I suppose the polymerase would fall off the strand at the end?
As for (2), I would think that the whole plasmid would fall apart as the replication bubble spreads, unless the nick is repaired somehow prior.
Thanks in advance.

Image taken from figure 1 of T.A.Holton and M.W.Graham, 1990.
T.A.Holton and M.W.Graham, 1990, A simple and efficient method for direct cloning of PCR products using ddT-tailed vectors, Nucleic Acids Research, Vol. 19, No. 15

To answer question (4):
A-tailing can be done in multiple ways, including the way you described. See here for the most common protocols:
https://international.neb.com/applications/cloning-and-synthetic-biology/dna-end-modification/a-tailing
The way I usually do it is to incubate the insert (e.g. from PCR) with Taq-Polymerase, which will always create a single A-overhang. Simply incubate at 72°C for 30 minutes and you are done (no need for ddNTPs, dNTPs are sufficient). Then you can use pre-existing vectors with T-overhangs for a straightforward ligation.
For the other questions I'm not very sure, although when you perform the ligation and transform bacteria with it, there is probably some way they will repair it. The endproduct (after miniprep) will certainly be an intact plasmid.


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What exactly is "Whole-genome sequencing"?
Newbie question: For few years I have seen news like “Whole-genome sequencing” is now under $1000 etc. I believed that this means all the base pairs of all chromatids in a single cell are identified and stored in a digital format in the original sequence. Just checked this Wikipedia article as well, which seem to align with my understanding.
Today I saw many news articles saying that Y-chromosome was fully sequenced for the first time. For example this article, which also mention that other chromosomes were fully sequenced only early this year.
What am I missing? Perhaps "Whole" is not "whole"?

So in short, the human genome project (HGP) and Greg Venter with his companies (fascinating story, I recommend to read into it) were unable to sequence many heterochromatic regions (with lots of repeats). Why? Because for repeats you need long-read sequencing methods (e.g., Nanopore, PacBio) that only became available in recent years. So apparently the HGP and subsequent attempts left out about 8% of the genome (https://www.science.org/doi/10.1126/science.abj6987), which simply consisted of some repeats and as the believe at that time was anyway that all these repeats are "junk" and the genes (about 2-3% of the genome) are the important stuff, they could argue that they sequenced the "whole" genome. Now of course we know that also repeats can be important for disease, gene novelty (evolution) etc.
Hope that helps.


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What distinguishes a colony from multicellular organism?
I would like to inquire what made biologists conclude that colonies such as the famous Volvox is an organism constituted by independent cells as opposed to a multicellular being.
I read that it has something to do with "degree of independence". However, what exactly are the parameters of a colony and the so-called "degree of independence" between cells and how is it different from multicellular beings despite possessing notable differentiation such as the latter?


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Current Fern Taxonomy
In our school, the manual exhibits an outdated taxonomy as expressed by my teacher. We're following the Kingdom Plantae, Division Pterophyta, then divided into three Orders:

Order Filicales
Order Ophogossum
Order Marattiales

However, I tried to look up what is the currently accepted taxonomy for ferns. What phylum is it under? Are its children taxa changed drastically? Does it still have a taxon dedicated to ferns only? What are also the morphological differences eyed in classifying these plants? These are some of the confusions I have. Thank you for answering :)


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How should I analyze proportional community data, in respect to habitat variables?
I want to analyze how the proportions of groups of species in a biological community correlated to habitat variables. I have 6 functional groups, defined by their similar traits, and I want to know how their proportions vary dependent upon changes in habitat size, and time since the changes started to occur (e.g. ramp disturbances).
I basically want to be able to say, "Group A species contributed more to the community makeup / function as habitat decreased. Group B species decreased in proportion, but not nearly as fast as Group C, which were extirpated by the time only 20% of the habitat remained" with some kind of stats to back it up.
I also monitored the communities as they recovered from the distrubance, and would similarly like to make inferences about which groups were contributing more early on vs. late stages recovery (e.g. could species with D-group traits be better at reestablishing?)
I don't think using raw abundance is appropriate because (generally) all groups decrease in abundance as habitat decreases, but some groups actually dramatically increase in proportion of the community, and thus would contribute more to the ecosystem services etc. etc.
Does anyone know how I should analyze this data? I have thought about using Spearman correlations to answer broadly if the groups do correlate with habitat changes, but this cant really tell me if one group is increasing or decreasing at a faster rate.
Thank you for the help!

What form are your observations in? Counts? Are they somewhat sporadic (like sightings of animals) or more systematic (like counts of plants within a grid)? How are observations structured over time and space? Are you measuring multiple habitats, or a single habitat over time?

I would say they're more sporadic, but we tried to make it as systematic as possible so samples could be compared. It was a timed-search method, using kick netting in streams to catch macroinvertebrates. We got roughly 1,000 - 10,000 individuals in each sample, and about 70ish species in total. Which were grouped via traits into those 6 groups.

Interesting... I'd highly recommend collaborating with a statistician with some experience in your domain. Proportions don't seem quite right, because it's probably not meaningful to consider individuals as equivalent/exchangeable, but you probably need some sort of control for the "sample size". I thought I'd have some suggestions, but I'm afraid this will quickly get beyond the scope of a StackExchange answer.

Sound like you want to do some compositional analyses of relative abundance data. It's a common approach used in microbial community analysis based on metagenomic sequencing data, but that's because the absolute count data is an experimental artifact from the sequencing methods and not necessarily reflective of absolute abundances in the samples.

Highly recommended read: McCune, B. and Grace, J.B., 2002. Analysis of Ecological Communities. MjM Software Design: Gleneden Beach. ISBN 0-9721290-0-6. 300 pp.. You might find a lot of interest in distance-based analyses (see "bray-curtis distance" for your abundance data), ordinations, and literally a whole host of multivariate analyses. Keeping track of temporal autocorrelations will also likely play an important role in your analyses.

I don't have complete grasp of the scope of your study/questions based on what you've presented here , and -- perhaps I'll be honest -- that type of statistical consulting advice is outside the scope of this site. If you already knew what you wanted to do or could more narrowly describe your question/analysis, some of us would certainly try to help. But I think at this stage -- especially given the complexity of your system -- I, like Bryan, recommend speaking more thoroughly with a dedicated statistician to ensure you're adequately covering all your bases and making the best decision.

Also, you're essentially asking multiple questions that each would require its own analysis approach. You might find a role of ordinations, mantel tests, structural equation modeling, etc for your 1st question, while MRPPs (multi-response permutation procedures), partial mantel tests, and mixed-effects models might play roles in other parts of your analysis. I guess I'll end by saying that your post is currently too broad and underdeveloped for our site. But again, I hope some of these comments steer you in the right direction. Read McCune & Grace (2002) and talk to a statistician. Good luck!


