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Do we have fundamental conflict in biology?
As saying "fundamental conflict", I mean something like two (or more) widely accepted results from different areas (or scales) can not exist logically together. In physics, there have been three conflicts1. I wonder if in biology, do we have such conflicts? And how biologists resolved that?
1  One of them is the conflict between Einstein's general relativism and quantum mechanics. String theory, if it is proved to be true, will reconcile this (read more). But it can also be like the controversy of the property of light. Some said it was particle, some said it was wave. Modern physics says it is both.

Several of them :P

Can you name some? I need a starting point to google

i think it is still not settled, whereas brain "computes" using mathematics, e.g. stores and solves equations, or process of vision is some stochastic MIMO black-box, which we represent as equations/math.models

But i think that googling should put you on right track. I haven't seen any relevant review, unless you consider latest Nature Methods article on p-value

This immediately came to mind, though it's not the example from different areas that you're looking for.

I think it is unlikely to have such (large scale/fundamental) conflicts in biology, because it is relatively easy to conduct experiments compared to physics. E.g. you wait for a proof of gravitational waves since when? Decades? The same with string theory, etc...

@canadianer Nice! :D We have exactly this kind of problems. I read many similar articles.

@aandreev this one turn out to be too technical to me...

Peto's Paradox is a great one. This addresses the disconnect in cancer incidence with cell number in an organism. It goes something like this:
Assume current oncogenesis theory to be correct in that mutation acquisition is the rate limiting step in creating a cancer, such that you need ~5 specific mutations in a single cell for that cell to be fully transformed into a cancerous cell. This then being the case, it is so rare that any cell can acquire all necessary mutations that in humans we don't see cancer incidence appreciably increase until the 5th decade of life.
Now, let's assume man has an average weight of 50kg and a blue whale has an average weight of 130000kg, with roughly equivalent lifespans. Assuming average cell weights are the same in both organisms, there are 2500X more cells in a blue whale than a human.
If linear mutation rate is the rate limiting step in cancer then increasing cell numbers is akin to increasing the number of times you flip a coin to try and get heads, which means there is a 2500X greater chance of getting all ~5 necessary mutations in a single blue whale cell than in a single human cell. If human cancer incidence starts to spike at 50 years, this means blue whale cancer incidence should spike after 7 days and blue whales should largely be eliminated by cancers within the first month of life.
Hopefully makes you question a bit what is causing cancer.
Make sense?

I never heard of that. It is interesting. However, it is the number of cell divisions that separate a given cell at the adult age and the zygote that matters and not the number of cells. Also, individuals that develop cancer rarely developed from a "clean" zygote. This greatly reduce your estimation as well. So is there still some kind of Peto's paradox or is it totally negligible?

@Remi.b -- More cells = more cell divisions required in the first place. Whale cells are not orders of magnitude larger than humans, despite being orders of magnitude larger as an organism. Since the vast majority of cells have some turnover, having more could also mean a hire rate of division even if the time it takes is higher. Peto's paradox looks fine (to me), but it does point out that DNA mutations do not always result in cancer. An extra stop-check prior to cell division seems to have a tremendous effect on cancers if you look at Naked Mole Rats. ;-)

Right, MCM is hitting a bit closer to the point. Remi.b when you say that the number of cells division is important, I agree, but once you have created an organism the cells do not stop dividing, they continue to divide and turnover for the rest of your life. And if you are suggesting by an "unclean" zygote, that it already carries something like an inactivating p53 mutation, this is a very special case resulting in serious problems for the organism because every cell in the body carries the mutation, and will oftentimes be embryonic lethal.

And I have to address the Naked mole rats because I think this is great evidence to the contrary of the mutation-centric cancer model. Naked Mole Rats have a higher density hyaluronin which may impede metastatsis, and hyperplasias. This is a great example of an evolved strategy to limit oncogenesis during potential reproductive years. And is doing nothing to change cellular mutation rate.

this one is something I'm looking for. Thanks for that.

Could not fit in a comment...
The question very much depend on what you mean by fundamental conflict (to the point that I am surprised to see nobody complaining that the question is primarily-opinion based). My first reaction is to think that there is no such fundamental conflict in biology just because biology is not really a "fundamental science". I am not sure what I mean by fundamental but I hope the comic will help understanding my point!

