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How do place cells switch their response patterns when the subject moves to a different environment?
So I understand that place cells form a map of each environment the subject has been in and responds accordingly in each environment. Question is how do they switch to represent a different environment when the subject moves to a new environment? It seems unlikely that a different set of place cells represent each environment the subject has ever encountered because it seems that would require too many place cells (and since the cell counts in the hippocampus is I presume relatively fixed, "free" place cells run out at some point), so it must be the same place cells "remembering" different response patterns to different environment and responding accordingly in different environments.
From the wikipedia page on place cells: "In a different environment, typically about half the place cells will still have place fields, but these will be in new places unrelated to their former locations."
Muller, R. U.; Kubie, J. L. (1987). "The effects of changes in the environment on the spatial firing of hippocampal complex-spike cells". The Journal of neuroscience : the official journal of the Society for Neuroscience.

Please, to the people who are voting to close: do not vote to close on a question as unclear simply because the question is an area outside of your expertise. It is possible to edit this question slightly to clarify, but this is actually an excellent question and actually provides a fair amount of background information and even includes an external reference.

So I'll try to answer my own question.. Not sure if that's usual but apparently it's allowed.
Ok. I think the question is fundamentally mistaken. Place cells do not "switch" into a different mode when the subject moves to a new environment. Rather, in a new environment, the inputs to these place cells are different, other parts of the brain is telling the hippocampus it is now in a different environment, so naturally, the place cell responds in a different manner. In this sense the place cell is a "computer"  (might be using the word too loosely but hopefully it makes sense), it makes a different output based on information from the senses.
This is my understanding. Hopefully it makes sense.

Imagine a 2x2 grid. Starting on the bottom left, how many different ways can you move to each box of the grid?
Two times: 1) up, right, down; 2) right, up, left
Now, say each of those combinations are used to store the memory of a different location. In order to activate either sequence, a different input signal would be required to tell the axon to send it's initial signal right, or up.
Your eyes will receive a signal in the form up light, and a specific electrical impulse will be sent down the optic nerve that allows your brain to perceive an image.
There are millions of nerves in your brain, and each combination of impulses serves to store a different memory.
Now, imagine a grid that has a million by a million boxes. How many combinations can you use to fill each box?
And, actually if I recall correctly, the hippocampus is one of the few areas in the brain that is consistently undergoes neurogenesis.

This answer does not attempt to answer the question asked: "how do place cells switch their response patterns in different environments?"

"Different input signals"... ie. from a different combination of signals from, what was my example, the optic nerve.

But how are those signals different? The optic nerve isn't rewiring to connect to different cells in visual cortex when you move from one building to another. You are answering the question "How does a radio tune to different stations?" by saying "Well your radio just listens to different stations depending on what you set the dial": it is essentially just re-stating the question, rather than providing an answer.

Do you think the optic nerve consists of a single neuron?

Absolutely not. I should have been more precise in my comment to say "axons of the optic nerve aren't" rather than the shorthand I used.

Then you tell me, why would the optic nerve only be able to conduct one type of signal? As I said, your eyes collect light - light has many different wavelengths. Does it make sense that collecting one wavelength of light would illicit a different response than would be obtained from a second different wavelength?

Let us continue this discussion in chat.

It is true that individual place cells will fire in many different environments.  However, the exact location where a place cell fires will vary in different environments.  Moreover, two place cells that fire in the same location in one environment could fire in completely different locations in a second environment.  Therefore, the pattern of activity of the network as a whole can be unique for each location in each environment.  The term for this scrambling of the association between place cells and locations in different environments is called "global remapping".
Try: L. L. Colgin, E. I. Moser, M.-B. Moser, Trends Neurosci. 31, 469–77 (2008). for a review.  http://www.cell.com/trends/neurosciences/abstract/S0166-2236(08)00167-7?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0166223608001677%3Fshowall%3Dtrue

why the downvote?

Can place cells be seen like the pixels on a screen, in that the same pixels can represent an infinite amount of pictures because it's the pattern of their activation as a group that actually matters, or is the analogy a bad one?

that is a good analogy


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What are these caterpillars eating a potato plant?
I saw these caterpillars rapidly consuming a potato plant in Central Texas:

They have thin, dark green-blue bodies with yellow-white longitudinal stripes and a bright rust-red head. Their body seems to be covered in fine hairs which may be difficult to see in the photo. They are about 1 cm long.
On some leaves of the same plant I saw what appear to be eggs - little black balls 1-2 mm in diameter, with a shiny appearance reminiscent of black caviar (well, I suppose they are black caviar). They seem to cover only a handful of leaves, in groups of about 100 or so (rough guess). Some can be seen in the photo.
Curiously enough, nearby there were tomato and strawberry plants, but they were not affected, while the potato was extensively predated (a few dozen leaves consumed).
What are these caterpillars? How do you kill them?

The "eggs" are poop (good for th soil, though I wouldn't call them caviar ;). As the caterpillars grow, their poop increases in size. (I've raised a number of caterpillars in an effort to increase the population of endangered butterflies.)

I think they are eggs. They are round and occur in clusters (can't see easily in this picture). The caterpillars leave what I think is poop as well, it is smaller, cigar shaped, irregularly shaped and fluid.

If they are in dense clusters, you are very likely correct. I don't know what you're describing is... I've never seen it. @theforestecologist will know, though.

@anongoodnurse They might be poop as well, it's hard to tell, but they seem like eggs to me (not in this photo). I'll see if I can get a high quality image of the eggs.

A better photo would help! I'm stumped. I've searched everywhere I know to. I like the rear end of these caterpillars: slightly bulbous with kinda fake eyes?

An Armymoth I think, probably Southern Armymoth(Spodoptera eridania). Id and
Management.

@anongoodnurse Well looks like you were right after all - I was really thrown off because the poops were concentrated in several (~20) clusters of 3-10 on certain leaves, while most leaves had very few of them. But the accepted answer has convinced me.

I believe this is the middle instar of a Southern Armyworm (Spodoptera eridania) larvae. Or some closely related species in the Spodoptera genus (family Noctuidae).

 © 2016 Wings, Worms, & Wonder
The larvae undergo six instars as they grow to attain a length of about 35 mm.

You can see a series of life stage pictures from Mississippi State.

Armyworms are so called because you typically find 100s at a time on a single leaf or plant. According to here:

Armyworms strike in the blink of an eye, and there are so many in their army that you will be finding them for weeks after the primary attack.

Behavior: larvae are mostly active at night and hide on leaf undersides, in curled leaves, or in leaf litter during the day.

This University of Florida site claims

Young larvae feed on under surface of leaflets leaving upper epidermis intact ("windowpaned"). Older larvae consume foliage and eat large holes in fruit.

Range: native to the American tropics (occurs widely in Central and South America and the Caribbean). Also found in US (principally in the Southeast but extends West to Kansas and New Mexico). It also is reported from California.

Here's a map showing some confirmed sightings [source]:

Host Plants:
This species has a very broad host range including important crops (including potatoes).

I would be concerned for your nearby tomatoes, because thy too are a favorite food of these insects.

See here for more information including management suggestions.

Defecation vs. Eggs??
The picture in the question shows S. eridania's feces.

This Mississippi State site includes a great zoomed-in picture of S. eridania's feces:

 © Lee Ruth
Note: caterpillars don't lay eggs. Only adult moths/butterflies lay eggs.
Eggs: large masses of 100-200 eggs covered with moth body scales, found on underside of leaves, hatch in 3 days.

 © 2016 Wings, Worms, & Wonder
Here's a picture of inside the seed casing of closely related S. exigua [source]:

 © 2016 Wings, Worms, & Wonder

Finally, here's a picture of the nocturnal adult:

Enter the cavalry! How did you find this?

haha :D. Well, truth be told, I don't know my lepidoptera as well as I could. So I simply started by googling a general description, then followed some links to seemingly related-looking species and eventually I narrowed it down. Took about 10 minutes :p.

Really nice answer and info!

source: Stack Exchange

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Why does scraped knee hurt more in hot water than cold water.
I was asked this question by my 5year old son. I do not know how to explain to him .

Cold decreases nerve ending firing. It's like a burn; ice feels good (but is not recommended!); warm water would make it hurt more.

The nociceptors i.e. the nerve cells that relay pain due to injury (mechanical), noxious heat and noxious chemical burns, get sensitized upon stimulus. I guess the injury sensitizes the nociceptors and hence they also become sensitive to heat (I am not finding a valid reference for this, at the moment). What @anongoodnurse says also makes sense but I am not sure if that is true. Extreme cold also elicits painful stimulus. Have a look at this post too.

I also suggest that you add some more content in the question body. The body does not convey any question. The title should be a one line summary of the body. If you do not have a lot of details to add then you can still restate the title content a bit more elaborately. We also appreciate some basic attempt from the side of the asked.

as objects heat up they vibrate more at the molecular level which accentuates interactions ... in your case raw nerve endings receive greater agitation ... cold reduces the frequency of this vibratory movement

2 reasons. The first (as anongoodnurse mentioned) is that cold temperatures temporarily knock out dermal surface nerves (in the winter you can verify that your face goes numb after a while outside).
The other reason is that a knee scrape produces inflammation (swelling and increased temperature). Cold water (or anything cold) counters these: stopping the inflammation temperature increase, then freezing out enzymes and proteins needed for inflammation and causing them to slow down or malfunction.