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Potential Function of Knuckle Popping?
Today I was walking past a door, when I accidentally hit my hand on the frame. All my knuckles popped instantly. I got curious and did the same thing but with my knuckles popped and this time the impact felt much more pronounced. Is the function of the popping of knuckle to retard the hand slowly, hence reducing the force when hit?

How do you propose that anyone knows whether that’s the purpose (if indeed there is a ‘purpose’, which it seems likely there isn’t)? (Genuine Q)

Is the function of the popping of knuckle to retard the hand slowly, hence reducing the force when hit?

No. The only physiological effect of popping the knuckles is to temporarily stretch the joint capsule improving range of motion slightly, which is why people often wiggle their fingers afterwards, or pop them before using their hands for something requiring a lot of dexterity (like safe-cracking in movies.) It may also cause the release of a small amount of oxytocin, which makes one feel good/less stressed/happy, accounting for its propensity to be habitual.
It doesn't seem to have a purpose. It's a phenomenon which can happen in many joints, including the neck and back. Some joints can click (e.g. the ankle) with certain movements, which is different.
It can be harmful to the joint capsule if forced.

What happens when you crack your knuckles?
For centuries, people have wondered about how knuckle popping works, and for decades people (usually older adults) tried to discourage their kids from popping/cracking their knuckles, warning them of future arthritis. However, it does not cause arthritis, and the mysterious phenomenon may have an explanation at last.
"Cracking" one's knuckles (or popping if you prefer; it depends on where you grew up) refers to the sound made when certain kinds of stretching are applied to the joints. One of my kids was addicted to it, so knowing if it could cause arthritis was important to me. In fact, there aren't any studies linking habitual knuckle popping to osteoarthritis. Knuckle-poppers are no more likely to develop osteoarthritis than non-poppers.

The [lack of] evidence for the association of knuckle cracking and osteoarthritis comes mainly from observational studies that have failed to show an association. [bracketed words mine to make statement clearer]

This has been born out by large retrospective studies and by small ones.
But what makes the noise? It's related to tribonucleation defined by Wikipedia as

a mechanism that creates small gas bubbles by the action of making and breaking contact between solid surfaces immersed in a liquid containing dissolved gas.

Knuckles, the joints between the flat part of your hand and your fingers, and those between the nearest and the middle finger bone) are solid cartilagenous surfaces surrounded by a fibrous joint capsule, and filled with a lubricating (synovial) fluid containing mostly proteins and dissolved gasses. When you pull the surfaces apart, the joint capsule stretches to the point that the dissolved gasses come out of solution and form a bubble (cavitation). The formation of that bubble produces a pop.
I don't understand why it produces a noise; a physicist might know. It has been compared to the noise that occurs when a suction cup is pulled off of a solid surface and air rushes in. Or my analogy would be clicking your tongue: placing the tongue to the roof of your mouth, creating a vacuum there, and then breaking contact produces a pop, how loud it is is proportional to the strength of the vacuum produced. It can be a soft "tsk, tsk" sound or if both surfaces are wet with saliva, a loud POP! I don't know why that causes a noise either, but it happens.
The formation of a bubble in the joint was first shown on xray in 1947. The noise produced was shown by MRI to be produced when the bubble formed by Kawchuk et al. in 2014, not when the gas was resorbed. You cannot pop your knuckle again until the gas bubble is resorbed into the synovial fluid.
On the left, no stretching action yet (normal joint); on the right, stretching applied to the joint with the formation of a bubble. Note how much more area the joint now occupies due to the stretching and gas.
[
Real-Time Visualization of Joint Cavitation

Do habitual knuckle poppers produce more sound than non-poppers? I have observed that people with that habit can crack it easier and louder than others. I also observe that they can do it more frequently than others.

@Aurelius - It's possible that habitual knuckle poppers have loosened the joint capsule a bit, so there might be a bit more synovial fluid in their joint space, thus more gas, thus a bigger bubble, thus a louder pop. (I don't know this for a fact.) I don't think they can pop their knuckles more frequently; it would take longer for the larger gas bubble to be resorbed, if my suspicion is correct.

(+1) Couple of doubts: 1. "It may also cause the release of a small amount of oxytocin, which makes one feel good/less stressed/happy, accounting for its propensity to be habitual" --> Is it actually? I always thought it is just placebo effect acting and there is no physiology involved. 2. "It doesn't seem to have a purpose" --> If that is the case, why did humans picked up the habit? Can it be considered an evolutionary habit?

@NilayGhosh re 1: "It may..." (emphasis mine). re 2: I don't know what an evolutionary habit is, so I googled "evolutionary habit" (scholar) and didn't get any hits. That piece is erroneous.  Lamarck was wrong.

I asked a follow up question on this topic: https://biology.stackexchange.com/questions/113071/is-the-habit-of-popping-knuckles-be-considered-an-evolutionary-habit


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ligand binding fluorescent protein
does anyone know of a fluorescent protein that upon binding of a substrate its fluorescence is activated? i've been looking on this and perhaps my keywords are not the right  ones. Thanks in advance

what is your substrate ?? Fluorescent proteins can be attached with a tag that specifically binds certain nucleic acid or protein domains..

There are only 3 classes of fluorescent proteins proteins known I think.  Two of them are relevant to your needs maybe.
The first are usually called 'fluorescent proteins'.  These proteins are usually derived from the A victoria jellyfish.  Its entirely passive in its fluorescence, but has been tuned to many levels of quantum yield and color.
There was a new sort of fluorescent protein cloned recently from japanese eels.  It is activated by binding to bilirubin.  Its so new that its not likely to be available, but there you go.
The third class would be the luciferases.  They are luminescent, not fluorescent but in producing light involves binding from a cofactor called luciferase which is oxidized to produce their light.  This is not really fluorescence since the electrical stimulation that causes light production is not from incident light, but since what you are looking for might not exist I wanted to remind you of the luciferases, which bind their redox substrates to activate.  The luciferin molecule actually varies as there are several classes of luciferase.  I think Flavin and NAD are the most common substrates.

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


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Plasmid maintenance
I have obtained some plasmids used as integration vectors, this question may apply to all plasmids. I would like to have a somewhat continuos source for these plasmids, let's say that the origin of replication is e-coli specific and can i then just transform the e-coli with the plasmid, let it grow to some density and then do miniprep? or can i also create glycerol stocks out of the bacteria that contain the plasmids and then harvest more plasmids as needed? i realize that both things are possible, but is this a good reasoning to follow?
Thanks

What I would usually do is transform E. coli with the plasmid, grow an overnight culture and mini prep the plasmid in the morning. Before you do the miniprep save a glycerol stock. Thus, you would have some plasmid to work with in the next couple of weeks, and also a glycerol stock to come back to. You can also keep the plate with your transformants, as you can go back to it within a month.