Of course, it is not true that biology is just applied chemistry (as I would expect the other relations to be wrong as well). Personally, I know nothing about chemistry and in my field of research (theoretical population genetics), we use math, statistics (which is just applied math) and algorithmic (which I guess is just applied math as well). Math is just applied logic by the way.
There are things we don't understand, but I don't think there are many fundamental conflict or paradox. There are many things that we have hypothesis (sometimes vague hypothesis) for it and have no idea how to test them.

i think question is about experiments that are contradictory, but haven't been refuted. Or contradicting hypotheses, both of which are supported by strong data and peer-reviewed publications. In terms of "fundamentalism", you are right, there is no "wave-or-particle"-type conflicts. Except on high cognitive level (see me comment to OP)

I always love this cartoon since I am in mathematics/engineering

@aandrev. I agree that there might have some cool fundamental looking stuff in neuroscience. It is a field that is in between algorithmic and neuroscience.

@dustin Yes, I like this cartoon. I'd appreciate to add philosophers even further to the right side. However, I apologize but engineering is by definition applied knowledge. So I would place engineering at a pretty low level of purity.

@Remi.b engineering is just applied physics if you think about it. The cartoon is also ordered in mathematical rigor so it would probably sit between chem and physics.

Have you read the explanation of it on explainedxkcd?

I think this is the most famous comic of xkcd. And I agree with @aandreev. So in your opinion, what is a "fundamental conflict"?

Well. I don't know but it is the OP's job to define the terms used in his/her question


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Problem involving genetic interactions in yeast
I'm having difficulty with the following problem:

In yeasts, genes MEC1 and SGS1 favor survival in response to HU
(hydroxyurea). In the figure below, Δ indicates homozygosis for the
mutant allele that causes loss of function. mec1-100 yeasts are
heterozygous (one MEC1 allel is wild and the other is mutant).
a) What genetic interaction do genes SGS1 and MEC1 maintain?
b) How do you explain the results at the molecular level?
c) How do you explain the difference in phenotype between the homozygous and heterozygous yeasts for the allel that causes loss of
function for the MEC1 gene?
d) Why would you combine the sgs1Δ mutant with mec1-100, instead of combining it with mec1Δ?

My attempt to solve this was as follows:
Observing the sgs1 Δ mutant in homozygosis for MEC1, we see that the phenotype that is produced is within a scale close to the WT phenotype. Further, in heterozygosis for mec1-100 without mutation we also see a phenotypical scale similar to the WT. When we see the heterozygotes for mec1-100/sgs1Δ the scale drops abruptly and the phenotype passes to be very far from the WT phenotype. This last one can be explained as an incomplete dominance in which the genotype of mec1 must present both WT allels to achieve its effect, because just one of the WT alleles cannot fulfill its function, so what we see in comparison with the sgs1Δ/MEC1 homozygote dominant is different from mec1-100/sgs1Δ. When we mutate the gen mec1Δ we see that the viability of the cells is reduced, even though the gen sgs1 is still present.
What has been observed and described previously could be explained as a recessive epistasis where regardless of what happens with gen SGS1, if MEC is mutated (double recessive) it masks the effect of Sgs1. That is clearly seen because when mec1 is present, the viability is close to the WT scale while when mec is mutated or in heterozygosis (which would work as a mutant by the incomplete dominance) it does not matter what happens with sgs1 (if it is mutated or not mutated) the phenotype of the molecular pathway is not produced (a phenotype of low viability is produced instead).
At the molecular level, it could be explained as follows:
A substrate exists that uses the enzyme produced by MEC1 to activate the viable molecular pathway. In absence of MEC1 the pathway is not activated, SGS1 uses MEC1 to carry out its function that also promotes viability, therefore if MEC1 does not exist SGS1 does not have an enzyme to interact with.

But turns out that the correct answer for this problem is that the genetic interaction is a redundancy between SGS1 and MEC1.
My question here is:
Can this problem, as expressed in the first paragraph, be taken as a recessive epistasis? Why can't it be considered a recessive epistasis? In cases where we have a logarithmic scale, if the correct answer is a genetic redundancy, can we take it as a viability generated by both genes anyway? Is the viability generated by each gene comparable at all?

This is a well-formulated question, but the prompts suggest that it is an exam question or other similar coursework. If that is true, you should add the "homework" tag. (You have clearly shown your attempt at an answer, which means that this question is appropriate for the SE Biology community.)

@MaximilianPress thanks! Will add it now. Yes, this is from a set of prep exercises for an exam that is driving me a little bit crazy.