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What is the fate of NADH produced in the liver during oxidation of lactic acid?
NADH (‘reduced NAD’) is produced during the oxidation of blood lactate in the liver. Glycolysis requires NAD+ (‘oxidised NAD’), whereas gluconeogensis requires NADH. However the NADH is apparently not always used for gluconeogenesis (How is NAD+ used in lactic acid fermentation after it is oxidized from NADH?), i.e. the Cori Cycle does not always operate — so what becomes of the NADH in this case?
My best guess is that, along with the pyruvate, it may be transferred in the blood somehow to do to the site where it is needed, and it will then be taken into the electron transport chain, while the pyruvate will be taken into the Krebs cycle.

I have condensed your question to make it clearer. If I have altered your meaning please say so.

The “best guess” in this question is incorrect and the question itself indicates a lack of understanding of the roles of NAD+ and NADH in energy metabolism. (To rectifiy this, Chapters 17 and 18 of Berg et al. are suggested.)
The production of NADH in the oxidation of carbohydrates and fats is the energetic rationale for these processes. Under aerobic conditions the re-oxidation of NADH to NAD+ via the electron transport chain in the mitochondria* generates ATP for the energetic processes of the cell.
The fate of NADH produced by the oxidation of lactate reaching the liver from the blood would be similar under conditions where it is not needed for gluconeogenesis (in the reversal of the GAPDH reaction).  In these circumstances it would be reoxidized to NAD+, generating ATP in the mitochondria*.
[Note also that pyruvate is most likely to be oxidized by the liver mitochondria to produce metabolic intermediates and ATP, rather than transferred to the blood. NADH is certainly not transferred to the blood.]
*Advanced Point: Cytoplasmic and Mitochondrial NAD
The statement above, that NADH is “reoxidized to NAD+, generating ATP in the mitochondria”, is correct, but may be taken to imply that the NADH enters the mitochondria. This is not the case becase the NADH and NAD+ cannot pass through the mitochondrial membrane (as @tomd has commented). However the electrons that represent the reduced state of NADH do pass through the membrane. They do this in the guise of other molecules which are reduced in the cytoplasm by NADH in what are known as electron shuttles. The electrons enter the electron transport chain and are finally accepted by molecular oxygen. More detail of shuttles can be found in section 18.5 of Berg et al.

@tomd — Thank you for that elaboration but the question was not about NAD transport (or effective) transport across the mitochondrial membrane. Including it in my answer would have reduced its clarity and obscured the basic principle of what the NADH is used for.

@tomd — I have now modified the question, the first paragraph of my answer, and added a footnote about shuttles. I trust this incorporates the points you raised.


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What is a gene transcript, how is it different from an allele?
Within human genetics,
My current understanding of a transcript for a particular gene is that it's the exact nucleotide sequence and position of a particular instance of said gene in some individual.
My current understanding of an allele is that it's a less granular breakdown of the instances of a gene in a population.  That is to say, one allele for a particular gene likely covers many (millions of?) unique transcripts for that particular gene, and groups them together due to their tendency to all have a similar phenotypic expression.
Is this correct?

Related http://biology.stackexchange.com/q/42521/3340

No.
A gene is a unit of the genome stored in the form of DNA. It can be transcribed into mRNA  (the transcript) to be used as a template in protein synthesis.
A gene can come in many different versions unique to an individual. That is, individuals can have different alleles, or versions of the same gene.
For example, in mice you can have many different fur colors. The color of their hair is determined by a series of biochemical reactions that are catalyzed by proteins. If each protein is functional, the mice will have a certain color of hair. If any of these proteins are not functional (because they are carrying a certain allele), then the mouse will end up being a different color than it would be if each protein functioned.
You can also have genes that produce somewhat faulty protein-products. As is the case with insulin-resistant diabetes.

But how come particular genes have so few recognized alleles then?  Isn't there way more variation in a particular gene across the population than the 2-3 alleles commonly associated to it?

Not really. Think of it this way. You are trying to assemble a car; you have ten sets of intructions, only one of the instructions will build you a functional car. How many types of cars can you build from these ten sets?

Two. It will either function, or it won't.

So you're saying that in a gene of say a million bp, that everyone will have one of ten possible million bp nucleotide sequences, without even a single SNP somewhere in there which deviates from one of these ten exact sequences?

Not necessarily. Not all mutations have an affect on the protein-product. Because of things like wobble-base pairing, and the overlap in amino acids to trinucleotide sequences. And some mutations might not have that much of an affect on the product. Usually, for a phenotypic change to occur, a protein needs to stop functioning, or have its function drastically reduced.

But wouldn't these SNPs then technically give rise to separate alleles?  Or must they result in some change in the protein product?

They could give rise to a separate allele if the protein is changed in such a way to produce a new phenotype.

So alleles are at a higher level of granularity with respect to the actual variation in the DNA nucleotide sequence.  What is a particular instance of a gene referred to then at the most granular level (SNPs included and all), just an instance?

I can't recall if there's a word for it. But, say an SNP occurred in a 800bp gene. You would jist refer to it at its particular point, eg. "the SNP at the 25th base"

Ah I see, since if it doesn't have a significant affect on the protein coded for then there's no point in referring to it beyond that, ok thanks!

I thought a transcript was the RNA sequence produced from transcription. The RNA copy of an allele that gets spliced and translocated to the cytoplasm for translation. Not sure if Wikipedia references are allowed here, but they seem to agree with my understanding.
An allele is a specific copy of a gene, i.e. you have two copies (alleles) of gene X; allele X1 comes from your mum, allele X2 from your dad.
I haven't heard of the less granular breakdown description of genes, so that might just be a different way of looking at it.

Yes I've seen the word 'transcript' used in that context as well, but I've also seen it used in the context of a particular 'gene transcript'.  As for alleles, just reading from here: https://en.wikipedia.org/wiki/Allele#Multiple_alleles, it says "For example, at the gene locus for the ABO blood type carbohydrate antigens in humans,[6] classical genetics recognizes three alleles, IA, IB, and i, that determine compatibility of blood transfusions"  But that can't be all, since basically every time you sequence another person's genome you should get a new allele.

Not quite, an allele can be the same between different people and a person can carry two of the same allele as two copies of the same gene.

Alleles in the traditional sense represent genetic variation in a population at a given locus. Usually this is related to a given phenotype or observable trait. They can refer to areas of the genome that may or may NOT be transcribed into RNA, whether or NOT that RNA gets translated into protein.
Alleles can refer to a single nucleotide difference (SNP), or an insertion/deletion of one more more bases (indels). Thus for a given SNP associated with heart disease, if 97% of the population has a T and the other 3 percent have an A at that locus, then the alleles are the A and T alleles for that SNP.
Note: the variation could be in a regulatory region of DNA and never get transcribed. But the phenotype associated would be varied expression of a transcribed region it regulates.
A transcript is merely an antisense strand of a region of DNA with U replacing T. Note there are many kinds of RNA transcripts, not all of which get translated to protein. The transcript always mirrors the DNA below. If the DNA has genetic variation, the transcript will reflect it.
In the last 10 years, with the discovery of epigenetics, we also have started thinking about a genetic locus where the variation is a modification of base or histone that the base binds to as DNA is compacted. So some now also include methylation of a CpG as an allele, where one person might have 40% of CpG at that location methylated, and another have 67%.  This difference can explain a trait difference and thus also be referred to as an allele (high methylation vs. lower).
Last but not least, much genetic variation results in no discernible phenotypes. Sometimes both Alleles still result in the same base being encoded during translation for example.

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Boiling A frog in a sous vidè bath
So if i were to use a sous vidè water bath and a frog and slowley raised the temperature say 1 to 2 degrees a day would they survive harsh boiling water through thermoregulation

How will it survive energy depletion?

could you perhaps provide a bit more context for asking this question?...

No.
No higher order organism has enough proteins that are stable at 100 degrees C to survive. Proteins denature at higher temps and all cellular functions that depend on them cease.
Some thermophillic bacteria have evolved proteins that are stable above 100 degrees C over eons of evolution.


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Why not replace the human genome with it's decoy genome version?

https://www.biostars.org/p/73100/
http://www.cureffi.org/2013/02/01/the-decoy-genome/

The decoy genome is an improved human genome from the regular reference. It's faster for mapping and it reduces false positive rate.
In this case, there shouldn't be any reason to use the regular human reference, because the decoy genome is simply better and faster. For instance, it has DNA sequence for common virus genomes presented in humans. It has everything in the regular reference.
Q: What's the point of the regular human reference (e.g. hg38) if the decoy version is more accurate and is a better representation for the human variation.

To clarify, when you say "decoy genome" you hopefully mean the decoy genome and the reference genome together; the decoy genome itself is not a complete reference, but a collection of contigs assembled from reads that didn't map to the current reference genome, but are known to be human sequence.
The decoy genome certainly seems to be a useful supplementary data set for speeding up read mapping to the human genome but it cannot be better than the reference because it is not comparable to the reference.

But you just said it has everything in the regular reference? And it has sequences not in the regular version too. Shouldn't it be just better?

The decoy genome does not have everything in the reference. It is separate from the reference; it only contains sequence that couldn't be mapped to the current version of the reference. From your second link: "an entire ‘decoy genome’ to capture reads from human exome or whole genome sequencing that fail to align to the human reference genome."

