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Are these cats calico?
Calico cats are cats that have 3 fur colors and are always female or males two X chromosomes.
I've seen many cats that will have 2 fur colors (one of them is usually white) and another, third, color which is a darker shade of one of the other colors. As exampled in the pictures below (taken from the internet). Are those considered Calico cats?

(source: mirror.co.uk)

I don't know much about calico cats, but from those pictures nobody can tell you for sure if they are female. One of the upper two closely resembles a male (and fertile) cat I know.

The relation to female was only through Calico cats. I don't really care about their gender.

I'd say, those could as well be normal tabby cats. Calicos are more often those with big brown and black patches on white. Or at least they have a distinctive amount of visible bright brown in their coat.

@skymninge, are tabby cats considered to be Calicos, and can they be of both genders?

Tabby is just another name for the color. Like Calico, it is not a breed. http://en.wikipedia.org/wiki/Tabby_cat Some Calicos could also said to be tabbys. Like Calicos, they can be of both genders. (It's just that most calicos are female, not all of them.)

they don't look like calicos to me. their patches don't form as stripes really.

We call this a White Calico with Tabby patches in my area.

I think you are misunderstanding "color" here. When applied to cats, it doesn't literally mean a color shade as used in color theory, but "coat color" which can in fact also be a "coat pattern".
The cats above are two-colored, not three-colored. One color is white. The other color is what is called "tabby" in English and is a pattern of dark spots arranged in regular stripes on a lighter background. These spots are not considered a third color in cats.

This is a calico cat. Her three coat colors are white, orange, and grey tabby. See how the orange and grey are irregularly interspersed, this is the pattern of paternal and maternal chromosome expression on her body. Again, the grey and black patches within the tabby part are regularly placed. They don't make two separate colors, grey and black, but a single coat coloring, grey tabby. There are also other color combinations in calico cats, for example white-orange-black, and they are more straightforward to recognize.

note two patterns is quite common in cats as some coat color genes can be affected by temprature.

Tortoiseshell cats (which is the normal name for Calico style cats in Europe) arise due to a gene on the X chromosome. Some patches are ginger, and some tabby due to the deactivation of one X chromosome in each cell at an early stage of development. This produces a tortoiseshell-like pattern.
What you see in these tabby cats with the white colouring is due to temperature dependence, this gives the patterning on the feet/nose etc. Tortoiseshell cats looks quite different, where the different coloured patches of fur are random.

Adding to this massively late, but while the cats in the first pictures are "just" black tabbies with minor white spotting, the cat in the second picture may actually be a diluted caliby! A diluted caliby (calico-tabby) is a black, orange and white cat with a tabby gene and a double dilution gene! This makes them a blue, cream and white tabby, shortly known as caliby. Unless the light is playing tricks on me, you can see a cream-colored patch on her right cheek that indicates the presence of ginger/cream.
As almost all cats that possess both a black and a ginger color are female, with only very rare exceptions, the second cat in this case would likely be female. Note that the color white is not a sex-linked color and does not indicate any gender! Important is the presence of both a black-based and a ginger-based color!
And a tiny crash course on the cats in the first picture: To tell the true color of a tabby cat, look at the stripes, especially at the tail tip. You can see their base color is clearly black, whereas the rest of their body has various shades of black due to the agouti gene, which gives each individual hair little stripes and creates the tabby pattern through that! If the cat is a torbie (tortoiseshell tabby, black + orange tabby) you will notice patches where the stripes are ginger instead of black.


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Is marriage with half-cousin's daughter more risky than marriage with others?
I want to know is marriage with half-cousin's girl more risky than marriage with a non-family girl?
Also I like to know if her parent are cousins(but from mother side), does it add more risk to this marriage or not?

The answers are yes and yes. However, I will have to dig up some sources before I can answer.

The marriage is obviously not an issue. The reproduction can be an issue.

Why is a girl connected with a girl? And she in turn marries a guy?

@TheLastWord it's an awkward diagram, but if you read the text of the post (her parents are cousins), you'll see that the lines connecting the family on the right side of the figure and the family on the left side of the figure are parent-child relationships, like all the black lines connecting boxes in this figure. The girl at the base of the figure is the child of the boy she is connected to with the black line and the girl she is connected to with the black line.

@TheLastWord: The (right side)girl is her mother and she is cousin with her father.

The medical term here is consanguinity, or a consanguineous union. The risks of consanguinity are well studied, and based on the principle that children born to parents with shared genes are more likely to be homozygous for recessive alleles. Population level measurements of specific risks for, e.g., fetal loss, major birth defects, or other problems vary depending on the population studied. Many of these studies look at first cousins, where typical numbers are between a 1-5% greater risk for major birth defects and 4-5% greater risk for late miscarriage or death of a child before age 10. The data on earlier fetal or embryonic loss isn't conclusive.  You can read more about this in the review I linked to at the end of this answer. The specific risk for a specific individual isn't on topic here, since it is a personal medical question. If you are looking for an answer to that question, I'd suggest scheduling a visit with a medical geneticist.
Your diagram depicts marriage between half first cousins once removed, with an expected shared percentage of genes of 3.125%, equivalent to second cousins, which fits the definition of consanguinity generally used in the medical literature and allows application of studies that use that definition. The fact that one of the potential parents in this marriage was also the product of a consanguineous union may increase the risk.
Consanguinity is an important risk factor for many birth defects and other diseases (see Cecil Medicine Chapter 41 and this review)

Thank you De Novo, but I can not understand why relationship between the girl's father and mother affects on her marriage, when that relation doesn't any issue with the boy who likes to marry with. I mean, why relationship of the right side family, can affect on this marriage when the boy has no relationship with the right side family?

@Hasani it suggests both potential parents are part of a subpopulation with a higher rate of consanguinity and less genetic variability. This means there is a slightly higher risk that the potential parents are both carriers of the same recessive allele for some disease. Empirically, when there is more than one consanguineous union in the family tree, we see a higher rate of birth defects and other diseases than you would expect form the expected shared percentage of genes alone.

Dear De Novo, May you explain how percent the risk of this marriage is more than a non-family marriage?

@Hasani the specific question about the risk of defects in your child should be asked in a visit with a doctor, ideally a medical geneticist. I've edited my answer to include more about what studies have reported in general.

source: Stack Exchange

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

sort: votes


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Why do we need to diversify our food sources to live healthy, where other animals live happy on one source?
We read about eating different food to get all vitamins and minerals our body need, and often you find people fail to get the daily amount of a certain thing.
I wonder why we humans need to do this where other animal live fine on grass only or leafs only

All organisms have some dietary requirements. Many organisms cannot synthesize everything they need from basic compounds and they have to obtain them from other organisms. This is not specific to humans.

OK, What about sheep as an example, do they eat anything other than grass? Does grass has all the nutrition they need?

Strictly speaking, humans, at least infants, can live on a single food source - milk. The current recommendations about eating something from all food groups may be exaggerating. Several studies have shown that vegans are not of greater risk of developing disease than omnivores, for example.

You say that like grass or leaves are easy to live off of, animals that live off these materials have highly specialized digestive systems to extract enough nutrients from it. Also note these herbivores are more than willing to eat things like meat and eggs when they can get it. Deer will stomp nesting birds to death and eat them. They can improve their health by obtaining these nutrient rich sources.

Also, grass and leaves are not simple things, but are quite diverse.  E.g. many humans happily consume the leaves of lettuce & cabbage (and other sorts like grape leaves in regional cuisines: https://en.wikipedia.org/wiki/List_of_leaf_vegetables ), but would be poisoned by eating the leaves of say rhubarb.

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


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Can an animal evolve after birth?
I am wondering if animals do evolve even after birth and gain DNA changes that give them advantages and make them more suitable to the environment while they are alive, then pass these "enhancements" to their children
UPDATE
After all, cell do split and multiply when the animal is alive, and it could end up with a totally different cells than the one born with, so if a mutation happened during this period that led for it to be the dominant "property", what stops it from being passed on?
Is there a research on this?

I would encourage you to look at this question, and maybe clarify in your question what you understand evolution to mean. I would note that typically, in the general sense, evolution is understood refer to changes in a population of organisms, but in some domains it can refer to changes in a cell population. This circumstance, though, doesn't involve passing on to the offspring of the organism, but the offspring of the cell.

No.  Certainly not.  There is only a very limited number of cells in the body of any creature which pass on genetic material to the offspring generation; these are referred to as gametes.  Mutations to these cells, however, do not affect the parent in the least, as their sole function is to produce offspring.
One gamete from the father & one gamete from the mother fuse to produce a child with a combination of genetic code, which means that mutations in those gametes (which did not affect the parent) will be present in every cell of the child's body, and affect the child.
Furthermore, do remember that most mutations are not "enhancements"; rather the vast majority of mutations are harmful.
After birth (and really, long before birth) mutations acquired in the organism are unable to be passed on to the offspring, unless they happen in the gametes, in which case they do not affect the parent carrying those mutations.

But doesn't gametes have the DNA of the animal?

Yes.  But the gametes rarely (if ever) express the portions of that DNA which will effect the rest of the animal.

Sorry but I don't understand, which portion and why it won't carry it?

Each cell in the body of an animal has a copy of the entire genome (all the DNA).  Some parts of that DNA only affect the cell it's in, whereas other parts of that DNA code for molecules which could effect the entire body.  Because of the function of gametes, they are specialized to express only parts of the DNA which allow them to grow and perform their function, which is to reproduce.  Consequently, they are kind of resident aliens with little / no effect on the parent until fertilization, when you have two distinct animals (distinct genetic code), one residing and depending on the other.