Yeah, I think this is a good backup.

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


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Why does hemagglutinin transfection fail in HEK293 cells?
I have tried to transfect HEK293 cells with the Influenza A H1N1 PR8 Hemagglutinin expression plasmid.
https://www.sinobiological.com/cdna-clone/h1n1-hemagglutinin-ha-vg11684-ch
I used PEI MAX as the transfection reagent.
After two days of transfection, I lysed the cells and performed SDS-PAGE and CBB staining, but there were always no bands representing hemagglutinin compared to negative controls (cell lysates without transfection).
I followed the protocol below.
The same protocol worked previously for a different plasmid expressing a different protein.

One day before the transfection experiment, I placed HEK293 cells in a 6-well plate to reach a confluence of 50~70% the next day.
Mix 3.5 µg of the plasmid in 150µl of DMEM without serum
Mix 11 µg of PEI Max in 150µl of DMEM without serum
Mix mixture 2 into mixture 1 and wait for 20 minutes at room temperature.
Aspirate the medium from the 6-well plate and wash with PBS
Add Mixture 3 to the 6-well plate
Place the plate in a 5% CO2 37°C incubator for 2 days.
After 2 days, aspirate the medium from the dish
Detach the cells using a cell scraper and suspend in ice-cold 2ml of PBS by pipetting
(I have also tried detaching cells using trypsin, but it did not change the results.)
Centrifuge at 400g at 4°C for 5 minutes, and aspirate the supernatant
Resuspend in 1ml of ice-cold PBS
Centrifuge at 400g at 4C for 5min, and aspirate the supernatant
Resuspend in 100µl of RIPA buffer containing protease inhibitor cocktail
Vortex for 1 minute
Sonicate for 15 seconds
Keep on ice for 15 minutes
Centrifuge at 15,000g for 5 minutes at 4°C
Collect the supernatant
Perform SDS-PAGE and CBB-staining

How do you select for positively transformed cells?

I did not select positively transformed cells.

I performed transient transfection and lysed all cells on a plate.

So you have no control which cells where transfected?

Yes. I thought that there should be a band at about 60~70 kDa, which is the size of the protein. When I used a different plasmid, I could see the band.

Band after CBB-staining in step 18

“Yes. I thought that there should be a band at about 60~70 kDa, which is the size of the protein. When I used a different plasmid, I could see the band.” This might be confusing, but I don’t have positive controls.

I am asking about this because transfection efficiency is sometimes a problem. The plasmid carries a hygromycin resistance gene, I would select after the transfection. If this works, then there is another problem.

Selection by hygromycin sounds a good idea to check if there are cells that are successfully transfected.

Actually, it is not clear which is the problem: transfection, cell collection, or cell lysis. When I detached cells, I observed that cells adhered to the dish more strongly than the negative control or other plasmid-transfected cells. So, thinking that the cell collection method might be wrong, I tried trypsin and cell scraper, but the result did not change.

That's correct. The later two can easily be tested and optimized with any cell. In my experience these two rarely failed while transfection is more often a problem.


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Are channel proteins considered a type of integral protein or peripheral protein?
I have conducted research, and unfortunately, I am unable to conclude whether channel proteins are considered a type of integral or peripheral protein. Based on my understanding, channel proteins are located on the peripheral surface of the cell, however, they have the function of integral proteins. Is my understanding correct?
All input in helping me distinguish between whether channel proteins are integral or peripheral proteins will be much appreciated.

Channel proteins are located on the peripheral surface of the cell, however, they have the function of integral proteins. Is my understanding correct?

No.
In this case of nomenclature, the context/reference point is the plasma membrane, not the cell - peripheral does NOT mean outside the cell, and integral does NOT mean inside the cell.
Integral proteins are integrated into the membrane, i.e. are embedded in the whole phospholipid bilayer that is the cell membrane, and peripheral means the protein is docked nearby, or associated adjacent to the membrane, and interfacing. They are still "at the membrane" but not integral to it.
By channel proteins, you are likely referring to membrane-spanning (transmembrane) proteins which feature pores that conduct molecules and ions. For example, aquaporins conduct or facilitate the transfer of water molecules across cell membranes, and ion channels such as Na+/K+ exchangers/pumps move cations in and out of the cell across the plasma membrane.
Transmembrane proteins such as (ion) channels or transporters are integral proteins (they are integrated into the membrane, not peripherally associated).
Personal aside: I will say that I don't often hear biologists refer to proteins as integral or peripheral... usually one would simply indicate whether they are transmembrane proteins or not. I guess this may vary by field but this practice is less ambiguous and less likely to throw someone off (as unfortunately was the case with you and plenty of others).


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Is TTGATATAT a gene?

Biologists use the sequence of letters A, C, T and G to model genomes. A gene is a substring of a genome that begins after the three-character ATG and ends before the three-character TAG, TAA, and TGA. Therefore, the length of the genome string is a multiple of 3, and the gene does not include three characters such as ATG, TAG, TAA and TGA.

I'm a little confused by the last sentence. Take a genome as an example, ATGTTGATATATTAG. Is TTGATATAT a gene? When the definition says the gene doesn't include ATG, TAG, TAA or TGA, does this requirement apply for every three characters TTG ATA TAT or for any character TTGATATAT?
ps: I don't have too much biology background. I'm currently doing a programming assignment on gene. The definition is all that is given to me. So excuse me if my question sounds really dumb...

Welcome to Stack Exchange Biology. Please finish reading the [Tour] to find out how this site works. It is primarily for "biology researchers, academics, and students", so if you "don't have too much biology background" you should play by the rules to justify posting here. This involves reading the Help on asking questions where you will see that posters are required to research their topic. The quotation you present (citation?) is unadulterated nonsense, as reading the Wikipedia entry for "Gene" would inform you. Please do so. (PS the answer is NO.)

I'd suggest reading more about genome annotation and gene finding for perspectives about these as computational problems. For your specific question, Bryan's answer should sort you out with regard to how codons can translate into protein outputs. This seems like a weird definition of either gene or genome, possibly there is more context in your instructor's questions that is missing.

The premise of the question should be accepted or the question closed. The existing answers don't even attempt to answer the question (the answer is "every three characters").

As a programmer, I'm irked by the fact that ATGATGA follows the "definition" of gene as indicated, yet its length is not a multiple of three.