Quote: "If you’re just starting alignment now, you can use hs37d5.fa.gz, which is all of human genome b37 plus the decoy" in the second link. I think the decoy version does have everything in the regular reference.

No, hs37d5.fa.gz has the "human genome b37 plus the decoy". The b37 reference genome and the decoy genome are separate sequences, but they are combined in that gzipped FASTA file.


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Can improper/inadequate exhalation in humans trigger migraines?
Is there any relation between  one's breathing pattern and occurrence of headaches? How does inadequate exhalation affect humans?

I'm voting to close this question as off-topic because it seems a better fit for Health.SE

I meant it in a general sense, was not seeking a personalized answer.

If so then please remove any reference to self and try to make the question interesting for the community at large.

I have reworded my question. Can it be re-opened?

It's still too broad for the format here. I would opt for Health. SE, another stack in the SE network


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Physiological effects of electrical shocks on human body depending on the energy
When discussing safety of electricity, one usually considers a constant DC or AC current with constant amplitude over a longer time. It is easy to find tables in books or in the web which lists different magnitudes of current and it's physiological effect on the human body. For example this (chest pathway):

If you consider a short time discharge, for example from a capacitor or an inductor, this description no longer applies. For example if you charge a small parallel plate capacitor with several thousands of volts and touch it, nothing dangerous will happen (just a slightly painful sensation). Initially the current through the body will be very high (such that it would be deadly if it was constant), but which decays exponentially in a very short time.
So one needs another scheme to evaluate the dangers to the human body in the case of a short discharge. One simple criterion is the energy criterion where one calculates the energy which may maximally deposited in the human body by the discharge. This is for example used in for electrical safety guidelines for German schools (http://publikationen.dguv.de/dguv/pdf/10002/si-8040.pdf, page 27), where for > 60 volts a discharge energy below 350 mJ is considered as safe.
My question is if there exists also an overview of the effects on the human body for short discharges depending on the energy (for the case of > 60 volt), or even a two dimensional map (one axis voltage, the other one energy).
If so, do you have a reference to the original papers.

Is there any source claiming that capacitor discharge with thousands of volts is not fatal?

@JM97: I tested it several times. But be aware, that this only works, if the discharge energy is low enough. Take for example the 350 mJ limit I cited in my post. Below this it should be safe. Then take a parallel plate capacitor without dielectricum, plate distance say 0,5cm and a square plate with $0,25\cdot 0,25 ,\mathrm{m^2}$ area. Then you get a capacity $C = \epsilon_0 \frac{A}{d} \approx 1,1\cdot 10^{-10} ,\mathrm{F}$ and with $U = 500,\mathrm{V}$ you get a  discharge energy of $E = \frac{1}{2} C U^2 \approx 1,38 ,\mathrm{mJ}$.

However take another commercial capacitor with say $1,\mu\mathrm{F}$ capacity, then at $5 \mathrm{kV}$ you get $12 , \mathrm{J}$ as discharge energy. I guess this would be fatal (don't worry, I am not going to test this :-)).

If there is more transfer of charge in less time that is higher amperes of current is passing then it will be fatal not only due to its effects on membrane charges but also due to intense heat produced by the fast moving charges. So the tables given in question are enough


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Is there a kind of 'rule' which decides whether the male of female is bigger?
In human race usually males are larger than females, and probably is this for all primates. But some animals there are the females bigger, but what determines whether the male or female should be bigger. Is this just random with no logical system as evolution can be or are there some marks which indicates that it is better that the female should be bigger?

I seem to recall that some primates show dimorphism in which females are larger than males.

See Sexual dimorphism

In short, there is not a rule of thumb whether a given species will have bigger males or females. In some cases females are larger (often insects, invertebrates or fish), in other cases males are larger (often mammals and birds) but even these generalizations have exceptions (Ralls (1976)).
When a males and females of a species have morphological differences other than differences in reproductive organs, this is called sexual dimorphism. These dimorphisms can be thought of as adaptations which have evolved due to a specific evolutionary pressure.
In males, larger sizes can evolve from sexual selection on males in competition with other males for mates. Simplified, the bigger males are better competitors. In females however, larger sizes can evolve from a number of different pressures, but rarely due to competition for mates. More common pressures resulting in larger females are rearing success, competition for resources other than mates.
Whether males or females of a species are bigger is certainly not random, but rather a precise outcome of numerous trade-offs and benefits of being bigger.


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What difference do trans and cis configurations of amide groups bring to the polypeptide chain?
Hi I was just wondering whether there would be any difference to the structure of the polypeptide chain, or any changes to a proteins characteristics, if it has more amide groups with a cis or trans configuration.
Apparently the trans configuration is more stable, so more amino acids with a trans configuration can be found within a polypeptide chain. Does this pose any significant characteristic to a protein, and if so what is this characteristic?

Apparently the trans configuration is more stable, so more amino acids
  with a trans configuration can be found within a polypeptide chain.
  Does this pose any significant characteristic to a protein, and if so
  what is this characteristic?

As you said, the trans- form is energetically more favourable. However, in proline the cis- form is energetically similar to the trans- form. The cis- structure introduces a kink or bend in the peptide chain which is seen in case of proline (see this section of wikipedia page on proline).


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Goodness of fit: How to decide which ratio to deal with?
While solving problems of Goodness of fit, I'm faced with an issue, how to decide which ratio to consider to find the test statistic from given set of observations.
E.g. 1

A supplied sample contains four types of seeds and the total number is 64. The types of seeds are large red 42, large white 8, small red 10 and small white 4. Calculate goodness of fit.

Problem: As df=3, Ratio= 9:3:3:1 / 1:1:1:1?
E.g.2

You are supplied with two different varieties of plant samples;tall-76 and short-24. Determine the observed number, apply Chi square test to state whether it is in agreement with expected ratio.

Problem:  As df=1, Ratio= 3:1 /1:1?
I was vaguely told by my propessor that which ever ratio seems to apply(by logical guess) we should choose that one to determine the expected values and thus the statistic.
I couldn't find any good read in this regard, except those that are full of mistakes. I've been reading Statistics blogs to understand the concepts but they don't cover these typical biological problems and those that did had the ratios mentioned.
I've another question in mind, from experimental result it is also likely that we won't get one of the four types of seeds (given that mating is random and the progenies appeared by dihybrid crosses) so determining the actual ratio behind becomes more difficult as df = 2  =/= 3!

Without more information, as in a specific hypothesis to test (which should come from your professor), you can't be expected to come up with the hypothesis yourself. If your professor won't be clearer with the questions, then I say you expect 42:8:10:4 for the first and 76:24 ratios for the second. Chi^2 = 0 and you are done.

I think she's supposed to decide which hypothesis to test, based on how genes are inherited

For Pearson-χ² test, you can use any one frequency (for instance the frequency of heterozygotes). However, both your example questions lack important information regarding what is the expected frequency. Why should you even expect 3:1? Any expected model has to have some basis. These examples do not indicate any. The first step of a statistical test is to define the null hypothesis.

@WYSIWYG 3:1 because there are two classes of the nominate variable (that's how we were expected to solve by our professor). So we can't actually proceed without information (as in this question) as which null to disprove? I also found some questions from a book. I can't get how they are deciding the H0? (should I post them as another question?)

@SanjuktaGhosh You don't have to find out what the H₀ is. The null hypothesis is your basic question. You will, of course, know that before performing the experiment. In your case of 3:1 you will have the assumptions such as: there is dominance, the cross is between two heterozygotes etc. This appears to be the case but I can invent arbitrary cases in which you may see 3:1 ratios. I can also argue that 76:24 is not 3:1 but actually different from it. Unless you have multiple samples, there is no way to prove it.

@SanjuktaGhosh, you don't always need to disprove the null hypothesis. In some cases it makes more sense to run a model to check to see if the null hypothesis is correct - particularly when you are not entirely certain about what the alternative hypothesis could be. This is what Chi-square analysis is for. You have determine whatever ratio would make the most sense, logically. Then you run the observed values against the null hypothesis's ratio - using the same number of samples. So, run a Chi-squared test with a ratio of 75:25 against the observed ratio of 76:24.

Example:   ∑ ( (Observation - Expected) ^2) / Expected = χ^2

( (24-25) ^2) / 25) + ( (76-75) ^2) / 75) = 0.0533.. Which is approximately equal to to an alpha value of 0.9. Therefore, the p-value = 0.45, and you can reject the alternative hypothesis in favour of the null hypothesis: there is no difference between the observed ratio, and the expected ratio

@WYSIWYG Thank you for your insight. It really cleared things up. But if I find a question like this I'll have to look for patterns as what the Ha they are expecting us to assume.