Based on the graph of experimental results, WT diploid yeast are able to grow in the presence of HU (hydroxyurea).  Deleting both copies of the MEC1 gene results in cells that stop growing in the presence of HU; therefore the wild-type product of the MEC1 gene is involved in resistance to HU (as described at the start of the homework question).  Deleting both copies of the SGS1 gene has a slight effect on growth in the presence of HU.  From this we infer that the wild-type product of the SGS1 gene has some role in resistance to HU, but these mutant cells can still grow, and therefore contain some other activity (or activities) that provide resistance.
The MEC1 gene is dose-sensitive; when you remove one functional copy with the mec1-100 loss of function allele, the cells resistance (or growth) is intermediate between wild-type cells and the mec1 homozygous null (knockout, or deletion).
mec1-100 heterozygotes, that also lack both wild-type copies of the SGS1 gene have much worse viability/growth/resistance to HU (when compared to either the sgs1 homozygous loss-of-function allele alone OR the mec1 heterozygous loss-of-function allele).  In other words, it appears "more" mutant, or closer in phenotype to the mec1 homozygous mutant.  Therefore the wild-type function of the SGS1 gene overlaps with the wild-type function of the dose-sensitive MEC1 gene.  Two genes with overlapping genetic functions are by definition redundant.
I would've described sgs1 as a recessive enhancer of a mec1 hypomorph.  Historically this can be a powerful way to identify genes that may be involved in the same cellular process.  When I see the term 'recessive epistasis' I think of trying to order genes in a genetic pathway.  As in, which gene is 'upstream' and which gene is 'downstream' in the genetic pathway.  It doesn't make sense (to me) to try to "order" two genes with redundant function.  Sometimes redundant genes encode proteins with homologous sequence (e.g., different classes of tubulins), but sometimes redundant genes indicate that there are parallel pathways at work (and one compensates for the lack of the other).  I suspect that you are using a different definition of 'recessive epistasis'.

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Why do Bactrian camels have two humps and dromedaries one?
Why has the Bactrian camel evolved to have two humps instead of the one that the dromedary has?
I searched on Google and I found nothing about it.
All I found was that the that humps store fat, that the fat can be converted into energy and water, that this lets them survive in deserts. As far as I know this is true also for dromedaries.
I also found that the Bactrian is smaller than the dromedary, that Bactrians are less numerous and they are at risk of extinction.
No site explains why Bactrian camels have two humps instead of one hump, as in the dromedaries.
Sources:
https://www.google.com/search?channel=fs&client=ubuntu-sn&q=why+do+bactrian+camels+have+two+humps#bsht=CgRmYnNtEgQIBDAB
https://en.wikipedia.org/wiki/Bactrian_camel
https://en.wikipedia.org/wiki/Dromedary

Why do you think there needs to be a reason as opposed to say genetic drift of two different lines?

@John Of course there was a genetic drift, but why dromedary was successful? I suspect that the fact that it's more small make it more adaptable to desert conditions. But I suppose this is another question.

First of all, it seems that the Bactrian is not smaller than the dromedary, and that dromedary and the Bactrian camel evolved from a common ancestor with two humps. So it seems it's the dromedary that evolved to have only one hump, and not the contrary.  I quote Wikipedia:

The modern dromedary probably evolved in the hotter, arid regions of western Asia from the Bactrian camel, which in turn was closely related to the earliest Old World camels.

It seems that the dromedary hump can store 80 pounds of fat:
https://www.nationalgeographic.com/animals/mammals/facts/arabian-camel
I failed to find how much fat a Bactrian hump can contain. A male Bactrian weights 590-1000 kg. Dromedary weights 400-690 kg.
So it seems a dromedary has only one hump because on average its weight is less than the Bactrian.
We can assume that the ancestor of the dromedary was a smaller camel with two humps. Over time, probably the second hump became smaller and smaller, until it disappeared. From Wikipedia:

the dromedary foetus has two humps, while in the adult male an anterior vestigial hump is present.

Be careful with conclusions. Does it only have one hump because its weight it lower or is its weight lower because it has one hump only? I tend to the second possibility.

@Chris good observation. I think you're right. I don't know if we have dromedary fossils, but I suppose a big camel with only one hump have smaller opportunity to survive than a smaller camel with two humps. I'll edit the answer.

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Bad Eyesight and Evolution
Why do many humans have bad eyesight, such as near-sightedness, which hampers performance in a wide variety of tasks? Shouldn't there be evolutionary pressure towards better eyesight?

Remi.b and Potterbond007 have put forward excellent answers. Would like to add something..
One of the reasons that Myopia (near sightedness) happens is because of use of eye in work like reading, which requires working with close objects. I don't think there was much working with close objects in the past. So very few people with myopia might have been present (and of course, they may have had disadvantages in catching prey.)
Other common disease is hypermetropia which generally occurs during old age, past the reproductive prime, so it could not have much evolutionary impact.

With nearly 40,000 years of natural selection on eyesight, prior to the invention of eye glasses, there needs to be a better explanation than the effects of 'modern' technology. There are two likely reasons for the persistence of "poor" eyesight in humans. First, humans are social animals and live in groups. Within groups there is frequently a division of labor. This division of labor deemphasized the importance of vision. Individuals with "poor" eyesight could easily maintain a high fitness (reproductive success) in this social structure. Second, humans have long term parental care (both within and among families - again a function of social living). Most human offspring maintain close familial connections up to and including the age of reproduction. The strength of selection on eyesight diminishes past reproductive age, allowing individual with poor eyesight to have relatively high fitness.