This is a very lazy (biologically) "programmer's definition" of a gene. It would be like if you found a biology textbook that said "a program in C is everything between main( and )" - maybe for some purpose this definition is useful, but it would be clear to a programmer that it is incomplete and misses too much.
You can read about "start codon", "stop codon" and "genetic code" to understand the concepts they are using for your programming assignment. Using these concepts, there is a specific 3-letter code that says start and codes one amino acid, and every 3 letters after that codes another amino acid, until you reach a 3-letter code that indicates "stop". So, if you want to simply write a program to get an amino acid sequence from DNA/RNA this is sufficient.
For your assignment, you probably want to find what your instructor wants you to define as a gene, not what a biologist would.

This isn't the definition of a gene.  In many organisms, genes include introns, and the regions upstream and downstream of the starts and stops (untranslated regions, usually called 5' and 3' UTRs), as well as promoters upstream of the 5' UTR, are counted as part of the "gene".  And of course, not all organisms always use ATG as the start codon, I'm pretty sure that some organisms have different stop codons.
But most importantly, if you looked up just the coding region of a gene, you'd definitely include the starting codon, because that's usually included in the final protein, and you'd want to include the final stop so you know you aren't looking at a truncated sequence.
That paragraph has nothing to do with how any real computational biologist would work with gene sequences.  It's just pretend.

According to the cringe-worthy biology from your assignment, yes the example that you gave - i.e. TTGATATAT - is a gene. The TGA that's out of phase (TTGATATAT) isn't relevant.
As for what makes the text that you quoted text so painful? I think it boils down to the line:

Therefore, the length of the genome string is a multiple of 3

If you're interested, a small amount of reading about the genomes of humans (or any other organism) should quickly reveal why it's nonsense.

note that a) that conclusion (in the given question) doesn't even follow from the rest of it, and b) i'm pretty sure they mean the gene string, not the genome string

true, my intent was to try to answer the question as posed (while also lending some color to the tone of the answers so far - mine included)


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Does a higher body temperature slow the corona virus down?
The corona virus appearantly does not like high temperature:
High Temperature and High Humidity Reduce the Transmission of COVID-19
Also it seems that higher body temperatures helps the immune system to work better: Elevated body temperature helps certain types of immune cells to work better, evidence suggests
Should therefore someone who suspect they may have the corona virus or possibly another cold virus and do not experience fever try to elevate their body temperature slightly (say 0.5-1 degrees celsius) by dressing extra warm?
This is postulated here.
Does this sound plausible to you?

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question asks for subjective view on measures to avoid the disease. Such questions are doubly off-topic here. I advise you to consult more appropriate reputable sources for such information, some of which are listed here.

SARS-CoV-2 is believed to have spilled over into humans from a Rhinopholus (horseshoe bat) reservoir. During flight, bats' body temperature is maintained at levels associated with fever in other mammals. Rhinolophus bats are reported to reach skin temperatures of 41 C during flight. (From this review which describes why bats might be special sources for zoonotic viruses)
So, this virus is likely adapted to survive higher temperatures than a human host.


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Why does these confocal images show concentric circles?
I recently got this confocal microscopic image from my microscopy facility. I am unable to understand why these concentric circles are there. They look like out of focal fringes in conventional microscopy, but this is from a confocal as I mentioned. (It is only appearing in red channel, if that provides a hint.)
They are present in several images toa varying extent.

Welcome user 80133. Could you provide a few more details such as the subject, medium and the approximate magnification or some other idea of scale. It seems like some artifact of refraction due to droplet surrounding the subject, but we'd nee more details.

“Does this” or “Do these”. A basic feature of English grammar is number agreement between subject and verb.


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How to identify unknown RNA species that copurified with protein
So I have been studying an E. coli protein. As the first step I purified it in a pretty standard way - overexpressed it in BL21 DE3 cells and placed it in an ion exchange column, followed by size exclusion chromatography. Interestingly on the size exclusion column the protein fraction from IEX seperated into my protein of interest plus a very defined RNA species (which on a gel ran at ~500kDa). our university has a sequencing service that can accept DNA. Would anyone have suggestions as to how I can identify this  I tried RTPCR for this protein using random hexamer primers but to no success.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on how this site works and what we do here.  We probably need a few more details on your experiment - How did you identify it as RNA? How do you know the RT-PCR failed? Do you have access to a MinION device?


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Multispectral photography and biology
I recently made a post to the Photography site at StackExchange and I was told this might be a better forum.
My original post can be found here. From a high level I have a friend who is beginning a research project and I suggested possibly using ultraviolet light to identify individual specimens of fish similar to what is done here.
The question I asked there had to do with using multispectral images to try and mimic mantis shrimp vision to see if there was any biological signal that is invisible to the human eye. The hope would be to filter out individual wavelengths to see if there are 'outlines' that are visible to the shrimp but invisible to humans and parse out any potential signals.
I found this paper discussing a proof of concept that mimics this vision but I was also curious to see if there has been any research done already to take multispectral imaging to match color hues that are visible to certain species that are not visible to humans. I've been able to find to some resources for multispectral image data files but I have not been able to find much research done in a context similar to what is described above, i.e. trying to capture images that would be visible to certain animals but invisible to humans.
Does anyone here have any good resources or leads to investigate work that's already been done?
Any feedback is appreciated!

You kind of got your answer there; It's doable and it's being done. Is this actually something you want to do or are you just curious? Do you have the funds to do this? Are you ready to carry out this research and with whom would you do it? Seems to me you need to speak with the folks who are actually doing this with something fairly concrete in mind, but that's only one opinion.

Say it's curiously for now but it could change into something actionable later.
I'm not actively involved in research at the moment but I could be doing some consulting and assistance for one particular project. It would almost certainly not use be using multispectral photography. After reading a bit deeper about photography and having it brought to my attention that cameras can capture light that would match frequencies certain animal eyes are attuned to but not human I was hoping to check in and see if anyone has good resources on work that's been done. I hope you can forgive the naivety.

It's not naivety at all nor is it a bad question (I upvoted it); lots of people are just genuinely curious about Biology, and that you've done some searching yourself says a lot that's positive. My thoughts (fwiw) I'm not familiar with anyone here doing that kind of research, or having a deep interest in it. I hope someone answers, but I kinda doubt anyone will, because we - well, most of us - have jobs, and mere curiosity questions get left behind because searches take time. If there's someone who's knowledgeable or excited about the field, you'll get an answer. If you don't, you'll know why.

Having said that, there are some neurobiologists here who might be able to answer, and one of them seems particularly interested in sight, so who knows? In advising you to talk to those who are already doing this, if it's just curiosity, you may or may not get an answer. If it were a collaboration you wanted to do, you would be taken more seriously. (When I was in research, it was pretty cut-throat, and people kept their methods close to their chests, but that was ages ago.) Also, people at conferences/profs are generally more generous and helpful. Sorry I can't help; my field is medicine.

*neuroscientists, duh.