OK, so let us assume that while multiplying/reproducing, a bone cell mutated and gained DNA information that makes the leg bones longer, you are saying that this info won't be passed to any other types of cells in the body other than bone cells?

Correct.  There's a process known as differentiation which sets in stone early on in the development process what kind of cell a cell will be, which in turn defines what its function will be.  In your simplified example (obviously it's more complicated than just "gaining information for longer legs"), the bone cell will be utterly incapable of passing that genetic material on to the gametes, so although the parent has longer bones, the offspring will have normal length bones.

@Mocas FYI, a cell mutating and migrating its mutated form to other tissue is basically a cancer that has metastasized (though it would not be infecting other cells with its mutations; only invading their tissue).


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Does the mutation CCR5-delta 32 increase the genetic info?
My understanding is that the mutation CCR5-delta 32 caused the CCR5 co-receptor to be of a different shape, resulting HIV virus to not be able to attach itself to it.
My question, this shape/mutation, is it a result of a more or less information in the genetic information of the person with the mutation as compared to one without it?

your going to have to clarify what you mean by "more or less information in the genetic information" and "increase the genetic info"

"Increasing genetic information" is a creationist buzzphrase, most recently popularized by "Intelligent Design" fraud Michael Behe in his most recent book; Behe claims that it's impossible for mutations to add information, only subtracting it, and that therefore evolution is impossible.

Whether or not a mutation changes the 'amount' (meaning the size of the genome) of genetic information present in an individual depends on the type of mutation and is independent on which gene is affected.
In general there are 3 types of mutations:

point mutation: this is the change of one base pair to another (e.g. A to C). The total amount of information/the size of the genome is unchanged.
deletion: this means that a certain stretch of DNA is missing, likely disrupting what was there before. The total amount of information/the size of the genome is reduced.
insertion: this means additional DNA was added at a certain place in the DNA and probably disrupts something that was there before. The total amount of information/the size of the genome is increased.

The CCR5-delta32 mutation is caused by the deletion of a few (only 32) base pairs, however this deletion causes a frame shift in the gene and therefore leads to an early stop codon, which renders the protein inactive.


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How do researchers define the region a lead SNP encompasses?
As I understand it, a lead SNP captures the variance for all unmeasured SNPs in a region due to it's low p-value and high linkage disequilibrium. However, in different papers the region size differs (e.g. from 500kb +/- to 1mb +/-), how are these sizes chosen and why do they differ?
Edit to add examples:
Xia et al. Transl Psychiatry. 2017 Aug
"Genome-wide association analysis identifies common variants influencing infant brain volumes"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5611727/
-500kb region
Polushina et al. Transl Psychiatry. 2017 Dec
"Analysis of the joint effect of SNPs to identify independent loci and allelic heterogeneity in schizophrenia GWAS data"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802566/
-1mb region

It would be great to reference papers which use the different sizes.  Otherwise it's hard to say why they chose the sizes they did.  Thanks!

Thank you for your response, added some papers I have been looking at now, is it likely to depend on the disease being looked at? As in, the more complex and heterogenous the wider the region you might look in? Or does it depend how many SNPs pop up how big you set your boundaries? Do researchers risk a loss of information with however they set these regions?


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Why is there a mass limit on biological powered flight?
So, this is a thing I never fully understood. There are a lot of reasons for a flying creature to be limited in mass (though I'm unsure if I'm familiar with all of them), from energy consumption to material strength. However, there seems to be an argument that goes along the lines that over a certain mass, no matter what, they can't generate enough power to counteract gravity.
What limitation could they exactly mean with that?

The design of the “wing” and its materials...

One of the physical limits to biological flight is muscle physiology.
Muscle force output is proportional to muscle physiological cross sectional area (PCSA) multiplied by its specific tension (Gans, 1982):
$$F = \text{PCSA} \times \text{Specific Tension}$$
PCSA is basically just the cross-sectional area of a muscle adjusted for its architecture. Pennate muscles have higher PCSA than parallel fibered muscles, because more fibers are packed into the area (at the cost of shorter functional distances). Specific tension is the force output per unit area. For a single species, specific tension is essentially constant.
So the way to make more force is to make more PCSA. But muscles don't scale only in area, they scale in volume as well. Increased volume increases mass as a cubic power, but muscle area only scales as a square power. So any increase in area that requires a volume increase (which is inevitable), will quickly outstrip any gains in force output.
Note that this doesn't mean that very large flying vertebrates were not possible: the largest pterosaurs (e.g., Quetzalcoatlus) had ~15 m wingspan and perhaps weighed 200 kg and the largest birds (e.g., Argentavis) had ~7 m wingspan with a mass over 50 kg. Both, however, were likely gliders.
Gans C. 1982. Fiber architecture and muscle function. Exerc Sport Sci Rev 10:160–207.

There's also the aerobic/anerobic issue.  If you look at the largest flighted birds, they actually use powered flight for very short periods, usually to get airborne.  Then they will soar (or like the albatross, use lift from ocean waves), which uses only a miniscule amount of muscle power for control.  Just as humans in sailplanes or hang gliders can stay aloft for many hours in favorable conditions, if they're towed up or launch from a high place.

Weird. Doesn't the square-cube law apply only when you scale an object in all three dimensions?

@Mephistopheles yes which is the problem the weight increases by the cube but the strength only increases by the square. so you reach a point were you can't add more strength without adding more weight than that strength can offset. And not just muscle, bone and connective tissue have the came problem.

@John I know, but can't you just... make it thicker without changing the length of the fibers?

@Mephistopheles the issues is if you make the muscle thicker you make it more massive, you also have to make the ligaments thinker and more massive becasue they are taking the load, then you have to do it for the bones., ect, then you have to do it for the digestive system and cardiovascular system supplying those muscles, and the lungs, and the ect. it is like the worlds least favorable rocket equation. If you just make hte muscle thicker without changing anything else it just tears itself apart, (which can happen to bodybuilders that put on muscle too fast).

@John So, in the end, it all boils down to material strength?

@Mephistopheles You also get the same problem with the wing themselves, the lift increase with the surface area (a square) the mass increases by the cube. soon the wings weigh more than the air they can shift. It is not just strength it also also things like oxygen (lungs also work of surface area) Muscle is just the most unalterable limit they hit first.

@Mephistopheles there are a few other problems you run into that are well covered in this fun video. https://www.youtube.com/watch?v=faBguu_6LBI

@John So, they also have to keep the wing loading constant. What's up with aspect ratio?


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Effects of direct and indirect cholinergics on cardiovascular system
If I give intravenous acetylcholine then the effects produced on cardiovascular system are hypotension , tachycardia and increased cardiac output.
Now if I give intravenous acetylcholine esterase inhibitors on another patient then the effects produced on cardiovascular system are hypertension, bradycardia and decreased cardiac output.
Ach esterase inhibitors also increase acetylcholine concentration then why does the effects are exactly opposite in the above mentioned two cases.
Reference for abovementioned data : Cholinergic drugs ,
katzung pharmacology, 14th edition.
Is it because Ach esterase inhibitors increase Ach concentration locally in the tissues which produce more direct effects while the Ach is rapidly metabolised in the plasma so can't reach into the tissues so it produces more indirect effects via baroreflex ?

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [MedicalSciences.SE], but please do not crosspost, instead request migration. However, please note that that site (and this one) expect you to document your prior research (ideally with references to reliable sources). Thanks!

Okk ,, I added my reference now

Now can you please explain something about that ? Does the way I m thinking correct ?

That's a start, but I encourage you to do more than read from a single textbook. In addition, given the poor fit between your question and this site you may wait a long time before someone posts an answer — that is why I recommended you check out what seems to me a more appropriate site ...


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Types of structures formed by various types of lipid molecules
Since Phosphatidylcholine (PC) and phosphatidylserine (PS) are roughly cylindrical in shape , they tend to form flat bilayers. Phosphatidylethanolamine (PE) on the other hand is conical in shape which bends the lipid bilayer when present asymmetrically along with PC and PS. What kind of structure will form when PE is present exclusively?

PCs are lipids with large head groups, so are more of a cylindrical shape, as a result, they tend to form flat bilayers.
PE is a lipid with a small head group, so is in a conical shape. However, they are generally present as inverted cones, providing maximum curvature to the membranes.
So, PEs are generally found in highly curved membranes , for eg:- viral budding, microvilli, micelle, internal vesicles formed for transportation, Inner mitochondrial membrane, Gram-negative bacterial membranes.
You can check out this article, where researchers performed lipid content profiling for E.coli. (https://www.sciencedirect.com/science/article/pii/S0014579315006912)

You can also check out this research article for lipid profiling of rat intestinal microvilli.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1186751/pdf/biochemj00720-0057.pdf)

Add figures to this answer if possible to make it complete.

Welcome to Biology.SE. This doesn't seem to be answering the original question, which was what would happen if only PE was present.


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Is there a resource that lists the quantity of active transposons for various species?
I read the thesis that transposons are a major factor in human aging. To study that thesis I want to see how the count of active transposons differs by species. Is there an existing database or study that lists active transposon count by species?

https://mobilednajournal.biomedcentral.com/articles/10.1186/s13100-019-0150-y

RepetDB (linked by Maximilian) and Dfam are both good databases for TE sequences and lineages, though I think determining which are active is a harder question, especially since TEs are highly polymorphic within a population.  A great place to start would be this recent review of eukaryotic transposable elements; see Fig 3, in particular, for a wonderful graphic giving the distribution and genome percentage of different TE classes across eukaryotes.