For any statistical test you need to know the null hypothesis. The alternative hypothesis does not matter. In fact all.the tests check if null hypothesis is valid or not. They don't really have any information about the alternate hypothesis. The alternatives can be infinite

Are there cases in which we have no established scientific theory  (that would have been be our Ho) to compare our data with? What do we assume our Ho then? @WYSIWYG

When the p-value exceeds 5% the result is called significant and when 1% it is called highly significant (given that the test is motivated by rejection of the null). But what about a p-value not exceeding the critical value (which is something certain when the Ho is true, well Type I error excluded), do we call the result significant then? What do we call the result in that case?@WYSIWYG

Statistical test cannot be performed if you do not have a prior hypothesis. Your hypothesis can be as simple as "both samples are the same". When you do a t-test you have one additional clause that both samples are normally distributed. P-value is the probability that the null hypothesis is correct. The smaller that value is the higher will be your confidence. In general, we define our confidence interval before performing the test. The choice of confidence interval is arbitrary; usual choice is 95% (p < 0.05 is considered significant) but you can be more stringent depending on the situation.

To solve this question you need to have a basic understanding of Mendelian genetics. Contrary to peoples' comments, this problem does provide enough information.
Genes are inherited from two parents. That is, the offspring will inherit one allele from each parent. Genes also interact with each other in a dominant/recessive nature. A dominant trait will be expressed, no matter what if this is carried by an organism. A recessive trait will only be expressed if the organism is carrying two copies of the same allele - the organism must receive the recessive gene from both parents.
In the first question, there are four genes. One gene encoding large seeds. One gene encoding small seeds. On gene encoding red seeds. One gene encoding white seeds.
The dominant genes are those that code for: large & red
The recessive genes are those that code for: small & white
For this question, you assume that both parents are carrying a single copy of each gene. This means, each parent has one copy of a gene coding for large seeds, one copy of a gene coding for small seeds, one copy of a gene coding for red seeds, and one copy of a gene coding for white seeds.
As a side note, this would mean that each parent came from a large red seed. There is also a chance for any of the four genes to be passed to the offspring.
Each parent could pass the genes for: Large red seeds, Large white seeds, small red seeds or small white seeds.
This means that the following gene-combinations are possible:
-large red, large red
-large red, large white
-large red, small red
-large red, small white
-large white, large red
-large white, large white
...etc...
And, I'm sorry, I've been trying for twenty minutes to upload a picture to show you what I mean. But, you can do this yourself also to see what I mean:
Draw a 4x4 grid, and in each box fill in each possible combination of genes that can be inherited by an offspring. They call this a Punnett square, and it is used to predict the phenotype of an offspring bred by two parents. If you search Punett square you will understand how this works.
But the thing to remember is this: If the offspring carries one copy of a dominate gene (large seed, red seed) then these phenotypes will be expressed. In order for a recessive trait to be expressed, the offspring must carry two copies of the genes (small seed, white seed), ie. it must have received the same recesssive allele from both parents.
Now, to solve the problem statistically, you will use the ratio 9:3:3:1. The null hypothesis is that there is no difference between the observation and this ratio. The alternative hypothesis is that there is a statistically significant difference observed from the sample in comparison to the test-ratio.
This means, a p-value < 0.05 indicates that the 9:3:3:1 ratio is false. And the gene-interaction must be explained by another means - not by Mendelian inheritance. Or, I suppose it could also indicate that the parents did not in fact carry one copy of each allele and some other combination, that maybe you need to find. Eg. One parent could have had two copies of each recessive trait, while the other parent could have had in had one copy of each trait. (Play with the Punnett square, and maybe you can figure out if this is true)

Oh yeah, and obviously they aren't a 1:1:1:1 ratio. So isn't this question basically "free marks"?

@Sanjukta Ghosh, my apologies - when I first answered your question I was under the assumption that you had an understanding of Mendelian genetics and inheritance. I have edited my answer, and provided you with some background information required to solve this question. I was also trying to upload pictures, but I had no luck with this. I'm sorry. I hope my new answer clears things up for you. If you have any more questions, please feel free to ask.

And this is a link to dihybrid crosses. It will explain why 9:3:3:1 ratios are expected. https://en.wikipedia.org/wiki/Dihybrid_cross

I'm aware of Mendelian genetics. Thanks for your efforts and this comment. I agree with them that the information(data) provided is not enough to establish a scientific hypothesis but questions like this are mentioned in books followed by my university.  I prefer your previous answer though. I would like to ask can you support your answer with some authoritative reference.

By your answer I meant the previous version where you talked about the technique.

Would you like me to change it back to the unedited version, or perhaps I could update my answer again if we are able to reach a conclusion on this problem? And, I have recently found this website from the University of Arizona explaining the purpose of dihybrid crosses. I think their links, numbered 10 & 11, will show example situations where a statistical model would successfully reject the null hypothesis.


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Reusing frozen blood
Considering the short supplies of blood in hospitals, why can't we freeze on our blood from time to time and and have it stocked for reuse in an emergency?
That could make ourselves responsible for own our blood supply in case of an emergency.

where have you looked for answers to this question? can you add some of that detail? it would definitely add quality to your question.

Freezing cells is difficult, almost an art form. It depends largely on the types of cells being frozen, the program to be used in freezing and the program used to thaw. You can end up with a massive loss in viability if a technician doesn't follow a freeze or thaw protocol to a tee, and there are release criteria where products of low viability cannot and should not be infused.
Being said, cryopreservation of blood for transfusion exists, and has since the Vietnam war. We're getting better at the process, but barriers such as cost and training probably still pose a hindrance.
Another barrier is maintenance of stocks, especially if you're considering monitoring your own blood supply. A cryogenic freezer would need to be maintained and monitored for constant -160-170°C. Cells do not undergo multiple freeze-thaws and thus once thawed you have a short shelf life.


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Signaling pathways with Receptor Tyrosine Kinase clarification
This question is regarding signaling pathways with RTKs, Receptor Tyrosine Kinase.  The picture posted has one thing wrong with it and I am supposed to figure out what that is.

What I have come up with so far is that the Ras protein shown that goes on to activate RAF, has GDP attached to it.  This cannot be true from what I understand, as Ras must have GTP bound to it in order for Ras to stay in it's closed conformation.  The closed conformation is what activates the rest of the signals.
I am wondering if I am correct in my assumption, or if there is something else in the diagram I am missing.

The active form of Ras should definitely be bound to GTP, to activate Raf. I don't see anything else wrong with the diagram. For reference, here is another useful diagram the pathway from Nature.

Please add some more details to your answer.


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What is the secondary structure distribution per AA in the Human proteome?
If one would classify each amino acid to either be in a Coil, Beta strand or Alpha helix what would be the distribution of these classes in the human proteome?
Is it 33%-33%-33% or is it biased? If it is biased why?
I thought it should be around equal, but I run the whole proteome through PSIPRED, and I found the distribution to be 60% Coil, 30% Helix, 10% Sheet. Why is it so?

I'm not sure what you're asking here. You seem to have answered your own question about the distribution (interesting, by the way!). So, by your own data, it is obviously biased. I don't know much about proteins, I'm a genomics person, but why would you assume no bias? Also, are you looking percent of total amino acids? Percent of total protein in each conformation? A bit more detail would be helpful.

A percent of amino acids in each secondary structure. I am just not really believing by own results, as far as i remember from the university these should be near equal (or like little bias). there are aprox 20k proteins in the human proteome, if we say each consist of 500 AA, we roughly get 10 million amino acids, which is in contrast with my results, as i get 6 million AAs in coils, 3 million in helix, and 1 million in sheets.

While I strongly object to the tone of the answer you've received so far, I see no reason whatsoever to assume an equal distribution. The properties of the different structures are not the same, so it doesn't make sense to expect such a distribution. Some explanation of why you would make such an assumption might be a helpful addition to your question.

The only answer I could give is very vague, unfortunately.  The distributions are not equal because these three SSE types play quite different roles in 3D structures. Sheets usually form in the core of a folded structure, and are short. Helices tend to pack around the outside, and can be longer. 'Coil' is everything else, and covers structure like long loops.

A major problem with my answer is the distribution of folds. If genomes were packed full of helical bundles, then the proportion of helix would go up. Presumably an organism with a lot of excreted extracellular proteins (that tend to have little secondary structure) would have a higher proportion of coil, and so on.

The question asks why the distribution of coil, alpha-helix and beta-strand is 60:30:10 rather than 33:33:33. The answer is:

“Why not”

This is because there is no reason whatever to expect that three types of structure (or in the case of coils, lack of structure*) should be present in equal amounts in proteins. It is like expecting that the percentage intron, exon and ‘junk’ DNA should be equal, or that the percentage of fuel reserves stored as glycogen and fat should be the same. Yes, they belong to the same category, but they are sufficiently different in each case for one not to be surprised if they are not required in equal amounts.
To understand this one needs to look a little more carefully at the occurrence of alpha-helix or beta-strand conformation in the three-dimensional structure of proteins. Three points may be emphasized:

Amino acids have particular conformations because they are part of an extended helix or sheet of strands the entirety of which leads to its structural stability — you don’t have a random mixture.
In many cases the helices or sheets are occur in particular combinations to give a family of proteins of similar overall structure. Again, the idea of random mixtures doesn’t enter into the equation.
These overall structures are suited to particular functions, so the abundance of proteins from a particular structural family will be determined by the requirement for antibodies or ion transporters or signal transducing proteins etc., not by some shake of the dice.