It seems like there are two pretty different things here; one is imaging into the UV (or infrared) relative to human vision; those things are pretty common by themselves for various purposes. Then there's oversampling the visual range, which doesn't actually reveal any "new" or invisible colors as in new wavelengths, but does add to the ability to resolve similar wavelengths as clearly distinct, which might help draw out certain patterns.


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What's the difference between a mitogen and a cell cycle stimulant substance?
It's been a week since I got this question asked and I still have no clue. I have thought that the main difference would be that the mitogen induces mitosis, and the cell cycle stimulant substance accelerates the cell cycle. I don't really know, to be honest.

What do you mean "got this question asked"? Was it part of an assignment for a course? In that case I'd look at the course materials or ask your instructor. If not, why do you need this answer? Where are you seeing these terms used and where are those usages in conflict? We expect questions to include some background information necessary to identify the specific question asked and the level of understanding it is asked with. "Cell cycle stimulant" is not something I find many hits for on e.g. Google Scholar, is this a translation?

Yes, it is part of an assignment, we don't really have course material, and the question was asked precisely by my instructor. The use of these terms is in the cell cycle topic. I am sorry that I did not give enough context to answer my question. The concrete question was "What is the difference between a mitogenic substance and a cell cycle stimulating substance?"

You have an instructor and a course and no materials? That doesn't really seem to set you up for success. I'd ask your instructor what they mean by this. It doesn't seem to be a phrase other people use.

Yeah, I noticed that too while searching about those terms. I'm gonna ask him tomorrow about this, because it's really confusing. I really appreciate you for taking part of your time to answer my question.

Sounds good, curious to hear what you find.


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Do larger multicellular organisms have an increased risk of mutation and thus cancer?
So I was thinking that if each cell has P(X) of becoming cancerous, then the chance of cancer is 1-((1-P(X))^n) where n is the number of cells in the organism.
Since larger organisms have more cells than smaller organisms (I'm guessing that larger organisms simply have more cells than smaller organisms as you can't have larger cells since there is an optimum surface area to volume ratio), does this mean then that larger creatures are more likely to have cancer cause they have more cells?

I would say that the question is more complicated since it really depends on the number of generations of cells. For instance muscle cells rarely get cancel but they also rarely divide.

You also have to take into account that a lot of larger organisms have a large genome with a low percentage actually encoding exons.

@GWW: Is there actually a correlation between body size and fraction of coding DNA?

As mentioned in the comments, this question is quite complicated. If the chance of a single cell from different organisms getting cancer was the same, then you would be correct, but this is not the case.
Different organisms have evolved to live different lengths of time. This is rather obvious when you think about it: mice have a maximum lifespan of ~3 years, humans ~80years (these figures are of course massive generalizations - but it doesn't really matter). Yet 'old' mice (> 2 years) still get age-related diseases such as cardiovascular disease, and cancer. It should be fairly clear that the risk of a 2 year old mouse getting (age-related) cancer is much higher than a 2 year old human.
The explanation for this isn't exactly concrete, but it goes something like this; mice invest a lot more resources in growing very fast and reaching a reproductive age very early, whereas humans develop much more slowly, and invest a higher proportion of their resources in maintaining tissue function, thereby reaching reproductive maturity much later than the mouse. The Hayflick limit for a mouse is about 10, whereas for humans this is closer to 60.
Thus the rate of aging in humans is much lower than that of the mouse, and it comes back to evolution: mortality in the wild is very high for the mouse, and thus mice that invest heavily in reaching early reproductive maturity are selected for - and those that invest in anti-cancer mechanisms take longer to reach reproductive maturity, and thus have less chance of actually doing it!
So to answer your question - smaller organisms tend to have higher risks of getting cancer because their lifespans are comparatively shorter, and thus they 'age' at a faster rate and invest less resources in maintaining function (e.g. genome integrity).

Would the OPs logic apply in the case of organisms from the same species?  For example would larger humans have a higher risk of cancer than smaller ones?

@Mew interesting question. Had a quick search and could not find a systematic study. The closest I could find is a report suggesting that BMI is positively associated with some adult cancers in humans (PMID: 18280327), however this could be confounded by a number of issues (>BMI could indicate unhealthy lifestyle? inactivity, smoking, drinking... only suggestions, but you can see what I mean). I can see that the logic of "large people have more cells" would imply higher cancer rates, but I don't see any evidence for this.


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What evolutionary mechanism caused felines to develop purring?
And why can some felines roar while others meow?

I guess the first question to ask is: "Why do cats purr?". If I remember correctly it is not really clear, so I doubt an evolutionary mechanism for it is known. As for the roaring I suspect that size matters.

Also, are you looking for an ecological answer (as in why cats perform the action of purring), or a physiological/anatomical answer (as in why a cat's purr sounds like it does)?

I just think there's no purpose to purring as far as I can tell. 'meow' seems like a more valid form of communication.

It makes sense that the ability to express your emotions improves the quality of the interaction you have with those around you. If a cat purrs those around it know it's feeling good, which can be useful information for future interaction.
I'm sure there have been cats who had a worse life because they didn't bond as well because they didn't purr, and consequently had a slightly lesser tendency to have their DNA end up in the next generation.
This argument goes for every ability to express emotions.

Indeed, so I suppose that cats use purring to communicate with one another?

I would think so yes.

http://en.wikipedia.org/wiki/Purr#Reasons lists several other possible reasons for purring. I'm not a big fan of antropomorphisation of animal habits, but I guess a clear response is still elusive in this case


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How to determine the most likely reading frame of a DNA sequence?
This question is from a past exam paper for an introductory bioinformatics module. I'm a computer scientist doing biology for the first time.
"A short bacterial gene has been sequenced, giving the following DNA sequence. Write out the 6 possible reading frames for this sequence and indicate which is the most likely protein translation of this sequence. Explain your reasoning for picking the given translation, and write all the translations in single letter amino acid code form.
5' - ttattcatccgccagcgccatgcgcgccat - 3'  "
I think I understand the 6 possible reading frames: three from the 5' end starting tta, tat and att; and three from the 3' end starting tac, acc and ccg.
I could also write out the translations for a given reading frame with a codon usage table.
It's the most probable reading frame part I don't get. I thought perhaps I was looking for the longest open reading frame. I can only see one start codon (atg). What is the correct way to recognize the most probable reading frame?
I can't find this problem exactly on Biology Stack Exchange. I did find:
Help reading chromatogram
It made me wonder if I'm getting confused between "reading frame" and "open reading frame", this question only asks or the former.
Thanks!

This is a terribly artificial question, but assuming that the sequence represents the whole reading frame, what do you need to consider as well as start codons? I like your suggestion of codon usage, but it's not as sophisticated as that.