Also be aware that the 'density' of transposons can vary hugely within a species — one example is in maize, where high latitude cultivars are selected for smaller genome sizes (to allow shorter generation times) and consequently have fewer transposons.


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Is it correct that the nicotinic acetylcholine receptor has nothing to do with Dopamin?
As I know Dopamine is almost exclusively produced via metabotropic receptors, is it possible for a nicotinic ACH receptor to influence a dopamineric neuron?
Can a nicotinic ACH receptor cause a dopamineric synapse to create dopamine?
Unfortunately I can't find anything about it.
Edit: rephrasing my question:  Do 2-neural systems exist where neuron A has a nACH-R and neuron B has a dopamineric receptor? And do dopamineric nikotinic ACH-R exist (receptors which react to dopamine)?

Your question doesn't make much sense because I think you have a variety of misconceptions all mixed together. Dopamine is not produced by metabotropic receptors, that statement is nonsense. The (general) order of things in the nervous system is: Cell A releases neurotransmitter onto Cell B, causing it to be more or less likely to fire for some period afterwards. If Cell A releases dopamine, it will affect Cell B if it has synapses on Cell B and if Cell B has receptors for dopamine. Cell A could possibly have receptors for any other neurotransmitter.

Thanks for your clarifications. Do 2-neural systems exist where neuron A has a nACH-R and neuron B has a dopamineric receptor? And do dopamineric nikotinic ACH-R exist (receptors which react to dopamine)?

Still doesn't make sense. Are A and B connected? What neurotransmitters do they release? What is a dopaminergic nicotinic ACh receptor to you? Do you know what acetylcholine is?

Yes, A and B are connected, A has n-ACHR and B has dopamineric receptors. is this constellation possible or not? Is it possible for a neuron with n-ACH-R to influence a neuron with a dopamineric receptor directly?

Let's simplify your question with correct terminology: you have a presynaptic neuron and a post-synaptic neuron. The presynaptic neuron can release multiple signals (neurotransmitters) into the synaptic space, or cleft. The postsynaptic neuron can be equipped with multiple sensors (receptors) that are specific to detect certain signals.
The signal and the sensor don't have to match, although this is costly if it's poorly tuned. Most neurons that are entirely unresponsive are pruned. Darwinian selection makes circuits much more efficient than what pure chance alone would produce, but remember that nature can be quite imperfect and stochastic.
However, you can have neurons that have a dopamine sensor (receptor) and provide an acetylcholine signal (neurotransmitter) and vice versa.
Acetylcholonergic and dopaminergic neurons can be connected. Here is an example.
Also, most people forget that neurons not only form chemical synapses but electrical synapses as well. That means the circuitry does not rely on ligands and receptors.

Thank you for giving a straight to the point answer.

"The presynaptic neuron can release multiple signals" - Although technically true, I think this statement is potentially misleading. Almost all neurons release a single principle neurotransmitter. "The signal and the sensor don't have to match, although this is costly if it's poorly tuned." - that's not how synapse development works, synapses are developed in an interplay between pre and post synaptic cells. "Most neurons that are entirely unresponsive are pruned" - did you mean synapses?

The answer he gave is fine, you don't need to downvote  because the ones you gave are complete trash that didn't help at all. Really pathetic that you are most likely the person downvoting both the question and this answer, which exactly provides the answer that I was looking for.

@BryanKrause My friend Bryan! I don't know what to tell you. You are woefully wrong on every count. These are neuroscience fundamentals we are talking about! Where to being? This is textbook from at least two decades ago. I'm also sure you must be aware that in development, a huge number of neurons are pruned through apoptosis, to remove most of the superfluous elements in the CNS. Lastly, I too thought you were uncharacteristically aggravating to the questioner; in my opinion it was counter-productive. After all, the question was very simple!

Yes I am aware that neurons release more than one substance, but they do not typically release more than one of the typical neurotransmitters. That is, neurons do not release both dopamine and acetylcholine, for example. Your source is talking about corelease of peptides which do not mediate the immediate synaptic response but instead influence the synapse itself. I am worried your answer is misleading to a novice.

My questioning was because the OP showed so little understanding of the underlying structure of the nervous system that I don't think they are ready for this answer.


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Issues with Mutant Allele Fraction Preparation
I am currently trying to prepare mutant allele fraction (MAF) solutions for an allele discrimination qPCR assay. I began with plasmids cloned with the different desired alleles. I amplified the the plasmids via PCR using primers flanking the mutation site. The amplicons were purified and quantified using qPCR with primers that flank the mutation site. The quantification was done with an standard curve of Ct values plotted against the log dilution factor of the solutions, with an efficiency of 84.18%.
Based on the Ct values obtained, the mutant allele and wild type allele amplicon solutions were then diluted to the log dilution factor that would give a specific Ct value (using the standard curve).
When I amplified the 100% mutant and 0% mutant solutions, I obtained roughly the same Ct values (values differed by no more than 0.5). When I mixed the 100% and 0% MAF solutions to prepare 5%, 1%, 0.1% MAF solutions and amplified them with the same primers that flank the mutation site, the Ct values from each MAF solution differed by up to 2, when it should differ only very slightly since the total DNA content for each of the different MAF solutions are the same.
Does anyone have any idea why this is happening?


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Absorbance anomaly
The standard concentration for absorbance of 1 for ssDNA is 33 ug/ml, while for RNA it is 40 ug/ml. I can't find the reason for the difference in this value for these two macro-molecules. My professor was unable to answer either. Would really appreciate some hint towards finding its answer.

DNA and RNA have different extinction coefficients - i.e. they absorb different amounts of light - because they have different structures.

This paper points out that uridine and thymine have different absorbances at 260, with uridine being higher. Perhaps that helps to explain the difference in absorbances? There seems to be very little difference between ribonucleotides and deoxyribonucleotides.

Another possibility is the ribose-phosphate and deoxyribose-phosphate backbones force different conformations onto the bases, which affects the base stacking interactions.

Thank you user137 for your response. However as you see in my question that actually ssDNA absorbs more than RNA. The paper points to the fact that at 260 nm the absorbance of uridine is higher than thymidine. It also shows that there is negligible difference in the absorbance between ribonucleotides and deoxyribonucleotides if the base is similar in both. So now I am more puzzled by the fact that uridine is absorbing more than thymidine at 260 nm.


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What can eating pink mold do to a healthy person (someone whose immune system is not weakened)?
I've tried searching it up, but my research has yielded nothing very specific.
The following website was the closest I came to finding something about pink mold on bread. It, however, said nothing about the effects of eating pink mold (https://moldcleans.com/pink-mold-on-bread/)
I also found another website, https://lookmold.com/detect/type/pink-mold, which states that healthy (people without compromised/weakened immune systems) people don't get sick right away from exposure to pink mold. Other sources, however, claim that only people with compromised immune systems will get infected by a fungal infection. Hence my question: what can eating mold do to a healthy (healthy immune system) person?
Edit: Thanks to all who responded! The advice was very helpful. I have also edited my question to fit the rules, for I am still curious about the effects of pink mold on a healthy person.

Just fyi your second linked source says "It’s not actually mold! That’s right, it’s actually bacteria. For the sake of this article we will refer to it as pink mold. The name of the bacteria is called Serratia marcescens." It's great that you did some research before posting your question here. It may not be true that what you saw in the muffin is the same as what is commonly found on bathroom walls. You should save all traces of the muffin you ate and any other muffins and consider seeing a doctor. Stack Exchange is not the right place to ask real personal health-related issues.

Was the patch fuzzy? If not it wasn't mold. But it could be pink yeast which can be found in spoiled dood according to wikipedia. https://en.m.wikipedia.org/wiki/Rhodotorula_glutinis

I reopened this question because I had previously unilaterally closed it for being a request for personal medical advice. I still think it could use a bit more clarity and prior research to be a good Biology.SE question, but I'll leave it up to the community.


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The exact points of muscle attachment and the "equal and opposite force" that skeletal muscles apply
I've been trying to make a simple simulation of the human body executing some motions in Mathematica (the details are irrelevant), but I need to know some more information about muscles and how they exert forces. To simplify the problem/question that I am asking, take just the bicepts for example. Suppose that you have just the chest, upper arm, and forearm attached, and ignore the rest of the body (and by that, I mean either remove or treat it as rigid, with the exception of the joints in question, which would therefore be just the shoulder and elbow joints).
One relevant idea that I should point out is that I'm simulating the guy basically jumping, and, whilst in the air, your body is in an inertial frame, meaning that Newton's Third law applies. Under the assumption of a constant moment arm, the usual simplifying assumptions that are made here, etc.. (actually, see the hyperlink below), does contracting JUST your bicepts cause an equal and opposite force at the shoulder, or just the elbow, and is this typical of muscles in the human body?
When the bicepts contract, if they're attached to the shoulder/chest they will (theoretically) pivot the upper arm towards you, while if they're attached to the upper arm they may pivot it backwards, the other way (I think). If they're attached to the upper arm, then the diagram here is essentially what I'd use, but if the muscles went all the way through to connect I'd have to basically "add" an additional segment to the diagram depicted in the link, and the muscle would pass directly over the upper arm, instead, for the purposes of contraction, attaching your forearm directly to your shoulder. This is why I think it's a problem of where the muscles seem connected.

Which of these is a more accurate representation of how human muscles accurately attach things, and therefore exert equal and opposite forces when they contract (and is what I've said so far even correct??)? Alternatively, how accurate is the image depicted in the hyperlink in the above paragraph?