Maintenance of Polymorphism and Mutation Load
There are many possible reasons why some amount of deleterious alleles are maintained in the population. One of which is the mutation-selection-drift balance. In short: Because mutations always occur, there is continually an input of deleterious mutations in populations genome resulting in some fitness decay (called mutation load). While mutations create this polymorphism, processes of selection and genetic drift cause a decrease in polymorphism. At equilibrium there is a balance between mutations, selection and drift called the mutation-selection-drift balance. You may also want to consider various population structure related concepts such as migration between patches. Haldane first explored this mutation load theoretically and estimated that the fitness of an existing individual in a population of perfect (deleteterious-mutations-free) individual is about 80% lower, which is huge! Such mechanism can explain various disease found in a population.
Age-specific intensity of selection
Also, for the question of disease appearing late in life (which is often the case of eyesight related disease), it is important to realize that those genes which are expressed late in life undergoes a lower selection resulting in a higher mutation-selection-drift balance. See this post for more info.
Impact of Medicine and social helping on the intensity of selection
As pointed out by @potterbond007 modern medicine allows to diminish the deleterious effect of some mutations. For example, one that has clubfoot may be operated and is likely to survive and reproduce and therefore propagating its deleterious alleles. This would be different in some past. Therefore, medicine diminish the selection pressure on deleterious alleles. However, modern medicine probably has a very low effect on our genomes because it is so modern. 100 years ago we could not operate clubfoot and 500 years ago (almost) nobody had glasses to correct for eyesight deficiency. We may go a bit further in the past and also consider that social interactions such as helping weak individuals in a tribe may also have decreases the selection pressure against deleterious alleles (more info in @theBIOguy 's answer). Of course, if selection is diminished the mutation-selcetion-drift balance is increased and deleterious alleles are more common and mutation load is greater.
Further investigations will be needed in Epidemiology
Assuming that eyesights disease are particularly common and deleterious, we should have a closer look to the epidemiology of the diseases of interests. If it seems to you that eyesight-related diseases are more common and more important in terms of their effects on fitness than diseases on other traits then, you may want to seek into some physiological and developmental explanations that may tell you why eyes are so likely to be impacted by genetic and/or environmental factors. I personally have absolutely no knowledge about the epidemiology and developmental mechanisms of any eyesight disease! Also considerations of the impact of modern environment should be considered such as the impact of TV and computer screens on our eyes (more info in @biogirl 's answer)

Your answer was technical, but I understood it.

Mainly because we haven't been forced to remove the bad genes that cause these defects from our gene pool. In ancient times, a bad gene that causes poor eyesight would have made it difficult for a person to spot prey or escape from a predator. However, we have glasses now which gives the bad eyesight gene as much a chance to propagate as any other gene. it also doesn't really matter since poor eyesight is never a factor for survival in present times. The same with poor hearing which we correct with hearing aid. Please read this for an article in the guardian and this article in the orlando sentinel. You could also read this discussion on reddit to see a few fun arguments.

Does is then indicate that if humans stop using artificial aids to overcome their shortcomings, then there is a chance that advantageous evolutionary traits would be observed in the future?

@rudstar no it does not since the existence of excellent eyesight is not such a limiting factor in present times is it. Even if we stopped using artificial aids, every individual with the defective gene is still going to survive and have kids. Would be significant if there was a defective hypothetical gene which lead to infertility and we did not have present day advances like IVF.

Yes, I get it. Reproductive fitness is what matters.

Glasses and hearing aids are very new inventions, only a few hundred years old.  There were hundreds of thousands of years of evolutionary pressure towards better eyesight, yet many people still have bad eyesight.

@Tiberia But human being's evolution to be at the head of the food chain is not a recent occurrence.. There is no pressure on the bad gene to disappear from the gene pool even less with the present advances in science.

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How do I identify the protein with the highest Disulfide bond density? i.e protein with highest ratio of Disulphide bonds per Peptide bond?
I want to list all proteins in the protein database and list them by the ratio of number of disulphide bonds per peptide bond.
I am not particular about the reliability of identification of disulphide bond.
--EDIT 1
I've been doing some research on this topic, and heres what i've found.