Images illustrating two such families are shown below:

(a) shows an ion transport proteins, predominantly alpha-helices, whereas (b) is an immunoglobulin domain with a distinctive pattern of beta strands (as well as some helix). For further examples and information I suggest the EMBL on-line course on protein classification and Berg et al. online, for example Section 7.3.
*Footnote 1: Situations where equal occurences might be expected
It is worth while contrasting the situation with protein secondary structure to some where the prior expectation might well be for equal usage, and the deviation from this could be regarded as bias and an explanation worth asking for:

The different proportion of the 20 amino acids in proteins (although a chemist would not expect equal proportions)
The different usage of synonymous codons of the genetic code in various species and mRNAs
The different usage of the similar molecules with a high phosphoryl group transfer potential: ATP, GTP, UTP and CTP (often loosely termed ‘high-energy’)

*Footnote 2: A coil is not a secondary structure
As is stated in the Wikepedia entry for Protein Secondary Structure:

The random coil is not a true secondary structure, but is the class of conformations that indicate an absence of regular secondary structure.

It might be mentioned in regard to protein structure that there are smaller three-dimensional motifs that the analysis quoted does not consider. These do not occur in equal proportions either, to nobody's great surprise.

Votes on a question have nothing to do with "sharing the mistaken scientific logic of the question". All due respect, get off your high horse. I upvoted it because I felt the underlying questions (why is such a distribution observed? Why are coils more common?) to be both interesting and worth investigating. Sadly, your answer doesn't address anything in the question apart from the obviously faulty premise.

This is not an answer i am sorry. This is a rhetorical something. I remember something from the university that the percentages of secondary structures are kind of equal. This must be a long known fact (either true of wrong) and all i want is a confirmation.

David, I see from your profile that you've done some structural work. Why don't you improve this answer and actually add something about the relative stability, functional plasticity or any other relevant properties that are different in the different protein conformations and how these can be used to explain the observed ratio?

@terdon — I'll stay where I am, I'm quite comfortable. I certainly answered the question. The reason that they differ from random — that was the question — is because there is no reason they should be random. If the question had been why is there more helix than sheet in proteins I would have voted to close as the answer is a matter of opinion. All you get is the sort of circular argument about something having more general utility. The poster needs to get away from his computer and read about proteins.

@GáborErdős — Your memory from the university is either faulty or you were told untruths. It is not a fact — long known or otherwise. If you do not believe me I suggest you search the internet (or read some books) to find evidence for this and cite it in your question.

@terdon — I've taken out the sentence that appeared to offend. And by the way my work on protein motifs is primarily computational — my colleague is the protein chemist.

@GáborErdős — I have now added some information to my answer to help you understand why your premise was incorrect. I have also restructured my answer and provided reading suggestions. If you are using bioinformatics tools you still have to think about the structure and molecular biology of the data sets you are working on.


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Where can I get fungal extracts?
Does anyone know how I can get fungal extracts from fungal isolates? I have isolates in PDA slants and I'm gonna need to get their respective extracts to impregnate in sterile discs. I'm a novice in the field and all the help I can get will be greatly appreciated.


text:
What does it mean when you "extract the filtrate with ethyl acetate three times?"
"The fermentation broth (600 mL) of each endophyte was filtered, and the filtrate was extracted three times with ethyl acetate at room temperature and further concentrated in vacuo to give dried residues prior to antimicrobial assays"

This procedure is referring to chemical extraction, which is a separation process used in chemistry (and biochemistry) to isolate compounds of interest by using two immiscible phases in which the compound of interest has differential solubility.
For example, in a liquid-liquid extraction, often one of the phases contains a polar solvent like water, and the other phase contains a nonpolar solvent like oil. Water and oil won't mix, but after stirring them together and waiting some time, the more polar molecules in solution will tend to concentrate in the water, and the less polar molecules will tend to concentrate in the oil. Because the phases are immiscible, it is relatively straightforward to separate them once equilibrium has been reached.
Ethyl acetate is a fairly non-polar molecule often used in organic extractions. In the process that you described, the result will be that non-polar contents of the fermentation broth will be extracted into the ethyl acetate, and hydrophilic contents will remain in the aqueous phase.
Because this process is never 100% efficient (the efficiency will depend on the concentrations of the solutes and relative affinity for the two phases), it is often repeated several times to improve the extraction.


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If you start with 1 cell how many are at the end of meiosis?
If you start with 1 cell how many are at the end of meiosis?
Can someone help me understand the process of what happens to the cells in the process of meiosis I and II

Welcome to the Biology Stack Exchange. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Please ensure your post is formatted correctly as well.

Meiosis is a process of cellular division involving two consecutive cellular divisions. Unlike the other process of cellular division-mitosis it leads to twofold decrease in the number of chromosomes in the cell, e.g. there are half as much chromosomes in the nucleus of the cell as there were before the meiosis. But the cell undergoes 2 consecutive division so the answer to your question is 4! There are 4 cells at the end of meiosis.
There might be what some people would consider (exceptions) in some cases like in the mammalian ovogenesis (this is the production of egg cells) where the products of one of the cells produced by the first division don't develop and there isn't second division so the total number of cells is 3 but this is considered an exception, so the proper answer to your question is still 4.

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

What do you mean by that comment?

This question can be easily answered by a search on google.Please avoid writing answers for questions that do not have any research effort because they are off-topic


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Are there knots in DNA?
This question may sound silly.
How does it come that the DNA molecules are not totally entangled with time in the cell ? If I take long strings in a box and shake it, that would create knots, and I wouldn't be able to easily isolate each string apart.
But during mitoses, the chromosomes are totally isolated from each others while otherwise, the DNA is freely floating in the nucleus.

Bienvenue Arnaud! ADN is french. It is DNA in english :)

thank you. That explain why I couldn't find ADN in the tags list ;)

Related (though not strictly a duplicate): Why DNA needs histones to be packaged and ordered?

There are enzymes to maintain DNA structure; one of the main ones are topoisomerases.

I think a key factor is that DNA molecules are not passive bits of string that are left to move freely (which is what causes knots in string-like things that are left alone too long).
For one thing the DNA molecule is an active part of the cell metabolism, as it is constantly being transcribed (to generate RNA and proteins) or copied or corrected and so on. And as part of its role in metabolism the DNA molecule is closely associated with RNA molecules, proteins and specifically proteins that the DNA is wrapped around called "histones". The Wikipedia page for "Chromatin" (what chromosomes are made of, basically) describes various aspects of this organization, including:

That DNA which codes genes that are actively transcribed ("turned on") is more loosely packaged and associated with RNA polymerases (referred to as euchromatin) while that DNA which codes inactive genes ("turned off") is more condensed and associated with structural proteins (heterochromatin).

So DNA is constantly being manipulated by all kinds of proteins and enzymes that affect its shape and position in space; it isn't just lying there. And insofar as it might get into knots, that would likely be part of the manipulations of the enzymes and proteins, or would fairly easily be dealt with by them. This doesn't mean DNA doesn't have knots however, in fact it appears it very much can:
DNA AND KNOT THEORY (from The Institute for Environmental Modelling at the University of Tennessee)

Conclusions: Principles of topology give cell biologists a quantitative, powerful, and invariant way to measure properties of DNA. Principles of knot theory have helped elucidate the mechanisms by which enzymes unpack DNA. Additionally, topological methods have been influential in determining the left handed winding of DNA around histones. Measuring changes in crossing number have also been instrumental in understanding the termination of DNA replication and the role of enzymes in recombination.

(note this paper looks at DNA in E.coli, which does not organize its DNA in chromatin the way Eukaryotes do).
Untangling DNA (from the Nature blog CreatureCast, 2013)
This link includes a video about topoisomerases, enzymes also referred to in the previous link that unentangle DNA.
A Monte Carlo Study of Knots in Long Double-Stranded DNA Chains (PLOS Computational Biology, 2016)
Quote from the abstract:

Even though our coarse-grained model is only based on experimental knotting probabilities of short DNA strands, it reproduces the correct persistence length of DNA. This indicates that knots are not only a fine gauge for structural properties, but a promising tool for the design of polymer models.

The active site of the SET domain is constructed on a knot (Nature Structural Biology, 200)
A knot or not a knot? SETting the record ‘straight’ on proteins (Computational Biology and Chemistry, 2003)
These papers discuss potential knots within a histone protein, not DNA, but illustrates that topology and knots can be important in macromolecules:

A knot within the SET domain helps form the methyltransferase active site, where AdoHcy binds and lysine methylation is likely to occur.
A novel knot found in the SET domain is examined in the light of five recent crystal structures and their descriptions in the literature. Using the algorithm of Taylor it was established that the backbone chain does not form a true knot.

Discovery of a predicted DNA knot substantiates a model for site-specific recombination (Science, 1985)
This link is a bit painful to read (and from 1985 so I don't know if it was superseded, but it has over 200 citations) so I will leave it at the title.
And finally this article, which I looked at last but probably should have looked at first because the first sentence of the abstract literally answers your question :
Direct observation of DNA knots using a solid-state nanopore (Nature Nanotechnology, 2016)

Long DNA molecules can self-entangle into knots. Experimental techniques for observing such DNA knots (primarily gel electrophoresis) are limited to bulk methods and circular molecules below 10 kilobase pairs in length. Here, we show that solid-state nanopores can be used to directly observe individual knots in both linear and circular single DNA molecules of arbitrary length.