Thank you in advance, so so much
Added TLDR; does (-from a conceptual viewpoint-) flexing purely your bicepts function to bring your forearm and UPPER ARM closer together, or is it really bringing your forearm and SHOULDER closer together? Is this how muscles work in general?

Does it help you to envision muscles (with tendons) as springs? The third law applies to the forces at the two connection points, like with any spring.

@BryanKrause kind of, I think that's a clarifying question though. I guess that what I'm asking is more like where the springs are attached; for example is the equal and opposite force at the other end of the spring exerted on the upper arm or shoulder; one moves the shoulder, the other moves the upper arm, too.

Muscle groups can be really complex, but individual muscles really aren't. I think you just need an anatomy reference and look where the tendons are anchored for any particular muscle you're looking at. It won't be attached to the "upper arm" or "shoulder" but to a specific place on a specific bone which will produce a specific degree of motion.

For major muscles you can probably find enough just on Wikipedia.


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Stopping all intracellular activity in a reversible fashion
I have never studied biology but the following question seems meaningful to me. Suppose I take a cell, not that of a unicellular organism, but a human cell. Normally, there are some intracellular processes going on. If I understand correctly, one way a cell is going to die is that enough mistakes happen during these processes and it can't take it anymore.
Suppose I really need this cell alive and well in two hundred years and I do not really care what happens in the meanwhile. Is there a way to stop all the intracellular processes (protein synthesis, intracellular digestion, etc.), in a reversible fashion, so that I (or probably not me but a great-great-great-great-great-great-great-grandchild) could "start" this cell again after two hundred years pass? Now, two hundred years seem like too much for an experiment, but you get the idea; say, a month would be OK too.
Surely, some biologist thought about this at some point. Any references studying this question would be great.
EDIT: Wikipedia says that

Many bacteria can survive adverse conditions such as temperature, desiccation, and antibiotics by endospores, cysts, conidia or states of reduced metabolic activity lacking specialized cellular structures.

So at least some unicellular organisms can temporarily slow down the rate of metabolism.
I also think that some mammals can enter the state called hibernation, when their heart rate significantly decreases. I think this is different from above in that the amount of time mammals can spend in this state is less than the amount of time bacteria can spend in the dormant state (see here). From this I infer that the maximum metabolism slow-down factor is lower in mammals than in bacteria.
Ultimately, I am interested in learning how far we could push, via artificial means, the slow-down factor in complicated organisms like mammals. However, taking an entire organ and making all of its cells to go to sleep and then waking all of them up in an organized way seems to be much harder than achieving the same for a single cell. Thus my question: can we, in a reversible and controlled way, slow down the metabolism within a single human cell? What is the maximum slow-down factor then?

What has your own research told you so far? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

@BryanKrause I am not a biologist Sir, I did what I could. Is this acceptable now?

i think you are asking about Cryonics

@aaaaaa not necessarily. From what I know, during cryonics freezing destroys some organelles and it has not been shown to be a reversible process. It is like a fancy way to die. Could others confirm this?

While the main idea of your question is on-topic in biology, your question itself tends to be opinion based (if something is possible in future). Not only bacteria and tardigrades (as pointed out by @user1136) but also many kinds of human cells can be frozen and revived successfully (a lot of them die in this process of course). Nematode worms can also be frozen and revived successfully (Wormbase). Freezing and reviving large complex organisms has not been attempted successfully.


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Did the number of rods changed from ancient time?
Correct me if I am wrong, but I know that rods work under limited light conditions only.
But now we are in a world that always have lights everywhere unlike ancient time when humans had to deal with darkness.
I also know that the humans adapt to its living conditions.
Since our eye only uses the cones and don't use rods often, will the number of rods decrease because of this?

Such evolutionary changes happen very slow - and the availability of light happened very recently in evolutionary terms. So if such a adaptation happens, it will take quite a while to happen. If at all.

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


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Who gives a newly discovered microbe its name?
Assuming a hitherto unknown microbe is found - who gives it its name?

I sthere any reason for your question to be specific to microbes? Whether a microbe or multi-cellular organism is found, the problem is the same. Who name it?

Who name it?

Whoever discovered it. Of course, discovering a new species is not as easy as just taking a picture. One has to provide a very thorough description of the species morphology and eventually argue that it should be considered as a new species and not just as a subspecies or something else. See here for discussion on the definition of a species.

How does the discoverer name it?

If the new species is considered part of an already existing genus, then the author has to keep the genus name. The species name the author chooses is mainly to up himself / herself. Consider for example Macrocarpaea dies-viridis (dies-viridis means "green day") was named like this because the researchers were listening to Greenday when they found it!

I know someone who found the first trilobite in a particular stratum in China and was able to name it Han solo. (https://en.wikipedia.org/wiki/Han_%28trilobite%29)

The person who discovers it. Or, maybe more precisely, the person who tells other people that they discovered it.
Journals and societies may have restrictions or guidelines on how those names are chosen, which certainly has some practical implications for the naming. Here is one example from the Journal of Clinical Microbiology:

For guidelines regarding new names and descriptions of new genera and species, see the articles by Tindall (Int J Syst Bacteriol 49:1309-1312, 1999) and Stackebrandt et al. (Int J Syst Evol Microbiol 52:1043-1047, 2002). To validate new names and/or combinations, authors must submit three copies of their published article to the International Journal of Systematic and Evolutionary Microbiology.
It is recommended that a strain be deposited in at least two recognized culture collections in different countries when that strain is necessary for the description of a new taxon (Int J Syst Evol Microbiol 50:2239-2244, 2000).
Since the classification of fungi is not complete, it is the responsibility of the author to determine the accepted binomial for a given organism. Sources for these names include The Yeasts: a Taxonomic Study, 5th ed. (C. P. Kurtzman , J. W. Fell, and T. Boekhout, ed., Elsevier Science, Amsterdam, Netherlands, 2011), and Dictionary of the Fungi, 10th ed. (P. M. Kirk, P. F. Cannon, D. W. Minter, and J. A. Stalpers, ed., CABI International, Wallingford, Oxfordshire, United Kingdom, 2008); see also http://www.speciesfungorum.org/Names/Fundic.asp.
Names used for viruses should be those approved by the International Committee on Taxonomy of Viruses (ICTV) and reported on the ICTV Virus Taxonomy website. In addition, the recommendations of the ICTV regarding the use of species names should generally be followed: when the entire species is discussed as a taxonomic entity, the species name, as with other taxa, is italic and has the first letter and any proper nouns capitalized (e.g., Tobacco mosaic virus, Murray Valley encephalitis virus). When the behavior or manipulation of individual viruses is discussed, the vernacular (e.g., tobacco mosaic virus, Murray Valley encephalitis virus) should be used. If desired, synonyms may be added parenthetically when the name is first mentioned. Approved generic (or group) and family names may also be used.
Microorganisms, viruses, and plasmids should be given designations consisting of letters and serial numbers. It is generally advisable to include a worker's initials or a descriptive symbol of locale or laboratory, etc., in the designation. Each new strain, mutant, isolate, or derivative should be given a new (serial) designation. This designation should be distinct from those of the genotype and phenotype, and italicized genotypic and phenotypic symbols should not be included. Plasmids are named with a lowercase "p" followed by the designation in uppercase letters and numbers. To avoid the use of the same designation as that of a widely used strain or plasmid, check the designation against a publication database such as Medline.

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


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Starting to learn biology
Well, I've not any biological background but I feel interested towards it. Can you biologists suggest me how to start? Like, from where I can start learning it, from the basic level.
I'm from engineering and physics background.
Edit- I was advised to add the fields of biology that interest me.
I would like to learn microbiology, genetics and plant biology. I should mention that I've very little to no knowledge in biology. So, advise me how to get started from basics. I really have no idea how and from where to start.

Biology is a broad field. What exactly is interesting to you? Identification of plants or animals? Genetics? Ecology?...

Things like microbiology, genetics, biology of plants and such things.


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If we can make magic bullets that are basically artificial antibodies, why has a cure for cancer not yet been developed?
So protonsil and salvarsan 606 where both used as the first magic bullets in the modern period of medicine in the 1900s. However, if we can create artificial antibodies that target specific diseases how have we not come up with a cure for cancer? It seems it shouldn't be that difficult. But if we COULD create artificial antibodies that target cancerous cells would we be able to do it effectively without the drug having any bad or quite noticeable side effects on the body?
By the looks of it chemotherapy is the closest we have gotten so far in chemical drugs, but it does have some nasty side effects.
I was aware of 5 of the approved treatments.
However each type of cancer is similar but different, would it be ever possible to create a generic treatment?
Edit: I have found something interesting, scientist have come across a way to change the antigen on a cell however it is not fully understood.

The Wikipedia article on cancer immunotherapy includes 9 different US FDA-approved anti-cancer antibody treatments. Can you clarify if your question is because you were unaware of these treatments or if you have some other question?

Adding to @BryanKrause comment: These therapies often show spectacular results in the patients where they work, but it is not yet understood, why they don't do this in all the patients.

To over-simplify is bit, the problem is that cancer is not caused by foreign agents like bacteria or viruses, it is caused by a small change in the body's own cells.  It's thus very difficult to create antibodies that recognize the cancer cells as "foreign".

This is a good question.
The first answer is that there are antibody therapeutics for cancer.
These fall into two categories which I will call therapeutic and immunotherapy (this is not typical naming but, keeping it simple they will do).
Therapeutic antibodies are designed to bind to an enzyme or signalling protein that will weaken the tumor specifically.  An example is an antibody to nutrient intake receptors (cancers eat a lot more than other cells). HER2 is a receptor that is heavily populated on breast cancer tissue.  Antibodies that inhibit HER2 activity can slow the growth of breast cancer specifically with minimal toxic effects.
There are also antibodies to proteins found only on cancer cells.  These can be specific antibodies (monoclonal antibodies) to proteins from a mutation that only the cancer cell has.