The PDB structure file lists all the Disulphide bonds in each structure.(SSBOND)
The PBD structure file does not list the number of peptide bonds, however it does
mention the number of amino acids. And number of peptide bonds = [no. of amino acids - 1].
We can generate a list of all PDB structure IDs with atleast 1 disulphide bond, using PDB.org's advanced search feature. This gives a list of 22543 structures.
Downloading all the 22543 structures and then parsing them using any programming language would be easy, except for the difficulty of downloading all the 22543 sturctures.

So the question now is:
 How do I parse all the 22543 structures to output only the number of disulphide bonds and the number of amino acids in each chain, without downloading the PDB structure files?

Count the number of cysteines and divide by total number of amino acids- that would be a not so reliable method.

That is the obvious answer for a single protein. I am looking for a way to do it across all the proteins in the PDB.
Essentially I want a way to query the number of Disulphide bonds from all proteins and the number of amino acids from all the proteins, and print a list.

You can download all sequences from the PDB in one file: (gzipped fasta format)

Thanks Mad Scientist, I did not realize that it would be such a small file. I guess i'll have to do a little bit of coding to get the rest of the answer.

@user8338 for PDB files you can actually find real disulphide bonds instead of counting cysteines. They would be annotated. If you are looking at all possible disulphide bonds, you can download the Refseq protein fasta file and count cysteines

@user8338 Parsing is a programming question and is off-topic; suitable for stackoverflow. However you should make an attempt at it before asking in SO.

I'm voting to close this question as off-topic because it is about text-parsing.

@WYSIWYG I agree the text-parsing part is off topic. My problem is about if it can be done on any server without me downloading the text files.

@user8338 I don't think so. The files are not that huge; you can download them without any problem.

@WYSIWYG the complete list of 22543 PDB files is in an excess of 2GB, compressed as gzip. I've been trying since last night to get them as a compressed file, and failed. Now I'm trying to download them uncompressed.

@user8338 Try doing with wget if you have a linux system. It is also available for windows with the GNUwin32 package.

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is it necessary that every theca of an angiospermic anther must contain two microsporangia
i basically don't know the procedure or sequence of steps involved in the formation of anthers but i have read it somewhere it is formed from the dedifferentiation of shoot apical meristem of the axillary bud through mitotic divisions

so is it necessary that every theca of an anther of an angiosperm must contain two microsporangia, if yes then why are they two in number., can i get an account on the development of microsporangial lobes [here i am not asking about the process of development of pollen grains in them].
i am asking how the microsporangial lobes itself are formed
a diagrammatic answer would be highly appreciated

Is the necessary that stamens have two microsporangia per theca? No. Many species in Cryptocarya group of Lauraceae have microsporangia that have fused such that they have only two microsporangia instead of the typical four (Rohwer et al. 2014). I interpret their description as saying that the microsporangia within a theca but it's not clearly stated as such.
Within the Magnoliidae, one pollen sac of a theca is lost is some taxa (Endress et al. 2008). Evolutionarily, the Hamamelidaceae have reduced the number of pollen sacs from two to one (Endress 1989). I could not find examples of plants with more than two microsporangia per theca.
Why do most plants have two pollen sacs per theca?  It's probably a result of the evolutionary history of plants in general because it is so common. Even those that have only a single pollen sac seems to start out developmentally with two.  It's probably due to the underlying genetics.
The genetics of floral development is complex but being slowly teased apart. The overall development of floral patterns is set by a group of developmental or regulatory$^1$ genes called MADS genes.  Collectively, the MADS genes (along with other regulatory genes) control the overall organization of the flower structure. For example, MADS genes determine the arrangement of floral whorls from sepals (outermost whorl) to petals to stamens to carpals (innermost whorl). Changes in use or timing of the MADS genes can contribute to different types of floral morphology, such as the loss of sepals or big, showy sepals but no petals.
Some of these same MADS genes contribute to the formation of the stamen structure. The review by Goldberg et al. (1993) gives a thorough but now dated review of the developmental genes that control anther development. The figure below (their figure 3) gives a nice overview of the stages that lead to development of the theca with two microsporangia and ultimately to the final stage of fertilization. Even more specific, Bowman et al. (1991) show that AGAMOUS is one regulatory gene that is active during the development of the theca and microsporangia.