Thanks for getting back to me so quickly. I'm still not sure but I had a few ideas.

Length of the frame, long enough to code something useful - but that would still be length between a start and stop codon.
Presence of expressed sequence tags - though I wouldn't know how to tell you if some sequence contained an EST and I suspect they are longer than 30 bases.
The presence of more or less "likely" amino acids eg, does the sequence have more of the most frequent amino acids (which I think are serine and leucine) - but I don't think we'd be expected to know this.

The presence of common subsequences that might indicate, say, common secondary structures - again, this is not something we've talked about in our course. 5) Sequence reading errors in the lab. Look for where there could be start and stop codons if you just changed one (or two) bases. For example, in the reading frame starting "att" from the 5' end, you could change that first triple to "atg" to make it a start codon, then perhaps the last "cca" should have been a tta stop codon. 6) Promoter sites?

Given that you've said it's easy, (2) to (6) all seem harder than what I was originally thinking about. More generally, I can't see how it can't have a stop codon and still be a gene.Thanks again.

OK, I've provided an answer.

The 3 reading frames from the 3' end use the "other" strand of dna, that is ATG and two others. Experts from mathematical and computational sciences contribute greatly to bioinformatics after a bit of education. Good luck!

This is what we classify as a homework question, but as it satisfies the criterion of the poster demonstrating an attempt to answer it, I provide the following suggestion of an answer.
I assume that as it appeared in an introductory bioinformatics module the exam question is just testing reading frames (obviously) and the punctuation of the genetic code. The meaning is not entirely clear, but as one reading frame would start with the initiation codon ATG/AUG (reverse complement of: cat - 3′)† and end with the termination codon TAA/UAA (reverse complement of: 5′ - tta) that will presumably produce “the most likely protein translation”.
This is reading frame F4 in the output from EMBOSS Sixpack, below, in which termination codons are indicated by an asterisk.
      L  F  I  R  Q  R  H  A  R  H                                   F1
       Y  S  S  A  S  A  M  R  A  X                                  F2
        I  H  P  P  A  P  C  A  P  X                                 F3
    1 ttattcatccgccagcgccatgcgcgccat 30
      ----:----|----:----|----:----|
    1 aataagtaggcggtcgcggtacgcgcggta 30
       X  N  M  R  W  R  W  A  R  W                                  F6
      X  I  *  G  G  A  G  H  A  G                                   F5
        *  E  D  A  L  A  M  R  A  M                                 F4

The conceptual translation, reading N to C, is MARMALADE, which is obviously meant to be humorous and suggests that it is indeed the intended answer.
Open Reading Frames
The poster asks for clarification of the difference between reading frame and open reading frame. There is a Wikipedia entry for open reading frame but I provide an explanation of my own to relate it to the example.
There are always six reading-frames for the conceptual translation of a piece of double-stranded DNA, as shown in the example.
I would define an open reading frame as one that is not excluded from being translated by the punctuation of the genetic code. It has the theoretical potential to be translated considering only the punctuation of the code, although it may not actual be translated. It can start either with the first AUG after a termination codon (even though it cannot be certain that this is the actual AUG used) or the start of a sequenced fragment of DNA (with the assumption that an AUG is possible preceding the 5′ end of the fragment). It can end either with a termination codon or the end of the sequenced fragment (with the assumption that a termination codon will lie 5′ to the end of the fragment).
By these criteria, reading frames F1, F2, F3 and F6, above are completely open (even though the internal methionine could theoretically be an initiation codon), F5 contains the open reading frame GAHGAGG, and F4 is a complete open reading frame, perhaps excluding the termination codon (depending on your semantic definition of the precise end of an open reading frame).
† Reverse Complement
If we take a section of DNA written in the 5′-to-3′ direction — according to standard convention — and use the Watson–Crick base-pairing equivalences (A=T, G=C) to generate the complementary strand, this will be in the 3′-to-5′ direction. For the strand in the question,
5′ - ttattcatccgccagcgccatgcgcgccat - 3′

the complementary strand is:
3′ - aataagtaggcggtcgcggtacgcgcggta - 5′

As shown above.
For ease of translation manually — and for any computer program that manipulates sequences — one needs to reverse this to the  5′-to-3′ direction:
5′ - atggcgcgcatggcgctggcggatgaataa - 3′

This is the reverse complement. Now the starts of the three reverse reading frames are easy to read as:
ATG...
 TGG...
  GGC...

Could be helpful (especially for someone without a solid biology background) to expand on the reverse complement subject. Based on the question it seems that this was most likely the part that was giving the OP trouble.

@David Well I feel silly, but also grateful for the excellent answer. I had tunnel vision but it's obvious now. Out of interest, what made you describe the question initially as "terribly artificial"?

@azure_reflection — Most proteins are much longer than nine amino acids, and programs predicting genes usually have a cut-off of perhaps 30. (Someone else might be able to give you precise size distributions.) There are exceptions (in biology there are always exceptions). In eukaryotes some small peptides are generated by translation of small orfs that precede the predominant AUG. But, from experience, I sympathize with lecturers setting problem-type exam questions.

@Astrolamb — done.


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Why doesn't copper affect human skin?
It's been known for a long time that copper has antimicrobial properties, but if it is so potent, why does it seem to have no effect on human skin or really any large animal?

https://en.wikipedia.org/wiki/Copper_toxicity

That's like if you ingest copper, not if you merely touch it.

Copper does affect human skin.  If you're in contact with it for a while, it will turn the skin bluish-green.

One possible reason is that humans are eukaryotes, while most microbes are prokaryotes.  There are significant differences in the cell chemistry, which explains things like why antibiotics work against (some) bacteria without much affecting the person that takes them.  See e.g. https://www.livescience.com/65922-prokaryotic-vs-eukaryotic-cells.html for more.

@jamesqf: Why does copper turn the skin bluish-green? Can you give a reference? Is the bluish-green color come from oxidized copper?

@Hans: My "reference" is having worn copper jewelry, and having seen other people wear it.  If you want to know more, typing "why does copper turn skin green" into a search engine redurns about 37 million hits.

@jamesqf: OK. My first reaction to your first comment was the greenish blue substance was copper carbonate Cu2CO3(OH)2 https://en.wikipedia.org/wiki/Basic_copper_carbonate.

The outermost layer of your skin consists mostly of dead cells, the Stratum corneum. Copper can't kill what's already dead.

Seems reasonable, but why doesn't it corrode the dead skin fast enough to cause more significant burn damage if it kills microbes quickly?

@Bangarang copper doesn't doesn't burn cells it poisons them. Dead cells aren't affected by being poisoned. The Status corneum is not just one layer, it's 15-20 layers. The cells are constantly being shed and then replaced from below.