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Why does hypocalcaemia cause increased muscle contraction?
Calcium is needed for  muscle contraction, so how does hypocalcaemia cause increased sustained contraction?

Consider the pathophysiology of tetany, which is the involuntary contraction of muscles caused by hypocalcemia.
From the tetany wikipedia page:

Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells and hypocalcemia effectively increases resting potential (rendering the cells more excitable) since less positive charge is present extracellularly. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required).

So, when Ca2+ levels are low, action potentials are spontaneously generated, leading to muscle contraction.


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Are peppers on the same plant genetically identical?
I'm a hot pepper growing enthusiast and on one unknown super hot cross there is significant variation in pod size and shape.
What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?
Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?
Appreciate any input!

Hello and welcome at Biology SE! Please take the tour to see how to ask a good question. You have multiple questions in a single post. Can you please narrow it down, clarify your example a little bit. Thank you!

Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?

Phenotypes are the quantitative or qualitative characteristics that arise from the interaction of an organism's genetics with the environment.  For pepper plants, height is a phenotype, as are leaf color, average fruit weight, and pretty much every other characteristic you can measure. Capsaicin concentration (mass of capsaicin per unit mass of fruit) is a phenotype that is relevant to hot pepper enthusiasts.

What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?

It's hard to know.  There could be a genetic component that results in inequitable distribution of resources to individual fruits during plant development. There could be environmental factors that determine why one fruit is larger than another -- perhaps the larger fruit developed during a time when water and sunlight were plentiful to the plant.

Are peppers on the same plant genetically identical?

See this excellent answer given by mgkrebbs to the question Are the seeds in a single capsicum fruit genetically identical?


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Why do doctors reccommend vegetable oils in high cholesterol and cardiovascular disease?
As there is high cholesterol in body why the patient need more fats and why the doctors are recommending it
Transcribed:

Vegetable oils are rich in polyunsaturated fatty acids (PUFA). The fatty acids present in such oils have more than one double bonds. Doctors recommend such oils to patients suffering from high blood cholesterol or cardiovascular diseases. This helps in lowering the cholesterol level in blood. When vegetable oils are hydrogenated, the unsaturated fatty acids become saturated and the oil changes to solid fat (vanaspati and margarine).

source please it will improve your question.

The subtext of the textbook excerpt quoted above is that when people are eating vegetable oil, they are not eating other fat sources. Saturated fats increase LDL levels, and unsaturated fats do not.
A C Beynen, M B Katan, Why do polyunsaturated fatty acids lower serum cholesterol?, The American Journal of Clinical Nutrition, Volume 42, Issue 3, September 1985, Pages 560–563.

Replacement of saturated by polyunsaturated fatty acids in the diet may lower serum very low-density and low-density lipoprotein concentrations because the liver preferentially converts polyunsaturated fatty acids into ketone bodies instead of into very low-density lipoprotein triglycerides. Thus unlike saturated fatty acids, polyunsaturated fatty acids are transported to the tissues for oxidation without leaving a trail of lipoprotein remnants in the form of low-density lipoproteins.


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What's the process for determining whether a GC -> AT conversion in bisulfite sequencing is due to degradation?
I'm working on an ancient DNA project (humans) examining the methylation patterns for a single nuclear gene on chromosome 5. I understand the protocols of bisulfite sequencing, and in general how the methylation is identified from the sequence results, but due the degradation in ancient DNA, some methylated cytosines may become deaminated to thymines, creating a GC->AT conversion. Since bisulfite sequencing allows for all retained C's to be classified as methylated in the original sequence, I'll be underestimating methylation depending on how degraded the samples are. Is there a way to address this?


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How dissimilar are the fingerprints of identical twins?
It is a very well-known fact, stated multiple times even in this Stack Exchange, that identical twins have different fingerprints. However, to what specific extents, and in what specific ways, do the sets of fingerprints of identical twins typically differ? Are the differences usually very minor (e.g., just a few stray loops and whorls here and there)? Are they perceptibly different but still fairly similar, with the similarities most likely stemming from heredity and/or cultural ties? Or does the determination of fingerprint patterns behave similarly to a uniformly weighted random number generator, with the fingerprint sets of twins being just as different as those of two people born on opposite sides of the world?
Obviously, due to the random/probabilistic nature of this feature, there may be no single answer to this question — there may be cases where one pair of twins has fingerprints that are more similar than those of another pair. But does anyone know what typical similarities and differences are present between the fingerprint sets of identical twins, and, if possible, the biological causes of such similarities and differences?

Identical twin fingerprints are different, but generally more similar than to random people.  For example:

Fingerprint recognition with identical twins is a challenging task due to the closest genetics-based relationship existing in the identical twins ... Srihari et al. [6] analyzed the similarity between twins' fingerprints in a study using fingerprint images from 298 pairs of twins. The authors analyzed this similarity using two-level features. With the features of level 1, they found that twins' fingers are much more likely (55%) to have the same pattern type than non-twins' fingers (32%). With the features of level 2, they concluded that the similarity between the fingerprints from twin fingers is higher than from two arbitrary fingers.

Fingerprint Recognition with Identical Twin Fingerprints

Dermatoglyphic asymmetry and diversity traits from a large number of twins (MZ and DZ) were analyzed based on principal factors to evaluate genetic effects and common familial environmental influences on twin data by the use of maximum likelihood-based Variance decomposition analysis. ... The present results are similar with the earlier results of finger ridge count diversity in twin data, which suggested that finger ridge count diversity is under genetic control.

--Inheritance of dermatoglyphic asymmetry and diversity traits in twins based on factor: variance decomposition analysis

Upvoted especially for the use of the word "dermatoglyphic", whose plural is the longest word in the English language with no repeated letters.


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How many different proteins are able to form prions?
The Wikipedia article on prions and other sources seem to only talk about variants of PrP protein.
I think I remember a previous version of Wikipedia saying something about another protein able to form a prion.
I know there are prion-like proteins, but for this question, I want proteins that are able to form true prions. It does not matter if the protein does not form prions in humans specifically, but does in other organisms.

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

@tyersome I tried searching, but it just ends up with a bunch of information of PrP, because there does not seem to be much interest in the others or how many there are.

No time to write a real answer but for the diversity see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5131755/ The 2nd prion thing you might have heard of may have to do with Alzheimer's https://www.ucsf.edu/news/2019/05/414326/alzheimers-disease-double-prion-disorder-study-shows I think it's still controversial.

@Fizz I think it was Doppel protein which I remember, which is called Prion protein 2. It is similar and takes a bigger role in PrP null mice. No idea why researchers didn't try knocking it out too.  https://en.wikipedia.org/wiki/PRND


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Is it OK to use predicted protein sequences from RefSeq for protein sequence alignment?
I'm doing a project, and my goal is to do alignments of a particular gene product to see if there is any conservation of secondary structures across different species.
So far, I have found a few from UniProt that are reviewed. I want to add more from different species, but the sequences were all created via AI prediction from a genome sequence.
Can I use those at all or no?

Welcome to Biology.SE! So, you are aligning protein sequences from some species with a known function, and you want to know if it's ok to include proteins from other species that are computationally predicted to have the same function? This is pretty standard practice, though you should expand on what you mean by "AI prediction". HMMs are common tools for searching for proteins with similar structural motifs, is that what you used?

not quite, I am aligning the same gene product from different species. The gene of interest is a human gene and I am searching for homologs. I have found homolog sequences in rat and mouse, which were reviewed and backed by experimental data. If i blast this human gene against xenopus tropicalis, I get a protein sequence that is "predicated by automated computational analysis...derived from a genomic sequence...annotated using gene prediction method: Gnomon, supported by mRNA and EST evidence." I am confused by the wording here...does this protein exist or?

Thanks for the clarification. I suggest editing your question to add the information you've provided in your comment. Concerning your question -- does this protein exist -- you should read up on how Gnomon works.

I did read that link before posting here...and I got the idea that the the answer is highly likely...I also have read the Refseq FAQ regarding the xp prefix (most of my sequences' accession number starts with that since they were all predications)...but I am still unsure...


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blackberry: what morphological features suggested the species epithet "bifrons"?
What morphological features suggested the epithet "bifrons" in Rubus bifrons? The scientific name of the familiar invading species "Himalayan Blackberry" (or "European Blackberry" or "Armenian Blackberry") in the US is Rubus bifrons (with Rubus armeniacus as an alternative if the two species are considered same).

Following the links given in the NCBI Taxonomy Browser, the International Plant Names Index gives the author abbreviation Vest, likely indicating that this species was named by botanist Lorenz Chrysanth von Vest sometime around 1821.

As @acvill pointed out, R. bifrons was named in 1821 by Lorenz Chrysanth von Vest. The original description can be found here (pages 163-164).
The latin bifrons translates to "two faces". I'm not sure, but I suspect this references the leaves of the plant, with the upper surfaces being dark green and the lower white (or much lighter)

Foliis subrotundo-ovatis subtus albentibus saepe villosis, tenue et confertim serratis...

[Leaves roundish-ovate, whitish on the underside, often villous
thin and serrate...]

However, I can't translate his comments after the description, so maybe there is another explanation included there.