I can't speak in detail about how regulatory genes work in flowers (I know a bit more about regulatory genes in animal development, especially from an evolutionary developmental perspective). In animals, regulatory genes often work by concentration gradients, both by the concentration of the regulatory gene itself, by the concentration of other regulatory genes, and by the concentration of the regulated genes. This process helps to determine the anterior-posterior axis in animals with bilateral symmetry, as well as the left and right sides.
I suspect that floral regulatory genes work in a similar fashion.  Changes in regulatory expression can lead to bilaterally symmetric flowers (think of mint flowers, monkey flowers, etc. See Hileman and Cubas (2009 for a good review.). I suspect it is some type of symmetric expression of regulatory genes that leads to the formation of two microsporangia per theca.  Mutations that cause changes in the expression patterns of other regulatory genes can cause the initial expression but subsequent loss of one of the microsporangia, as noted for the Lauraceae and the Hamamelidaceae.
Footnote
Broadly but simply, regulatory genes are genes such as transcription factors that regulate or control the expression of other genes.
Literature Cited
Bowman, J.L., et al. 1991. Expression of the Arabidopsis floral homeotic gene AGAMOUS is restricted to specific cell types late in flower development. The Plant Cell 3: 749-758.
Endress, P.K. 1989. Aspects of evolutionary differentiation of the Hamamelidaceae and the Lower Hamamelididae. Plant Systematics and Evolution 162: 193-211.
Endress, P.K. and L.D. Hufford. 2008. The diversity of stamen structures and dehiscence patterns among Magnoliidae. Botanical Journal fo the Linnean Society 100: 45-85.
Goldberg, R.B., et al. 1993. Anther development: Basic principles and practical applications. The Plant Cell 5: 1217-1229.
Hileman, L.C. and P. Cubas. 2009. An expanded evolutionary role for flower symmetry genes. Journal of Biology 8: 90.
Rohwer, J.G., et al. 2014. A phylogenetic analysis of the Cryptocarya group (Lauraceae), and relationships of Dahlgrenodendron, Sinopora, Triadodaphne, and Yasunia. Phytotaxa 158: 111-132.


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Are there any cases of observed extreme speciation
Is there an observed (direct not indirect) speciation on record showing a species shift within the span of history of recorded science?

I think this post may interest you. It is maybe even a duplicate.

a simple google search would have provided this page showing examples of speciation, even artificial ones (http://en.wikipedia.org/wiki/Speciation)

I'm looking for something more along the lines of a fruit fly evolving into a june bug or an ape evolving into a human. Obviously those examples are ridiculous, but they explain my point. I'm looking for something where one kind becomes another... and I hate using that word...

I should add that I don't expect to find anything like this, but I figured this would be the place to ask.

Darwin in origin of the species makes several examples from live stock and pets.  During his time creationists argued that all (or many) of the different dog breeds came from different origins, each of which was created separately by god. Darwin makes good arguments for conversion by man, your modern creationist is unlikely to argue the multiple dog origin in light of  modern science.  The lesson here is that, your creationist, has been fed, a hand picked question that can not be satisfied, and when it can they will pick a new question.

Rebuttal question "Show us documented proof where the amputee has their limb instantaneously restored"

This question seems to involve an attempt to respond to ID rhetoric. Instead of asking a precise but open-minded question OP is asking for an example of something that may not be directly observable. This site wastes too much time (IMO) responding to faux-naif questions from evolution deniers masquerading as open-minded middlemen.   There are plenty of these questions in the record and on the net. This is not the forum for them even if the OP is in fact well-intentioned.

As much as I can agree with what you are saying daniel, I am asking because I had hopes that someone WOULD have an answer. I have already answered my debater with this: https://docs.google.com/document/d/1S5tX2H4J4hR41mD7-oT5qw3o9cq46u6ipgV2SQFeJS4/edit?usp=sharing

So to sum it all up, the question still stands. My reason being that surely someone has either an example that I can use to both answer and respond to these types of questions as well as something that will educate me. I TOTALLY get that ID rhetoric is a huge problem for the scientific community. But just ignoring it won't make it go away... it makes them think they have valid questions. Then they go and get valid lawmakers to support them... ugh

How on earth is this 'off topic'????
I am asking for biology-based evidence of speciation. I didn't realize that my REASONS for asking a question would matter one whit. This is fairly ridiculous and casts quite a pall over all other questions that anyone can ask on these boards as far as I am concerned. I thought that the clarify, simplicity, and reasoning behind my question followed ALL of the 'scope' requirements of this board. There wasn't a drop of philosophical or any other non-biology related characteristics to my question. Simple biology 101. Someone needs to re-review this hold.

ID proponents' belief that their questions are valid is not a reason to entertain them here. You are not asking for evidence of speciation, you are asking for "fruit fly to june bug" speciation. You can raise the issue at the Meta site. I don't expect in my lifetime to see fruit flies turning into june bugs.

Fair enough. THAT makes more sense than the blanket hold with standard answer. Thanks @daniel

But I do think Remi.b's comment is responsive to this question. Also you should post a question on Meta so we don't drag this out here.

Hi @randomblink.  Please note that your question was put on hold by the community and up till now has had no moderator intervention.  Privileges are earned by the amount of reputation a user has on the site, which is a indicator of how trusted that user is.  In this this way, it is the community that determines the scope of the site.  I can see that you have made efforts to improve your question to get it out of the hold - can I ask why the first question linked to would not be a duplicate before I vote to reopen?  At a glance it seems to provide you with an answer.