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Toxicity of stannous fluoride in toothpaste?
I recently purchased a new brand of toothpaste, and when I looked at the medicinal ingredients, it listed stannous fluoride 0.454% w/w, instead of the regular sodium fluoride. I was a bit concerned because I thought that tin was toxic to humans, and that it might be absorbed in the mouth.
A couple of studies like this one say that stannous fluoride is great, and I can't seem to find any studies on how toxic tin ions are to humans, but on Wikipedia it says that stannous fluoride readily forms tin metal and ions in water. Should I be worried?

Readily soluble in water, SnF2 is hydrolysed. At low concentration, it forms species such as SnOH+, Sn(OH)2 and Sn(OH)3−. At higher concentrations, predominantly polynuclear species are formed, including Sn2(OH)22+ and Sn3(OH)42+. Aqueous solutions readily oxidise to form insoluble precipitates of SnIV, which are ineffective as a dental prophylactic.

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. In particular note that personal medical questions are not appropriate for this site. ——— Please consult with a dentist or other medical professional instead — any advice on medical subjects obtained over the internet should be regarded with extreme suspicion. Thanks!

https://fluoridealert.org/studies/acute01/


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Reverse oxidative phosphorylation?
I noticed that all of the cellular energy production methods that I covered have a fixed ratio of ATP to NAD(P)H out. For example, in the combined process of glycolysis, pyruvate oxidization, and the Krebs cycle, 10 NADH, 2 FADH2, and 4 ATP are produced (based off of my high school's bio text book, if I'm adding that right). In this way, NADH and FADH2 can easily be exchanged for ATP through oxidative phosphorylation. That got me wondering what would happen if a cell was using so many electrons (from NADH and/or FADH2) that there is too much ATP. (Just as a hypothetical: It seems fairly unlikely to me)
I was looking for a way that oxidative phosphorylation could be reversed, but I didn't find much. I did find that anaerobic bacteria can oxidize nitrite in this way, but I couldn't find much evidence of an O2-forming version. Does such a thing exist?

I am not clear whether you understand how ATP is produced in oxidative phosphorylation when you talk about producing oxygen. If you are still following a course you should wait until you have learned how a proton gradient, produced by the oxidative electron transport chain, is used to phosphorylate ADP. When you are at that stage you will be in a position to appreciate how hydrogen ion transport can be accomplished by essentially the reverse of this process. (If you need to learn this yourself, we can suggest suitable reading.)

Sorry, should've clarified... My question is basically whether there is a mechanism in any organism to split H2O (into H+ and O2, like PSII) using energy from an existing H+ gradient, possibly created by an ATPase.

I cannot see any biological rationale for what you are suggesting (much less any chemical likelihood), but I should point out that the production of ATP (like other biochemical processes) is tightly regulated. If there is sufficient ATP, there will be a switch from energy generation to energy storage.


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Why seeds won't sprout given excess water?
What would cause a seed to not sprout despite showing signs of germination given excess water? Oxygen, temperature, and light were sufficient for germination and sprouting in seeds of a slightly lesser amount of water.

What kind of seeds are we talking about here - some have special requirements

I think the answer to this question is like this.   Some seeds can sprout with this much water - even germinating underwater. The seed could sprout, but why doesn't it?  Some living things actually have adapted highly specialized conditions for growth - why should this be?  I'll try to come back later and put an answer up if this is right, and nobody else does.

You've stated in your question that oxygen was sufficient for germination, but if there's too much water this probably isn't the case. It's likely given excess water seeds will drown- that is they have not got access to sufficient oxygen to continue germination.


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How cotranscription events affect splicing?
I want to know how and how often does cootranscription takes place? Can transcription regulators influence splicing during cotranscription?

Can you give some background to why you are asking? Is this a study question or based on your own research?

Co-transcriptional splicing (CTS) is very widespread. Different studies (which are done on different cell types) report different frequencies of CTS. Most of them report a frequency of ~0.8 in different cells except for mouse liver which was reported to have a frequency of 0.45
This is the article that summarizes these different studies.
Can transcription regulators influence splicing during cotranscription?
Yes.. including factors such as nucleosome positions.. this post may be helpful.


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Could total 2020 flu deaths be low due to Covid19 countermeasures?
A working assumption is that Covid19 countermeasures will also reduce seasonal flu transmission and mortality.
Could this effect be so large that the 2020 total global deaths from both causes will be lower than the annual expected deaths from seasonal flu alone ?
I understand global seasonal flu mortality is around 40k/month

This seems too speculative to me - do you possibly have a citation for this "working assumption"?

Contact minimisation will reduce all pathogen transmission. Are there references to the contrary ? https://royalsocietypublishing.org/doi/full/10.1098/rsif.2009.0302.focus

In the regions where they heavily restricted public events, closed schools, etc. because of COVID-19, it's very likely there will be lower flu incidence and mortality. The problem is how to prove that, because the incidence of flu differed grossly from year to year in past years when there were no countermeasures.

This is a question and answer site for problems about biological processes. Such problems should be capable of being answered objectively. Questions about the expected effect of a current epidemic of one disease on the future mortality caused by another disease are not about biological problems in terms of this site and are only capable of speculative opinions. Your question is therefore off-topic. Some reputable sources concerning the current coronavirus pandemic can be found here.

@cumfy if they don't go down after all this fuss it will be embarrassing. I have to go to the bathroom when my nose itches just so I can wash before scratching it. Gonna be annoyed if that doesn't save anyone, covid 19 or not.

@David I'm sorry this epidemiological question isn't to your taste. Viral transmission mechanisms, their efficiency and analysis of their variation and sequelae between similar viruses is a central topic in epidemiology. Many statistical inferences can be drawn from carefully recorded epidemic data.

@cumfy — Please read what I have written — it is not a matter of taste. I explained that your question only admitted of speculative answers and was therefore off-topic according the standards of this site. You post here without even finishing reading the Tour (you lack the corresponding badge), never mind the Help on asking questions where this is laid out. New contributors are welcome to SE Biology, but they are expected to read and follow the "rules".


text:
Did we first have swimming birds or flying birds?
Looking at the swimming birds building nests just across my garden, I suddenly wondered how evolution came to swimming birds and whether flying birds started swimming or whether swimming bird like animals started flying.
What came first and when and why?

Wouldn't we have had running birds first?

Flying came first, as far as we know. The earliest known bird (currently), Archaeopteryx lithographica, already had aerodynamic feathers (Feduccia and Tordoff, 1979). The Solnhofen Limestone, where it was discovered, is ~145 million years old, so we can place the "when" flight evolved to greater than or equal to that time.
Gansus yumenensis is regarded as the earliest aquatic bird and is dated from ~120 million years ago. The Hesperornithiformes are the sister taxon of Gansus (less derived) and also aquatic. However, they date from ~85 million years ago. It is not clear whether the ancestors of Hesperornithiformes were also aquatic. Because they branched off the main line of birds before Gansus, these ancestors would likely predate Gansus, but those relatives have not yet been discovered.