As far as I can see, nothing in Vest’s comments offers any further explanation of bifrons.  The Latin description reads in full: ‘Foliis subrotundo–ovatis subtus albentibus saepe villosis, tenue et confertium serratis, caulium fertilium plerumque teretibus, caule tereti rarius per intervalla subangulato, aculeis validis rectis, petalis obovatis stamina subaequantibus.’ — I don’t know botanical Latin enough to properly translate it, but nothing seems more relevant than the part you already translate.  [cont’d]

The German note reads: ‘Er ist häufig in den Wäldern um Gräß, und wird gewöhnlich für den R.fructicosus gehalten, der ein aufrechter Strauch ist, mit eckigem Stamme und krummen Dornen u.s.w. der unsrige liegt am Boden, sowohl der blühende Stamm, als der unfruchtbare (flagellum, stolo).’ — this translates roughly as ‘It is common in the woods around Gräß, and is commonly mistaken for R. fructicosus, which is an upright shrub with square stem and crooked thorns etc., whereas ours [i.e. R. bifrons, I guess] lies on the ground, the flowering and non-flowering stem alike.’


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How did plaques form in Salvador Luria's Bacteriophage experiment (discovery of restriction enzymes)?
I was watching Eric Lander's lecture online describing Luria's experiment (see below for link), and I couldn't understand how plaques form. From my understanding,

Bacteriophage infect strain B
Viral DNA is incorporated
Restriction enzymes cut out viral DNA (mostly)
Some viral DNA is methylated before step 3 occurs.

At this point, to replicate, we would need the infected bacteria to produce more bacteriophage to infect nearby virus. However, due to step 3, the newly incorporated viral DNA will be cut out through restriction enzymes. So in my mind, we only have one bacteria with viral DNA (along with its descendants).
So how does the plaque form?
https://youtu.be/_TdJBLu6hPc?t=890

In the experiment, the genetic material of a single bacteriophage was, by chance, methylated and thus protected from restriction. In order for the phage to propagate, this DNA must be replicated within the cell. Before replication, the phage DNA is methylated on both strands of the recognition palindrome. During replication, the strands are separated and used as templates for DNA synthesis. The methylation is retained in the parent strands, leading to a condition of hemimethylation in the replicated duplex. This hemimethylated DNA is protected from restriction, allowing time for the daughter strand to be methylated (this is the same mechanism by which the bacterial DNA itself is protected after replication). In other words, once the phage DNA is methylated, the bacterial cell no longer recognizes it as foreign and continues to propagate the methylation through subsequent rounds of replication.
Jen-Jacobson L, Engler LE, Lesser DR, Kurpiewski MR, Yee C, McVerry B. 1996. Structural adaptations in the interaction of EcoRI endonuclease with methylated GAATTC sites. EMBO J 15(11):2870-2882.

...our data for the hemimethylated GAmATTC site show that [the rate of cleavage of the unmethylated strand] is reduced only -330-fold relative to an unmodified GAATTC site. ...this would seem to be an inadequate degree of protection, taken alone, during the transient existence of such hemimethylated sites in vivo after DNA replication. Even if a hemimethylated site were to suffer a single-strand nick in the unmethylated DNA strand, however, it is very unlikely that this would progress to double-strand cleavage because the [rate] for the second cut (in the methylated strand) is reduced by 4200-fold. This rate is so slow that the endonuclease would dissociate from the nicked DNA before making such a second-strand cut, and the single-strand nick would then be repaired by DNA ligase.

[image source]
Note that the lecture mentions the sequence GAATTC, which is the recognition site of the type II restriction enzyme EcoRI (discussed above). This enzyme is naturally found in E. coli RY13. In their 1952 paper, Luria and Human used E. coli B, which does not have type II restriction modification systems. Rather, the effect observed was probably due to a type I restriction modification system (EcoB in this case). In such systems, hemimethylation not only reduces nuclease activity but also increases methylase activity, thus actively protecting newly replicated DNA.
Vovis GF, Horiuchi K, Zinder ND. 1974. Kinetics of methylation of DNA by a restriction endonuclease from Escherichia coli B. Proc Natl Acad Sci USA 71(10):3810-3813.

In E. coli B, the DNA immediately after replication should possess only [hemimethylated] sites. Such sites must be modified rapidly. If not, another round of DNA replication would yield some completely unmodified [recognition] sites which would make the DNA susceptible to restriction. On the other hand, if bacterial or viral DNA synthesized in a foreign bacterium should enter E. coli B, it would do so with unmodified [recognition] sites. These sites would be expected to be poor substrates for methylation but excellent ones for eliciting restriction, the appropriate protective reaction. The in vitro action of... EcoB, i.e., rapid restriction but very slow methylation of molecules with unmodified [recognition] sites and rapid methylation but no restriction of molecules with [hemimethylated] sites, is entirely consistent with the above in vivo scenario and suggests that this enzyme is responsible for both restriction and modification in vivo.

I don't know if this increased methylase activity on hemimethylated DNA also occurs type II systems, which have separate nuclease and methylase enzymes.

This indeed a very interesting experiment. In the lecture, you can see that the obvious explanation for the initial inhability to grow in strain B indicates that the bacteria is resistant to the virus. However, ocassionally, a virus is able to form a plaque in strain B, which initially seems to indicate that it mutated. However, in a second passage from Strain A to Strain B of this initial "mutant", we observe that there are no plaques in Strain B. This indicated that something beyond the DNA (unlike a mutation) was at play, and eventually led to the discovery of these epigenetic markers (methylation) that are made by the machinery of the bacteria (thus, Strain A lacked such machinery, so it maintained the viral DNA but did not mark it as 'viral').
Because these experiments occurr in Petri dishes, where there are millions of cells (billions, in fact), there is always some probability that the restriction machinery does not work. This probability (small, but detectable) of no detection is what is observed in the "original" plaque formed in Strain B. In addtion, when the virus is just added, it is still not marked, so it needs some time to be marked (more cell replication cycles), and during this time the virus can be infective. Either of these possibilities will produce a small fraction of plaques in Strain B.


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Examples of things that are undefined in terms of living and non-living
I'm putting together a class on basic biology for kids and I will discuss living and non-living.
I'm looking for examples of things which are undefined in terms of living and non-living, if there are any.
People expect viruses to be alive but they are defined as non-living. Other examples of things that go against intuition are also welcome. Or things which were once classified one way and later redefined.
I couldn't find anything online.

Viruses are not undefined - they are seen as non-living.

@Chris: Most people who study viruses consider them to be living organisms. Many consider bacterial plasmids to be alive, along with other transmissable genetic elements.

Does this answer your question? Is there any definition of life which makes viruses undeterminable?

relevant xkcd: Alive or Not

@user1136 Haha :)

People expect viruses to be alive but they are defined as non-living.

This is actually one of the most widespread misconceptions I see. I think it's just one of those interesting but dubious factoids that spreads around in dinner party conversations. There certainly are some who take that position. But, after 11+ years of formal university education in biology, I can't think of a single professor or colleague who firmly embraced the position that viruses are non-living. Most (including myself) have been firmly in the camp that viruses are, in fact, alive. And the rest are more-or-less agnostic or ambivalent on the topic.
There's an intesting mini-debate between experts on the subject found here, I'll share this quote from one of the participants below because I think it's on point.

"In many ways whether viruses are living or non-living entities is a moot philosophical point."

There isn't one single, universally accepted definition of life. So ultimately, the answer to whether viruses are living or not will depend on ones chosen definition, and that's the case with most other controversial things.
However, viruses are unquestionably classified as biological replicators. There's a review on that topic (found here). It also includes discussions of other replicators which some experts also think of as living entities (but many don't). Examples include certain genetic elements like plasmid and integrons.
One notable exception that I didn't see mentioned in that review is prions. The first virology professor I ever had strongly advocated definitions of life that were inclusive of prions, but I haven't found that position quite as common among other academics. I'm a bit more agnostic on the prion debate, because it's hard to find prion-inclusive definitions of life that arean't also inclusive of something like an inorganic crystal.
The problem is that scientists like consistent definitions that don't have lots of exceptions, or require us to split existing categories. Between viruses, plasmids, and prions, there's a lot to talk about in terms of what characteristics they share with other life forms and what they lack that makes some question their classification. It's also interesting to consider whether any of the attributes common to living things occur in silico (or if they could in the future).

It's kind of contradictory that you use dismissing language such as "widespread misconception" and "dubious factoid", but then cite a debate article because to whom is the paper targeted to if not to experts with opposing view points? And calling it a moot point because there is no universal agreement is counterproductive as there aren't many thoughts that are universally agreed upon. It's like saying studying phylogeny is pointless because my next door neighbour believes in creationism.

Also your post puts a lot of emphasis on replication although it's not a key necessary trait of living things. A yeast cell with a temperature sensitive allele of a telomere capping protein will arrest permanently in stationary phase at a restrictive temperature unable to divide. Humans can become sterile in their lifetime. Both of those are incapable of reproducing, yet are unambiguously living things. Conversely if the vegetative yeast cell or the human completely lack metabolic activity they are unambiguously dead. Metabolism is a more important criterion.

@Cell. It is a widespread misconception that viruses are non-living, not becuase it's false, but because it isn't settled fact (which is how it was framed in the question above). I never implied that sterile humans weren't alive, I merely referenced one classification encompassing viruses and other biological entities. I'd happily reply to your critiques point-by-point, but I don't think the comments are an appropriate place for it. If you find my answer factually inaccurate, please specify where and I'll try to fix it. If you find it incomplete, consider writing your own.