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Oxygen dissociation curve and temperature
Say, we have a container with a mixture of gases. The concentration of oxygen is $C_{oxy}$ and its partial pressure is $P_{oxy}$. We then introduce a sample of hemoglobin (deoxygenated) in that container. A certain fraction of the sample gets saturated  with oxygen. Afterwards, we increase the temperature of the gas in the container keeping everything else constant. $P_{oxy}$
obviously increases. Does this mean that the percentage of saturated hemoglobin increases as well with the increase in $P_{oxy}$, according to the ODC curve?
Or, will the oxygen saturation decrease, as at higher temperatures the $Hb-O_{2}$ bond starts getting denatured? If the latter is the case, does this imply the ODC curve is temperature specific? And if that is the case, wouldn't the ODC curve (partial pressure Vs saturation curve for a specific temperature) be a mere concentration vs saturation curve for a specific temperature?

Welcome to BiologySE... can you give some evidence of effort on your part to try and figure this out? where have you looked for an answer?

Added my idea. Can you help? @VanceLAlbaugh

..saturation actually depends on the concentration... If thats the case then why do we experience mountain sickness?

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


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Why do cells divide (or copy themselves)?
What I know
I learned about cells (not too much, but I've studied them a little bit. So don't feel offended when I say something which isn't really true. If something I write is wrong, please correct me (if it's not too much of effort).
Question
Imagine the first cell on earth.
Why would this cell "think" of dividing itself? How would a cell come up with the idea of dividing itself? The process of dividing itself isn't that simple, so ... how could that be? I don't really see a reason for devision from the "standpoint of a cell".
One of the solutions would be, that there's an intelligent creator, but I want to know the answer from the point of view from science.
Layman explanation would be appreciated
Just don't go too deep in the answer, I really just want to know if there is a solution to my questions. And if scientists really found out something, please just give me a very (VERY VERY) easy explanation.

There are two different points in your post. 1) Intelligent design. It has been explained thousands of times throughout the net why this pseudo-science hypothesis makes no sense. 2) Why did cells evolve to replicate. This second is IMO a good question (the answer of which lies into the existence of external causes of mortality). You should narrow your point down to this element I think.

As a sidenote, you might want to follow some very easy and very introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

ok, I changed the question. I really just was wondering how that could be, because as I studied the cell, this question came to me, and my teacher couldn't give me an answer.
Thank you for the link!

I think this is as much a question in philosophy of biology and metaphysics as it's in biology alone. You might also be interested to look in this SE question in the philosophy section-http://philosophy.stackexchange.com/questions/15596/why-is-it-necessary-to-survive/41102#41102 . There I gave a brief answer from both philosophical and biological point of view that might be related to your question. If you are interested in the broader perspective of your question you may check it out.

if I have an ocean with two things one that copies itself and one that doesn't, and I wait a while, then I am more likely to have more of the first because it, you know, makes more of itself. Thus there are many of the first and few of the latter. certain chemicals copy themselves, certain strands of RNA are a good example as are some prions. It's like asking why stick in a fire want to catch fire, there is no want it's just chemistry.

You're assuming that a cell somehow came into existence and then began to replicate. The situation is most likely the opposite: there were self-replicating molecules (perhaps RNA, nobody really knows) long before there were cells as we know them today.

"One of the solutions would be, that there's an intelligent family of creators" - thought of that too?

The "Why" question
Why do organisms replicate?
Given that there is (extrinsic and also eventually intrinsic) sources of mortality, organisms that did not replicate just ended up disappearing. Those that did replicate eventually ended up giving rise to important lineages.
In other words, replication occurs because those who did not replicate disappeared. It is also because unique instance of things may disappear that you regularly backup your computer (if you do).
The "How" question
By what mechanism did early replication occur?
You actually did not really ask about it but here are a few words anyway.
The mechanism by which first replication occurred are mainly unknown as it is hard to investigate specific processes that occurred such a long time ago. The field that studies the origin of life is called abiogenesis. You might especially want to read the section on Self-enclosement, reproduction, duplication and the RNA world. You might also want to read about Autocatalysis.
I am afraid that a summary of existing hypothesis on early reproductive systems are 1) out of my capacity and 2) would hardly fit into the wish to receive a very (VERY VERY) easy explanation.

Good answer; the others seem to overshoot the simple observation of what happens when one molecule reproduces itself and another doesn't.

There are two issues with your question that both lead to potential answers.
First, the assumption that there was ever "a first cell" is wrong. Life in general occurs in populations; if there's one of something then there usually are others. And the same is true in chemistry; usually if you have a certain molecule in a certain place there are probably others there too (that got there in the same way the first one did), and they're all having similar reactions (because similar molecules behave in similar ways). As abiogenesis, the general term for the development of life from non-life, involves complex chemistry resulting in self-replicating systems resulting in life as we know it, all of those principles would apply there too.
Second, the assumption that the first life was a cell is likely wrong (except if God created life, and started with a cell, or some other such ad-hoc idea of course). Life is partly defined by self-replication, and self-replication is also what allows the optimization of systems for specific purposes via the processes of biological evolution (which requires, and is a consequence of, imperfect replication); meaning that as soon as you get a self-replicating system you're well on your way to having life - and the first cells as we know them likely developed quite far along that process, because they already are quite optimized.
In this perspective, the answer to your question is that there was never an issue of "the first cell" "deciding" to "replicate" - the first life replicated by definition - and whether it was a cell or not is a completely different issue.
As to how the first life "decided" to replicate - replication is a chemical reaction, it's not like modern DNA "decides" to replicate, it is a chemical reaction that occurs when the conditions make it inevitable. Biologists currently do not know what the first self-replicating molecules or systems were and how they replicated without the complex mechanisms that allow the chemical reactions that make DNA replicate, but the assumption is that it was a chemical reaction that happened for the reason chemical reactions happen - the components and conditions are such that following the laws of physics results in the chemical reaction happening. For what it's worth though it should be noted that while DNA cannot do anything outside of the mechanisms of the cell, the same isn't true of RNA; in fact small sequences of RNA can pair off on their own in solution, and it is generally thought that RNA came before DNA in the development of life.
Abiogenesis is an unanswered question of science, but if you want more ideas of what biologists think might have happened you could look here:
https://en.wikipedia.org/wiki/Abiogenesis
Otherwise I can't help but mention my favorite hypothesis of abiogenesis, which I find most exciting and (to my layperson eyes) convincing, and more importantly illustrates how "the first cell" could have been a fairly late step in the development of life. Here is a video of one of its originators talking about it:
https://www.youtube.com/watch?v=gb7pZyks_HE
Basically those researchers started out looking at the energy of the chemical reactions that make the building blocks of life, and figuring out how natural reactions could generate that energy. They found that the conditions that occurred in hydrothermal vents were conducive to such reactions:
http://journalofcosmology.com/Abiogenesis107.html
In more recent papers they connect this to comparisons of existing cells to try and figure out which features the Last Universal Common Ancestor of all life had, and putting those things together they build a fairly coherent picture of the first "organisms" developing inside pores of the material of hydrothermal vents, involving chemical reactions that produced complex molecules which promoted the production of further such molecules (including proteins, enzymes and RNA that can both self-replicate and promote the creation of proteins),  and the development of membranes not so much as a protection from the outside world but to maintain the energy difference between inside and outside the pores ("proton gradients") that further promoted the reactions in question, and bacteria and archae being the result of two independent events of cells "breaking off" from the porous rock and becoming free-living.
http://nick-lane.net/wp-content/uploads/2016/12/Sousa-et-al-Phil-Trans.pdf
Here is a figure from that paper:

(And this goes a bit to my first point about there not having been a single first cell - you can see in this hypothesis there would have been many pores/reactions occurring along proton gradients/groups of complex molecules reacting in positive feedback loops/self-replicating systems/membranes forming/cells breaking off/etc at any one time, making it more likely for any one "step forward" (in quotes because it's only a step "forward" in hindsight; at the time it would be a variation among others) to occur somewhere in that population).

this is nice answer but energy is not always associated with the emergence of Life. See for example here- https://en.wikipedia.org/wiki/Dissipative_system an article about what scientists call dissipative structures. They too can consume energy and self-organize but would you consider them alive? Actually the big question concerning your post really is: Can there be Life without cells? And if the answer is not, then the OP has a point about equating Life with cells.

@YordanYordanov I never said "life DID originate without cells", I said "life COULD HAVE originated without cells" (well ok to be fair I said it LIKELY originated without cells, which is still less absolute than what you're claiming). OP started out assuming that the first life was a cell; this is a valid assumption if we know that life cannot exist without cells, as you say, but it isn't a valid assumption if we don't know that, which is the point I was making. Also, I don't see how your comments about energy relate to things I said in my answer.

Actually if you want to know more how difficult it is to actually define Life and why all those who favor one or other property to define Life have so much problems defending their point of view here are 2 papers related to the subject-http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&ved=0ahUKEwjutJqR29bSAhXG6xQKHSn3C_sQFggnMAI&url=http%3A%2F%2Fspot.colorado.edu%2F~boonind%2FCleland.Life.synthese.pdf&usg=AFQjCNGkPTHYezOUG7D2_aajhmclkpq5Pg&sig2=rj31QVZo9Ge-BYKuNIel5Q

and http://quod.lib.umich.edu/p/ptb/6959004.0006.001/--proper-activity-preference-and-the-meaning-of-life?rgn=main;view=fulltext . They make an excellent example of the difficult (both philosophical and scientific) of prescribing Life to anything. I guess you should check them out. My argument is you can claim anything about Life at this point of development of science. What we know for sure is that Life is within cells but this doesn't mean we can prove Life is possible without cells. If you ask me (for my subjective opinion) then I would gladly agree viruses are alive,too

But the scientific community won't back me up 100% because as I say-"There is NO definition of Life, yet." at our current level of development of science. Therefore the only case for Life we can all agree on is cells and the OP has the right to ask his/her question in the manner it is asked, but the claim that Life is defined by self-replication is not valid in the context of modern attempts to define Life because as, I show you, we have no universal definition of Life yet, So how can you claim what defines Life we have no definition of it?