@RoryM the reason that the question linked to would NOT be a duplicate because the questioner in that instance is referencing reproductive isolation as the definition of another species. This is something that fruit flies are famous for as well as several lizards and a few plants and bacteria. I am searching for a more pronounced evolutionary step whereby more than just reproductive isolation or minor coloration is the defining marker of speciation. I'm looking for a larger gap between the original species and the new one.

Could not fit in a comment…
What kind of observations will you accept to be an observation? If we can demonstrate showing genetic data that two current species where actually only one some time in the past would it represent an observation to you? Or does it has to be a lab experiment (experimental evolution)? Experimental evolution with big animals take much time, I am afraid we probably have no evidence (not counter-evidence) of a mammal species that evolve to be phenotypically speaking as different than a fruit fly and a june bug (example coming from your comment). Would you accept considering microorganisms (I have no example in head though right now)?
As you noted yourself I think, it is difficult to know how different (phenotypically or genetically?) should two sister populations (populations who derived from a common ancestral population) be so that you would consider that one of these populations at least evolved into another "kind" (compare to the ancestral population).

I 'knew' that there would not be an answer that would give me what I wanted after 'thorough' online searches. But I had hope that someone would have an obscure link that Google had missed. The level of evolutionary steps I was searching for are just not going to happen within the tiny historical steps as little as decades or even millenia. I was being WAY too optimistic.

but I had to try!

Good to try $\ddot \smile$ Hope you agree that you have to decide 1) what you will accept as being an observation (Not all methods of observation in science are easy to understand for non literate) and 2) what kind of differences you are interested in.


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Free energy difference between change in protein structure and its reverse?
I have seen in many articles that a protein variation (A- > B) and its reverse (B- > A) must have the opposite value of the free energy difference (ΔΔGAB = − ΔΔGBA).
But i’ve alse heard that in experimental data this is not true!
So i am a little bit confused; can anyone explain it? Which is the case?

Welcome to Biology StackExchange! The Gibbs free energy $G$ is a state function, hence the free energy difference of the reversal process $\ce{B->A}$ has the opposite value of the forward process $\ce{A->B}$, $\Delta G_{\ce{B->A}} = -\Delta G_{\ce{A->B}}$. Please edit you question and include references (articles, books ...) where they state that this is not true. Otherwise, we cannot know what exactly they mean, and also cannot give you any meaningful answer.

I have modified your title to indicate the type of “variation” you seem to be referring to on the basis of one of your tags. But you should make this clear in your question, or if this is incorrect say precisely what you mean. “Protein Variation” could mean many things, and protein folding would not be on my list.


text:
What is the difference between digesting sugar and carbohydrates?
To understand where I'm coming from, first some commonly distributed (mis?)conceptions:
(Obviously to be taken with a big grain of salt because they are somewhat contradictory)

Sugar is bad for your health, because it goes into the blood quickly and thus creates a blood sugar spike upon consumption.
Snacking often is bad for your health, because it puts the body in a state of permanent digestion and keeps blood sugar high.
Carbs are better than sugar because they release the glucose over time a supposed in a spike.
Slow carbohydrate food (food that is supposed to release the glucose extra slowly, due to the chemical composition of the carbohydrates inside, or the physical structure of the food?) is better than carbohydrates, because it releases the glucose even slower.

Now the second one and the other three ones are somewhat contradictory, because if it was solely about the peak glucose levels, snacking should be healthy (which it probably is not), so something's off...
So I'd like to know:
What are the biological differences between the digestion of sugar and different types of carbohydrates as constituents of different types of food in humans?
Edit:
For more context:
I would like to understand what the most important aspects of carbohydrate digestion are, in order to be able to conclude a diet that helps me optimize my health from that.
I am very well aware that:

Sugar is carbohydrates.
Many carbohydrates will eventually be broken down into sugar.

I am also aware that "carbohydrates can be bad".
What I do not understand is how exactly "carbohydrates are bad".
In particular, I got confronted with three viewpoints:

High average blood glucose levels are bad.
High peak glucose levels are bad.
Snacking is bad.

Which seem to go in different, rather contradictory directions.
Also, Studies partially supporting either viewpoint can be found:

Study considering hemoglobin A1c levels
Study considering peak glucose levels
Study considering snacking

Which leaves the non-biologist asking themselves which is the "major effect" (certainly, there will be some truth to each position, but the question is which one(s) got the "main point"), and if there are any other important effects to be considered, hence this broad question here, so I understand, from a biological standpoint, what happens to the carbohydrates when I eat them, so I can conclude for myself how to adapt my diet for "optimal" health.