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How many signals can one neuron send and/or receive simultaneously?
I've been researching this question online and finding opposing answers. Some articles say that one neuron can only send one signal at a time while others says that one neuron can send more than one signal.
What is the the exact answer, if it is a known fact in biology? If both cases are there, is a typical neuron in our brain sending one signal at this time or "multitasking"? Does the answer depend on the type of neuron?
Even further, if each neuron is sending more than one signal at a time, what would that imply to our current medical detections of brain? Can different signals happening at the same time be distinguished at all with our technology of detection and brain scanning?

It would be helpful if you provided more information about what you read - where did you read it, and can you provide a short quote of what was said?

I'd also ask you to clarify what you mean by "medical detections of brain"... no clinical uses of brain activity care about single-neuron stuff.

You're asking a pretty broad question here. Basically it's asking for a mini-course on how the different types of neurons work. Please narrow it down to a specific question, and your last question as already been answered by @BryanKrause. While every neuron is important, we can only examine/detect large groups of neurons at work.

A typical neuron receives in parallel many signals, both excitatory and inhibitory, from many different sources (usually other neurons). At any given time, if excitation exceeds a certain threshold, the neuron fires a single outgoing signal (the so-called action potential).
Thus, the simplest possible answer to the first part of your question is that neurons can only send out a single signal at a time. However,

each action potential is distributed to many targets at once (usually other neurons)
a single action potential is hardly meaningful as a signal; instead, the firing rate, i.e. the frequency of outgoing signals, is regarded as the most fundamental (but not the only) neural code.

For example, a neuron along a sensory pathway might respond with a barrage of several hundred action potentials to the onset of an appropriate stimulus (a sound, a blinking light, a touch on the skin, etc.). In turn, these signals would be transmitted to many other neurons, and so on.
Mind you, this concise description barely scratches the surface of an immensely complex topic. As mentioned in the comments, the question as a whole is too broad and ill-defined.


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How do non-ionic polymers help precipitate proteins?
Some non-ionic polymers (e.g. chitosan and polyethylene glycol) are also commonly used as protein precipitating agents. What is the principle of protein precipitation resulting from the addition of these polymers? Is this type of precipitation reaction a reversible or non-reversible precipitation?

Perhaps a bit too technical, but would this answer your question? At least in part?

Two interpretations of such precipitation events have been proposeda while ago according to the paper above: attractive depletion (Asakura & Oosawa, 1958) and excluded volume (Iverius and Laurent, 1967, Polson, 1977). These are discussed there too!

Protein precipitation by these non-ionic polymer is based on the principle of steric hindrance. These polymers compete with proteins (Mahadevan, 1992) for space in the solvent. Congestion caused by the physical presence of surrounding polymers force the proteins to exclude from region occupied by the polymers and concentrate together until their solubility is exceeded (Atha & Ingham, 1981). In this case, protein precipitation occurs.

"Steric hindrance" is usually invoked in the context of molecular shape as it relates to chemical or enzymatic reactions, i.e. how the relative organization of atoms in a molecule constrains the shape space of that molecule. I'm not sure if it's the right term to use in discussion of this system, but I'm open to differing opinions.

Moreover, your answer could be improved by replacing some of your terms with more concrete explanations of the physical interactions. Re: what electrostatic phenomena underlie polymers competing with proteins and congesting the solvent space? There is also a minor logical jump from exceeding solubility to protein precipitation that could be addressed.

@acvill - yeah, this is mechanism is molecular crowding, not steric hindrance


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Limitations of 16S rRNA sequencing
Looking at the microbiome analysis literature there seems to have been a shift away from 16S rRNA sequencing analysis toward shotgun sequencing of the whole genome. While the motivation given is typically that there is more information obtained by the latter, I am curious about the actual limitation of 16S rRNA analysis. Is the problem that:

There is simply no variation in the 16S rRNA gene between different species/strains that it would be useful to tell apart for a more accurate analysis.
There is some variation that would be useful, but the noise in the current sequencing methods and the capacity of the current computational analytic techniques are not able to capture it.
There is some variation that would be useful, but it is not clear how this correlates with the phenotype it would predict therefore scientists prefer to use shotgun sequencing to investigate causal relationships between genome and phenotype.
Something else (please explain!)

Thank you very much

Ask yourself and then tell us what the objective is of the sequencing in the two cases? Is it the same in the two cases? You should also find out how long the two techniques have been available. This will provide a better basis for your attempts at an explanation.

There is simply no variation in the 16S rRNA gene between different species/strains that it would be useful to tell apart for a more accurate analysis.

The amount of sequence variation depends on the region of the 16S rRNA gene amplified, and the choice of region depends on the desired universality of your primers as well as the read length constraints of the sequencing platform. Put simply, choice of target for 16S amplicon sequencing is a tradeoff between breadth and specificity. Typically, 16S sequencing connotes the use of primers targeting the V3, V4, and/or V5 regions of the 16S gene. Such primers are often optimized for taxonomic breadth (i.e. to differentiate as many organisms as possible) and designed to create amplicons that are readily sequenced on an Illumina platform.1 Thus, strain-level differentiation is limited in vanilla 16S analyses, though use of a multi-region framework can greatly increase phylogenetic resolution.2

There is some variation that would be useful, but the noise in the current sequencing methods and the capacity of the current computational analytic techniques are not able to capture it.

Modern short-read sequencing platforms (primarily Illumina) are considered quite robust in terms of sequencing error rates. However, for amplicon sequencing techniques like 16S, the per-base error rate might exceed the expected relative abundance of low-abundance organisms, making their detection and differentiation tricky.3

There is some variation that would be useful, but it is not clear how this correlates with the phenotype it would predict therefore scientists prefer to use shotgun sequencing to investigate causal relationships between genome and phenotype.

You've identified the major benefit of metagenomic / shotgun sequencing over 16S amplicon sequencing. When you are trying to extrapolate microbiome functions from 16S data, you are constrained by the existing phenotype-to-phylogeny mappings that are present in your databases. With databases of sufficient size, such analyses can give very good estimates of microbiome function.4,5 That said, strains that are closely related at the 16S level may have very different functional profiles due the inherent flexibility of bacterial genomes. Increasingly, pan-genomics is revealing that the so-called "peripheral genome" carries genes of consequential function, and the carriage of such genes in a particular strain cannot be detected by 16S amplicon sequencing alone.6

References

Caporaso JG, Lauber CL, Walters WA, Berg-Lyons D, Lozupone CA, Turnbaugh PJ, Fierer N, Knight R. Global patterns of 16S rRNA diversity at a depth of millions of sequences per sample. Proc Natl Acad Sci U S A. 2011 Mar 15;108 Suppl 1(Suppl 1):4516-22.
Fuks G, Elgart M, Amir A, Zeisel A, Turnbaugh PJ, Soen Y, Shental N. Combining 16S rRNA gene variable regions enables high-resolution microbial community profiling. Microbiome. 2018 Jan 26;6(1):17.
Schirmer M, Ijaz UZ, D'Amore R, Hall N, Sloan WT, Quince C. Insight into biases and sequencing errors for amplicon sequencing with the Illumina MiSeq platform. Nucleic Acids Res. 2015 Mar 31;43(6):e37.
Langille MG, Zaneveld J, Caporaso JG, McDonald D, Knights D, Reyes JA, Clemente JC, Burkepile DE, Vega Thurber RL, Knight R, Beiko RG, Huttenhower C. Predictive functional profiling of microbial communities using 16S rRNA marker gene sequences. Nat Biotechnol. 2013 Sep;31(9):814-21.
Wemheuer F, Taylor JA, Daniel R, Johnston E, Meinicke P, Thomas T, Wemheuer B. Tax4Fun2: prediction of habitat-specific functional profiles and functional redundancy based on 16S rRNA gene sequences. Environ Microbiome. 2020 May 18;15(1):11.
Gordienko EN, Kazanov MD, Gelfand MS. Evolution of pan-genomes of Escherichia coli, Shigella spp., and Salmonella enterica. J Bacteriol. 2013 Jun;195(12):2786-92.

In my experience, the primary impetus is number 3 on your list, but it's also related to number 1. There's a lot you can learn from 16s sequencing, but reviewers want functional data that can help elucidate causal mechanisms. 16s is mostly limited to providing information about the taxonomy of a community. While there are ways of "predicting" the functional capacity of a metagenome from 16s sequences, like PICRUSt, these approaches are reliant on a some shaky assumptions that are baked in to the predictions. This is where it relates back to number 1 on your list. When I was doing my first 16s run on a 454 platform, I recall reading about different E. coli isolates that could have identical 16s genes but genomes that shared less that 50% sequence similarity (don't have source on hand, but will edit post if I find it). So, effectively two strains with identical 16s genes could have substantially different functional capacities, and there's only so much a prediction algorithm can do with that.
Another big driver is the lower cost and improved efficiency of newer sequencing technologies and bioinformatic analysis pipelines. The cost of getting a plate of 16s sequencing done ten years ago was probably comparable to the cost of doing as many high-quality shotgun metagenomes today.

Other answers are excellent by and large.
One point that is left out: 16S copy number itself varies among organisms, which leads to significant analytic complexity for trying to really estimate relative organismal abundance.
As this is the main use case for 16S analysis (using relative 16S OTU/whatever abundance to describe communities), you can see that there are issues with it.
You can still likely learn something from e.g. distance analysis between samples, PCoA plots, etc. Different communities will still look different by these measures. But the copy number itself is not directly interpretable.

This is a good and necessary addition to the existing answers. An important caveat to 16S

"As this is the main use case for 16S analysis…". Really? What is your basis for saying that? And please don't use terms like "use case" that are borrowed from computing science where more straightforward English would be more accurate and more comprehensible to biologists.