@YordanYordanov Neither of those papers seem relevant to abiogenesis. The first is closest but is about applying the definition of "life" in a general enough way to include potential extraterrestrial life (which the author is right that we currently don't know enough to do), not about the intermediate steps that would have led to modern Earth life. The second is purely about definitions; again, not useful for abiogenesis where the parameters are already well-defined in the sense those philosophers are thinking of.

@YordanYordanov I am not talking about a universal definition of life, and neither is OP. We are talking about how life started on Earth. In this context it's true that defining "life" is a matter of boundaries, and it's also true that "self-replication" isn't the only possible place to set the boundary (that's ignoring that the boundary WILL be fuzzy, and will be so even if we use "self-replication" as the boundary) (...)

my point is that if we have no universal definition of life and we can claim only that cells are the definitely alive, then the OP's question is justified in the way it's asked but at the same time the argument that Life begins with self-replication is not justified because as you can see in the papers it's still a matter of debate which is the property that defines Life so your point of view of equating Life with self-replication isn't justified. Can you understand me?

@YordanYordanov  ...but the justification I gave for using it is a good one: self-replication, aside from being a definition of life, also defines the point at which the process of biological evolution starts; in other words, the point starting from which the features that develop are the result of evolution (and the optimization that implies) and not only abiotic processes.

I understand your point but setting boundaries arbitrarily isn't possible without some deeper understanding of what the phenomenon which you put inside the boundary is. And we don't have that for Life, yet. This is why you can't "just use" self-replication for the definition of Life. The only thing you can use for sure is a cell because everyone agrees cells are alive. Otherwise I can put up the argument that even a hurricane (e.g. dissipative structure) is alive if it can self-replicate. Do you agree hurricanes are alive?

@YordanYordanov "Can you understand me?" I understand you fine, you are simply wrong and confusing definition games with scientific enquiry. "All modern living things have this feature" is not a good justification for "the first living thing had this feature", because the development of life would have been gradual, i.e. would involve intermediate steps between life and non-life, i.e. would involve entities that had many but not all features of modern life, i.e. we cannot affirm that a feature occurring in all modern life implies it existed in the first life, or worse defines a boundary.

Let us continue this discussion in chat.

@YordanYordanov Two last points: first, I don't know how you can claim I "just use" self-replication when I have justified this choice twice now and you have addressed the reasons for that choice neither time (I addressed in my previous comment why "is a cell" is way more arbitrary a criterion for setting the boundary). Second, please read Sousa et al, or look at the diagram, and tell me by what criterion you call the free-floating stage "alive" and the immediately previous stage "not alive".

@YordanYordanov I have to leave, I'll be in the chat in half an hour or so.

Here is a story,
Lets imagine that we go back a long long time ago.
Lets imagine a bunch of cells. Some divide. Some do not. And every so often a cell gets randomly damaged from UV light, toxic chemicals or just gets eaten by another cell.
So what happens.... cells that divide soon out number cells that do not. And in say 1 years time, all cells that you find are cells that divide.
And this is why cells divide. A self replication machine soon outnumbers a non-self replicating machines by virtue of being able to replicate.
There is no thinking required. Also no intelligent design is required either. Anything, any random mutation that makes the self replicating machine work better, even a little, will soon cause that better more efficient revision to out number the original version.
It isn't intelligence so much as water flowing down hill.
In fact that this is how some man-made ribozyme are made. A scientist first makes hundred of millions random RNA sequences. Then feed the mixture into  a test for activity. If activity occurs the molecules is copied by RNA dependent RNA polymerase. And more copies are made... and since RNA polymerase makes many error... you have a mutation rate. The products go through another round of selection. And so on.
And when the scientist comes back later in the week... they have an efficient ribozyme. Did the scientist design this molecule.. some intelligent design? Nope. There was next to no intelligence in the design of RNA. In fact said scientist wants to study this mixture of ribozymes and find how they work.
In nature that test is simply survival. Being around as long as possible to replicate as much as possible.
The experiment I am describing is a generic experiment to demonstrate how the RNA world could develop. Several examples
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652413/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390851/

can you show the paper where this experiment is described. Can you provide some references? I mean the artificial rybozome experiment.

First of all, there are cells that don't divide. For example, the nerve cells of mammal's central nervous system are shown to be very long lived and the rule is they don't divide through time. The same is true for most of their muscle cells, but yet, the point you infer is correct-cells do replicate, otherwise all the cells would have died of old age by now and the Earth would be lifeless. Therefore, the answer to your question is more in the line of the answer of the question: Why do there are always cells which want to divide? Do you agree?
Now, I have one question in the philosophy section that you may find relevant to yours. It's here. There I ask about the relationship between the ability to "act on your own" which is defined as agency there and the notion of choice-e.g. the ability of anything to move into different states in a non-deterministic way. I will cut down the philosophical terminology and give you the short answer I made for myself after reading and discussing this question in the Philosophy SE. Basically, the cell doesn't have a choice other than choosing to replicate. Yes, I know this answer may seem very hard to grasp but you need to think of the cell not as a free will creature as you are but as a kind of "computer" which has instructions in its "program", e.g. DNA when and where to replicate and when and where to stand still. So it has agency (the ability to choose) but it doesn't have free will on its own like you or I have. Just like a computer can't really choose what to do-it's its program that tells it what to do.
This is the answer to your question-there isn't such a thing as a "standpoint of a cell" because it really does not have free will. If it has no free will it can't have a "standpoint". Just like computer can't have "standpoints", too. It divides because it's programmed to do so. It only appears to us the first cell had any choice what to do and what not. The reality is the cell is nothing more than your computer with Windows OS. If Windows say-divide, it will divide (if of course, it was able to). There is no choice for the cell to divide or not. It's just what its program is. So, until there are cells programmed to make more copies of themselves which program their descendants to make more copies of themselves there will be cells dividing because the program is self-replicating. And just like any other computer virus until the hard drive (e.g. the environment) provides it with the means to reproduce-it will do so. Can you understand me?
P.S. If you however, kind of "translate" your question as to why the first cell had this "program" to replicate, then the answer lies in chemistry, not in biology. There is this thing called chemical evolution. It literally mean the origin of the "drive to reproduce" which eventually became the "drive" to divide was a direct result of the interactions between chemical, not biological reactions. And chemical reactions are deterministic, e.g. they have no free will. A reaction just can't possibly choose to occur, or not to occur. It happens under the natural conditions of the environment and when chemical evolution was eventually replaced by biological evolution the cause of the first became the cause of the other, too. This is how to explain the origin of the "will" of the cell to replicate and as you can see everywhere around you this "cause" is pretty much still in action everywhere. I hope you can get my point.


text:
Why do same type of fruits come in different sizes?
Why don't fruits come in exact same size even they're the same type of fruit?
This sounds like an obvious question,
but why are some apples bigger than others?
and why are some bananas larger than other bananas? or some trees grow taller than others?
What affects them to grow in different sizes, although they are from the same type of trees?
Is it because the fruits grew in different conditions?
Are there any articles or research about this?

Phenotypic variance
This variance in the appearance of living things is called phenotypic variance. There are a number of reasons for the existence of such phenotypic variance. In other words there are a number of underlying variances that can explain phenotypic variances.
Primary source of phenotypic variance
The two most obvious source of phenotypic variance are

genetic variance
environmental variance

Genetic variance is caused by individuals having different genetic predisposition in the population. Environmental variance is caused by the fact that different individuals experience different environments (both macro and micro - environmental differences).
Monozygotic twins look alike because, among them, they have no genetic variance. Even if raised in the same home, they still experience slightly different environments. If raised separately (which sometimes happen) then twins will differ a little more as they experience very different environments.
Other source of phenotypic variance
The other sources of phenotypic variances include
- epistatic variance
- developmental noise variance
- all covariances between all of these causal factors.

Are there any articles or research about this?