Thanks for the extensive answer, so there's a gap of at least ~25 million years, considering the current state of knowledge.

Another way to look at this is: How do you evolve flight when you're aquatic? There are three proposed models (or even five) for the evolution of flight:

wings helped predators to better jump at prey from high positions
wings helped a jumping animal to make longer jumps
wings helped a tree-living animal to get around

All of these models assume that you have a high or solid surface to start flying from. Water, in contrast, is a difficult underground to start flying from (being flat and soft).
In contrast, to evolve swimming for "terrestrial" bird seems much more straightforward.

Ok, seems a fair line of thought, but if this were true, why do we have flying fish (ok, not really flying, but still, they could have evolved from there)?

Fish have been around for 500 million years, and no true flying fish has evolved during that time. However, in tetrapods (which evolved from fish), flight has evolved in bats, birds, and pterosaurs. In contrast, "flying fish" are actually gliding fish that accelerate in the water (and not in the air, as birds do).


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Can viruses be reintroduced to humans from ice sheets?
A comment on reddit mockingly say

because the ice is melting away due to global warming, this new virus came out of the melted ice sheets

It has 60+ upvotes and no one replied
Is it possible for viruses that are frozen in ice sheets to reinfect humans when they are melted?

Yes, pathogens have been shown to survive freezing temperatures under ice and still remain potentially dangerous after the melting of ice.
This has not only happened for relatively simple molecules such as the ones that viruses are made out of, but it has also even happened with larger pathogens such as bacteria (anthrax outbreak in 2016).
Unlike high temperatures which can cause molecules to dissociate due to excess kinetic energy, freezing temperatures usually preserve molecules and even cells such as with the aforementioned anthrax outbreak. This means that viruses can survive cryogenesis.
In 2015, researchers in Tibet discovered 28 'new' species of viruses in (melting glaciers).
These sort of discoveries lead many to believe that with global warming, previously unknown viruses could appear once again.
As for SARS-CoV-2, it seems that melted ice sheets are unlikely to be the source of such a virus considering (among other reasons) that the virus was first noticed in Wuhan China, a place lacking permafrost.


text:
how does acetic acid induce pain?
how does acetic acid induce pain? I am finding the whole mechanism of it but cannot find any papers or writings. please help.
If you have links that would be nice too.


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Can there be significant new changes in physical features of Humans due to evolution in 10000 years of span?
Humans migrated from Africa about 60000 years. And in these years humans physical features undergone significantly in terms of skin color, hair, eye color and facial features.
So, with this we can say that given 10000 years of span we can see a significant noticeable new changes in physical features of humans? like some humans with new skin color (apart from today's white, black and brown), new color eye balls, big heads etc.?

@tyersome Below answer gave me appropriate answer. Thanks

@tyersome : The link you provided was more specific to evolution of human in future whereas mine was more specific to evolution changes in terms of a window/range of 10000 years. So, below answer is more appropriate.

Yes & perhaps (or probably?) no, depending on what you define as significant changes.
Less than 10,000 years ago everyone in the british isles & the rest of europe were dark skinned so the answer if (unlike me) you consider the change in skin color a significant change is obviously a resounding yes.
Here's what English people looked like 10,000 years ago

Darker skinned than you were expecting perhaps.
If as suggested in this article white skin arrived in Europe around 5,000 years ago that only leaves 2,000 years before early Greek & Roman art we have available which shows it as ubiquitous, so it perhaps took only 2,000 years or so (maybe less) to become dominant in europe, that's fast.
Using 20 years as the measure of a generation that's only 100 generations, so, very fast.
Timeline of human prehistory
The first reconstruction in the link below is a reconstruction of a Neanderthal woman found in a cave in Gibraltar. She died at least 30,000 years ago.
Here she is, the skin tone may not be accurate but we do know from gene's recovered from Neanderthal remains that they were relatively light skinned.

Personally I don't consider her appearance to be significantly different from modern humans.
29 Reconstructed Faces Of Ancient People
So my answer based on what I consider significant changes would be no.
But for you or others the answer may well be yes.
And of course a mutation for a new eye colour could appear at any time in one individual & spread like wildfire practically overnight just because we think it's unusual & 'cool' (aka sexual selection) so if eye color ticks your boxes it's a very definite yes.

Your first link - https://curiosity.com/topics/the-earliest-humans-in-england-didnt-look-the-way-youd-imagine-curiosity/ gives me the answer. 10000 years before there were no light skinned in Europe and it took less than 10000 years for homosepiens to get the lighter skin? I presumed it would take about 100000 years for such big change like skin color.

I thought it might :)

"about 10,000 years", nope, a mutation can spread pretty fast if it's beneficial or selected for by sexual selection, once it appears, blue eyes spread fast too when they turned up, what takes a long time is the mutation, it's a lottery & useful (or just non-damaging ones) aren't that likely so 'on average' are often a long time apart, reduce it to only ones that provide a noticeable phenotype change & rarer still.

@barath : Which all means a single change of some sort can just happen, & pretty quickly, but multiple changes to a phenotype such as you need to go from something chimp like to something man like will take a really long time & for that 10,000 years isn't even remotely long enough.

@barath : "such big change like skin color" : Skin, eye or hair colour may be noticeable & obvious but they aren't 'big' changes, not really in any qualitative sense, they can occur with just a single mutation to a single gene so they're really pretty small changes genetically speaking.

@barath : "what takes a long time is the mutation" : Ooops, edit required > what takes a long time is waiting for the mutation to turn up : mutations themselves are of course pretty instantaneous, caused as they are by DNA copying errors or random background radiation jiggling with a single strand of DNA, they (or at least noticeable non damaging ones) are just few & far between, useful  or desirable ones more so.

Yes, I didn't consider mutation into account. Probably there was a mutation for light skin among very a few human beings and other human species might have attracted/preferred to those lighter skin and produced more offsprings with them and eventually lighter skin spread significantly across Europe as a natural selection of humans.

@barath : It's pretty much all mutation somewhere up the line. Light skin may have arrived in europe as little as 5,000 years ago, lactose tolerance in adults as little as 4,000 years ago, so yes, the spread can be fast if the mutation is beneficial or desirable to the opposite sex.

@barath : Light skin is an advantage for vitamin D production in a 'less sunny' climate (europe, compared to africa) so it had a definite advantage for health & survival to offer & doesn't need the sexual selection angle to explain it's rapid spread.

Yes, agree. Thanks.