@David As someone in the field, I can affirm Maximilian’s statement that 16S amplicon sequencing is most commonly used to estimate species relative abundance in environmental and host-associated samples. Though if you have insight into it’s historical use for other analyses, I think that would be good to add.

In addition to the points raised in the other answers, organisms like bacteria frequently engage in horizontal transfer of genetic material.
This means that the relationships between organisms are more complex  than the relationships between the stable core elements like ribosomal RNA (see, for example the mosaic genome of Rickettsia felis). Focusing on only 16S rRNA thus gives only part of the story and can be highly misleading.

But horizontal transfer never affects ribosomal RNA, which is why it is suited for phylogeny. However as the poster doesn’t say we don’t know whether that is what he is talking about, and it would be better to ignore his question until it becomes worth answering.

@David My point is that phylogeny itself can become a fuzzy notion for microbes. I've added a linked example to illustrate the point.

@David: HGT does seem to affect the 16S (not at as high a rate as other loci, of course). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC296235/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558861/, https://www.frontiersin.org/articles/10.3389/fmicb.2017.02225/full

I think that the HGT fuzziness is a good thing to keep in mind, however this is not really solved by shotgun metagenomics! You are still kind of trusting the central tendency of the tree for each gene independently.


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When I use isopentane to freeze tissue, which kind of purity should I choose? GR, AR, or CP?
GR: Guaranteed Reagent
AR: Analytical Reagent
CP: Chemical Reagent

I want to use  mouse liver, brain and freeze the complete organs at -80℃.

You would like to prevent the formation of ice crystals?

Depends on what you are doing with the frozen tissues. If you're flash freezing for histology, it probably doesn't matter. If you're doing some kind of metabolite extractions for analysis, you'll probably want to use a reagent suitable for HPLC or mass spec (probably AR in this case, but many manufacturers will sell products described as HPLC grade).

Those reagent 'grade' labels are done by manufacturer and are not standardized; see some examples:
https://chemistry.stackexchange.com/questions/575/what-do-the-different-grades-of-chemicals-mean
https://www.emdmillipore.com/US/en/lab-technical-resources/grade-definitions/c9Ob.qB.r7MAAAFEgSYWq.DI,nav
https://www.avantorsciences.com/pages/en/grade-definitions
https://www.westlab.com/blog/2018/04/06/a-guide-to-chemicals-and-chemical-grades
Some companies break these down into very fine scales. Personally, I think about them in roughly 3 grades: 1) ultrapure reagents that are the best of the best, used for the most delicate protocols; these come with a huge price premium, 2) normal academic laboratory grades that are as pure as is efficient - the specific purity depends on the chemical and how separable it is from contaminants, and 3) junk grade for budget experiments in teaching labs. I'm sure other people will bicker with me over this, but it's the system I've always kept in my head when ordering. I'm not certain in all cases that the actual contents you will receive are any different among some of the grades, depending on manufacturing practices it's more about what has been tested.
I don't know if your three grades listed are going to fit into these three categories that I personally came up with, but I'd probably put your GR and AR together in that second/middle grade; CR might belong in the third.
That said, I don't think the purity is going to matter much between those grades for your use; don't spend 3-10X the cost to get something more pure, I'd select something from my "middle" grade. Your samples themselves aren't "pure", and you're not really using isopentane as a reagent in a reaction but instead as a liquid interface for transferring temperature. Higher grades are probably more free of water and other contaminants, but the stuff you pour out is going to get filled with (small amounts of) water from the atmosphere anyways while you chill it. I've never seen a freezing protocol that was explicit about needing to use a very high purity of isopentane.


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Has there been evidence that there has been coevolution in E. Coli strains with the T4 bacteriophage?
According to Evolution of T4-related phages, there have been multiple instances of evolution in the T4 coliphages. Per the article, there are many T-even phages that have insertions from other coliphages. Per Oechslin's paper, different bacteriophages have different effects with different strains of E. Coli. Has there been evidence that there has been coevolution in E. Coli strains with the T4 bacteriophage? I have found a paper on the coevolution of E. Coli and PP01 at Coevolution of bacteriophage PP01 and Escherichia coli O157:H7 in continuous culture. Still, I have not found any information regarding T4 coliphages and their coevolution with E. Coli.

High-level answer: Yes. Almost by definition there might have to be coevolution between a phage and a host, in the same way that humans coevolve with our viruses (in the form of e.g. immune repertoire). Pathogens kill/disadvantage susceptible hosts, imposing a selective cost to susceptibility.
Detailed answer: Yes. E. coli has CRISPR arrays that target T4, and T4 has mechanisms for escaping CRISPR processing by E. coli. This is pretty textbook coevolutionary arms race. This is reflected somewhat in the different host ranges of phage, as you suggest.


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homologous recombination and non-homologous recombination ratio during S-phase
Can I assume that it is easier to do targeted gene knock-in in rapidly dividing cells because they should have a short period of G1? Is there an easy way to measure the relative amounts of homologous recombination (HR) and non-homologous end joining (NHEJ) during the S and G2 phases? Is HR favored over NHEJ during S-phase for all cell types?


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In lichen, do the fungi consume the oxygen produced by algae?
Is the oxygen produced by algae in photosynthesis consumed by the fungi, specifically in marine lichens where oxygen is less abundant? I am wondering this because of a speculative evolution project.

Exchange of gases between lichen symbionts has been demonstrated for Flavoparmelia caperata. Note that this is a foliose lichen species, though the findings may be generalizable to marine lichen.

We discovered the first evidence that photosynthetic O2 and respiratory CO2 mutually power the lichen symbiosis, together with the previously recognized exchange of Calvin-cycle sugars and water.

Ten Veldhuis MC, Ananyev G, Dismukes GC. Symbiosis extended: exchange of photosynthetic O2 and fungal-respired CO2 mutually power metabolism of lichen symbionts. Photosynth Res. 2020 Mar;143(3):287-299.

Thank you! This was very helpful

@katzenklavier if mine was indeed a helpful answer, I would appreciate if it was accepted. Seeing no other answers in the weeks since this was posted, I think this is reasonable.

done, sorry, I'm not to knowledgeable about this site


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Detection of bacteria to measure quality of water
I have been working on a science project were I have built a water filter.
To prove that it works I would need to test if there are bacteria in a sample which has been treated vs a sample that hasn't been treated.
I really just need to know if there are bacteria not how many. I looking to do this at home.

Put your filter on a nice and rich medium in a petri-dich and it will give you an idea of whether there are bacteria. Fitlering different amount of water will allow you to quantify. There are always potential bacteria you will not be able to grow on this specific medium and therefore it is pretty much impossible to really prove that something is completely sterile.

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

There are many techniques. You should add some details to narrow down the question, which include- the available infrastructure, ease of experimentation, monetary budget, time required for analysis and other relevant information.

There are many ways to do this. User Grb's answer is good but his method requires access to equipment.
If this is a highschool level project, you could make two Nutrient Agar petri plates. Spread 1 milliliter of unfiltered water on one and 1 milliliter of filtered water on the other. Make sure this is done in a sterile environment (using a Bunsen burner for example). The presence of colonies on your filtered plate would indicate that there are still bacteria in the filtered water.
You can also count the number of colonies on both plates. If there are less colonies on the plate with filtered water, your filter works to a certain extent. If the counts are identical, your filter does not work. If you use colony counts, make sure you repeat the experiment multiple times to obtain statistically rigorous result.

IF you are looking at a much faster technique but don't mind spending a bit and have some research equipment access, there are ways by which bacterial contamination can be detected by measuring ATP (Adenosine tri-phosphate). See this research publication. There are commercial kits available which you can use: Here is one of them by Thermofisher.
Again, this is only if you have access to the research equipments and funds.


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Why isolated, recombinant plasmid DNA without any restriction is often detected in agarose gel electrophoresis as three DNA bands?
I don't understand why three bands are found without any restriction digest. Please answer me as soon as possible.

today, i have seen fourth band first time after plasmid(pNL4-3) isolation

These are the three forms of the plasmid: supercoiled (smallest 3D-structure, runs fastest), linear (runs in the middle) and relaxed, nicked plasmid (runs highest). You can have another fourth band, which is the circular single stranded plasmid (runs faster than the supercoiled version). See the following figure (from this article, which I recommend reading):

Thank you a lot. I have another question,                  How many DNA fragments are generated from a circular plasmid DNA, when this DNA is restricted by EcoRI three times and each of these EcoRI fragments is restricted one time by PstI?

Can you please make this a new question? And if an answer is satisfactory answering your question, can you please accept it? This is a nice gesture towards the people who anwer.

Thank you Dear  Chris. I accepted your ansewr. I got confused again. I found in wikipedia that relaxed plasmid(mentioned that both strand are uncut) is different than open circular(one strand is open). But here both are considered as same. In case of second question, Already I asked as a different question and I didn't get any answer. waiting for response. Thank you


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Which countries do not feature mosquitoes?
Please, I am so itchy, I need to know: which countries are free of mosquitoes?

Iceland is a good choice.

You'll get itchiness due to dry skin if you move to cold places where there are no mosquitoes.

According to India.com, Chris is right and Iceland has been declared mosquito free.
The science behind this is quite interesting and there are various hypotheses regarding as to why Iceland doors are shut to mosquitoes. The most preferred hypothesis by scientists, according to New York Times is >>

When mosquitoes lay eggs in cold weather, the larvae emerge with a
  thaw, allowing them to breed and multiply. Iceland, however, typically
  has three major freezes and thaws a year, creating conditions that may
  be too unstable for the insect’s survival.