Well yes! Your question is underlying an entire field of knowledge which is called quantitative genetics.
More information
For more information, I recommend having a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


text:
Is cell-free Life possible?
I think most of the people on this site know about the famous Baltimore paper describing the ability of the poliovirus to replicate itself without the need of cells but I want to expand on the issue and ask could it be possible to have truly "cell-free" Life-e.g. life forms that do not have cells in any form according to modern biology but yet can be considered "alive" by its standards? This is the first paper in historical context describing the possibility of creating a self-replicating molecule in the laboratory. Well, it's about a viral genome and it only can self-replicate so it's not like it's alive according to what we consider "true" living organism, but nevertheless it triggers an interesting chain of assumptions in my mind. What if we could design a system where nucleic acid can evolve outside of cells? Then, what if we managed to provide an energy source t drive this evolution outside of the context of cells? Would such nucleic acid evolving on its own in a test tube depending only on the energy source we provide and on the specific conditions in the test tube be considered equal to a gene evolving in a "true" living organism? What if then we managed to add more nucleic acid's molecules to the system, just enough to have all the components involved in the replication of the evolving nucleic acid molecules synthesized by the system itself? Then can we consider this system analogous to a living organism, e.g. truly alive? What if we continued adding nucleic acid molecules to the system to the point when it was able to produce ATP from organic molecules used by what we commonly consider to be "alive", e.g. entities we prescribe the name living organisms, like glucose, for example. Then what would be the difference between this chemical reaction system and a genuine living organism? What if we continued building up this "in vitro metabolism" to the point when we have a genuine "molecule laboratory" testing the fitness of new nucleic acid molecules to itself. A true evolving, replicating and self-organizing molecular "machinery" we could "grow" in a test tube. Would we then consider such a thing a genuine living organism and if so why?
Yes, I know it's a "fringe question" and out of the scope of almost all branches of biology but nevertheless I think it's one of those questions that can "capture our mind". So, do you think there could possibly be such a thing that we could deem "alive" but have no cells at all? Something organized in such a way that we can readily call it a life form but yet not organized in the "way we think" about Life in general? If this is possible, when do you think this system of reactions could be called genuine living organism?
To the moderators-my question is different than the question "Why isn't a virus alive?" because it has a much broader perspective than it-a cell free form of Life can be anything-from a self-replicating "grey goo" to an evolving tornado. Viruses are only one small particular subset of possible answers. Plus the question you are referring to isn't about synthetic biology and the possible diversity of life forms as is mine but is only about a particular aspect of what we call a virus-its pertaining to the set of life forms or not. My question has both different direction and different set of objects it's aimed at. How can the two be identical, then?

The link is broken.

Possible duplicate of Why isn't a virus "alive"?

I fixed the link.

Oh, no this question is not about viruses! At least not only about viruses. here I ask the question can we even characterize something as alive if it has no cells at all. Could we call something alive if its organization isn't based on cells? The issue is much broader than the question: Are viruses alive?. For example, the first living organism at the origin of Life might as well have been the entire ecosystem. Then how is this connected with the question are viruses alive?

I only briefly glanced at the paper, but it sounds like they are describing viral RNAP activity in cell extracts. You could hardly say it can "replicate itself without the need of cells".

Nevertheless, it's the first paper mentioning the ability of something to be able to replicate on its own without the need of cells. My question is: How far can such molecules go? and further Can we ever consider anything replicating and evolving without the need of cells truly alive?

@YordanYordanov, although, like some of your other questions, I think this question might be closed. But I have to say, I really enjoy reading what you write. Never change =D

This web site is not for discussions like "So, do you think there could possibly...". Please provide definition of Life that you like and we can argue.

-1 because not a real question

The answer entirely depends upon your definition of what is life. Such definitions are to be discussed on Philosophy.SE, not here. Once you came up with a clear definition (probably a list of clearly defined conditions; which will be hard to do) we can discuss what forms could satisfy those conditions.

Everyone should probably note that the cited paper only depicts poliovirus polymerase replicating viral RNA, not the virus itself. This is merely polymerase doing its job; similar to what happens in a PCR reaction, but with RNA. PCR reactions do not constitute living organisms. Additionally, the replication of RNA and the replication of a full virus are massively different things; it still needs the cell to do that.

This question is basically asking, "what would a thing that we currently don't know exists be like, with as few constraints on it as I can come up with?". I don't know whether to flag is as too broad, opinion-based or unclear. I disagree that this requires a definition of "life" to be answered, but it does (at the very least) need more constraints on what kinds of features would be required for something to be "considered alive" by the standards of modern biology. Or is that what the question is asking for? Again, unclear, too broad, whichever.

I edited my question. Now, can you accept it isn't a duplicate of "Why isn't a virus "alive"?" or you still have issues here?

You've added constraints and specified the question, that's for sure. Now the problem is it betrays a deep lack of understanding of how cells work, apparently thinking it starts with nucleic acids that self-replicate and things like energy, every other molecule in the cell, ATP (!!!!!) are optional bells and whistles that can be added later. It is too long to be addressed in comments and an answer isn't appropriate to ask further questions; if you want a discussion on this I would be willing to chat though.

I agree to continue our discussion in the chat rooms but I would prefer to stay in the same room we opened yesterday- http://chat.stackexchange.com/rooms/55362/discussion-between-yordan-yordanov-and-rozenn-keribin .It's on another question but I think it's better to stay there and not create a new one specially for this question.

Oh, come on people, how do I have to modify my questions so they can be able to stay on this site?

The references I site in this answer may interest you: http://biology.stackexchange.com/a/19737/6307

Thanks for the reference canadianer, however, as far as I can see they haven't got as far in "artificial evolution" as I describe in my hypothetical example here, so I put the question in a broader context.

Your updated question, as I said in a comment is much more precise but also describes a biologically and thermodynamically absurd scenario that betrays deep misconceptions about how cells work and what they need to work. Having said that I've realized it has an answer, so I'll give it:

Would we then consider such a thing a genuine living organism and if so why?

As in every case in science where previously-sharp categories become fuzzier through the discovery or creation of entities that fall in previously-empty intermediate zones, "we" would debate ardently about whether those things should be considered "genuine living organisms" or not. There would be several possible outcomes to these debates:
1) All of the new intermediate entities demonstrate that in the space of characteristics things can have, the old category as previously defined no longer forms a sharp cluster, but a sharp cluster still does exist that is pretty close to that old category; in that case the old category gets a new definition, and as a result some entities might change their classifications, or not. Real-world example of this kind of definition change (though not necessarily caused by the appearance of intermediate steps): how stars and planets went from their antique definitions of "stays put in the sky vs moves around" to their current very-different definitions.
2) The new entities demonstrate that what was thought to be a sharp cluster in the space of characteristics is just... not. A clear, universal, unambiguous definition is thus impossible. One possibility is that the cluster dissolves entirely; the category as a whole is thus abandoned (many abandoned taxonomic terms can be seen as examples of this).
3) The old sharp boundaries no longer exist, but there is still a definite cluster in the space of characteristics that can be pointed to, it just has fuzzy borders. Like colors, which blend into each other but we still know there is "red" and "blue" and they're not the same. In that case, like with colors we might abandon the edge and focus instead on doing like we do with colors; defining the entity by looking at what "a good representative of this category is" and "what an ambiguous representative of this category is", thus giving a reliable idea of where the cluster is, where it isn't, and where the boundary is, even if it's fuzzy.
4) Sometimes you do need sharp definitions though, especially in science. In that case there are two possibilities:
4a) Use different definitions in different contexts, depending on which characteristics of the cluster interest us at any given point. "Species" is an excellent example of this; a paleontologist, a vertebrate biologist, a plant biologist, and a bacteriologist will use the same word to talk about similar concepts (a grouping of organisms with specific ecological and evolutionary significance), and they will use different criteria to determine what a species is in each case, meaning they have different definitions.
4b) Settle on an arbitrary boundary based on certain criteria that cuts through the fuzziness, with the understanding that it is arbitrary, other criteria would have yielded a slightly different boundary and different classifications for given entities that exist in the fuzzy zone, but it is useful for whatever purpose to have that boundary and thus a boundary will be chosen. Debate might continue a long time over where the boundary is, and potentially involve different people using different boundaries as in 4a, or not. Classic recent example is the definition of planet, and the process that led Pluto to no longer be considered one. This can also involve the creation of new categories, like "dwarf planet" in the case of the redefinition of "planet".
So to answer your question "would this be considered genuine life?", the answer will be "yes", "no", "it depends" or "neither" depending on which of those outcomes the debate ends up settling on. And we cannot know which outcome it will be, because the choice that will be made will entirely depend on what the space of characteristics will be like that makes a currently-sharp boundary fuzzy... And obviously we do not already know what the space of characteristics is like because those discoveries or inventions that will prompt us to revisit what we think of as "life" hasn't happened yet ! (well, not the ones you posit. Obviously the definition of "life" itself has already undergone the processes I describe many many times as it got better understood !).
(note I'm not even getting into the vernacular, and whether it will follow scientific usage or not and at what rate if so. It's interesting to note it still in many ways hasn't caught up with (or is just unrelated to) today's biological definition of "life" !)
(I will also add that I cannot posit an outcome even based on the specific scenario you describe, for two reasons: first, the decision would be a communal one made by professionals in the field, and I am a single person and not a professional biologist. Second, the specific scenario you describe already goes against everything we currently know about life, so, yeah.)

This is actually a big part of my question @tomd . How to determine the precise moment when something becomes a form of life but at the same time go out of the "specifics" of any one's particular field? However, it's part of my question this answer doesn't answer so I will wait the author's response here in the comments section.

@YordanYordanov "How to determine the precise moment when something becomes a form of life but at the same time go out of the "specifics" of any one's particular field?" You keep assuming that such a precise moment exists. It might, and it might not. If it exists then the answer to your question is trivial, but currently unknown: a clear discontinuity will be observed and be the basis to decide if something is life or not, but you're talking about observations that haven't yet been made so we can't say what the discontinuity would be. If it doesn't exist then your question is a non-sequitur.