Sugar is a carbohydrate. If you want scientific answers to your questions, you'll have to start with scientific sources that make these specific claims. Anyone can claim whatever they want is good or bad and write a book about it, that doesn't mean it's right or useful for anything besides selling the book.

This site is for students of biology and biology professionals. Its purpose is not to provide textbook information for non-biologists. If you wish to learn about the metabolism of carbohydrates you need to buy a textbook and study it.

@BryanKrause I added some studies as references, as expected, you can find studies to argue either way, so who "got it" then : (

well for a start, cellulose is fiber and is not digestible so yes different carbs are digested in different ways, but I suggest breaking this into 3 different questions since otherwise you are asking for a dissertation on carbohydrate digestion. Also several have already been asked and answered. https://biology.stackexchange.com/questions/31352/do-blood-glucose-spikes-contribute-to-insulin-resistance-or-is-prolonged-elev?rq=1

The level of detail of a Wikipedia article would suffice : )

If your goal is to have "a diet that helps me optimize my health", then I suggest talking to a doctor, specifically a nutritionist. If for some reason or another that is not possible, I would suggest reading articles on trustworthy sites, such as www.cdc.gov or www.who.int. Just so you know, pretty much everything you described is about blood sugar levels, which your body does a very good job maintaining using insulin and glucagon. The condition of this regulatory system not working is called diabetes. If you are not diabetic, then daily calories is much more important than blood sugar level.

The problem is there is conflicting information out there, and the CDC and the WHO each have a track record that is neither abysmal nor perfect, just like most other sources too, so I don't trust either side, and try to gather as much information as possible, with a coherent big picture drawing from multiple sources as primary goal, because if things from different sources fit together well, they are more likely to be true.

That being said, I will of course also consult a nutritionist.

I do not see any conflicts in the sources you cite. There is no reason a snack can't cause a blood sugar spike for example. If you are after nutrition guidance there are lots of guides that do not require an understanding of sugar metabolism. Basically, eat lots of plants, avoid added sugars and excess fats, eat a varied diet.

Scope of Answer
The original poster provided ample context for his question, which related to health considerations. It was perhaps for this reason, among others, that the question had not received an answer at the time of writing: questions relating to medical or health advice are off-topic here. However, his actual question is primarily biochemical:

What are the biological differences between the digestion of sugar and
different types of carbs as constituents of different types of food in
humans?

Although this might be answered with a little internet search, I felt it would be hospitable if someone offered him an answer to this — and this only.
Definitions
The basic sugar unit is a mono-saccharide, those of relevance to this question being hexoses or pentoses, having six or five carbon atoms, respectively.
What in non-technical language is called sugar, refers to a specific molecule, sucrose, which is a disaccharide of covalently-bonded glucose and fructose.

What in non-technical language are referred to as dietary carbohydrates generally refers to the storage polysaccharide of plants such as potato and other root vegetables, rice, and other cereal crops used to make bread. This is a homo-polymer composed solely of glucose units.

Summary of the differences in metabolism
Arising from these definitions, the following differences in metabolism emerge:

Different enzymes (amylase for these polysaccharides, sucrase for saccharose) are used to catalyse the hydrolysis of the linkages between the monomeric units.

Absorption in the gut is different for glucose and fructose, as is transport into cells.

Both glucose and fructose are (or can be) metabolised to pyruvate. However fructose is first metabolised to fructose 1-phosphate, and only enters glycolysis at the triose phosphate stage. A consequence of this is that it by-passes any regulation that occurs for the metabolism of glucose after conversion to glucose 6-phosphate. (In addition, glucose 6-phosphate has alternative metabolic possibilities not shown).

Postscript
This provides the framework for considerations of the consequences of dietary intake of sucrose, which are not part of the question and off-topic here, as already mentioned. Despite that, this topic has been addressed in questions in SE Biology, as well as elsewhere on the internet. I try not to offer advice to others (nor to take it from strangers). However my wife, whose advice I am sometimes obliged to take, professes the following:
“All things in moderation, and moderation in all things.”

Nice answer. Also fits very well with other information I recently acquired.


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How many proteins are in the Earth's proteome?
Humans alone have thousands of proteins. With that in mind, it seems like the total number of proteins among all species would be very large.
Are there any available estimates for how many proteins exist on earth in all organisms? I'd also be interested in how many of these are unique proteins as opposed to proteins that are very similar to other proteins, i.e an estimate of non-redundant proteins alongside the redundant proteins.

Well, remember that just about all proteins are evolved from other, related proteins, so how many you consider unique is really a matter of definition. If you and I have a protein with a single amino acid substitution, is that a new protein? Kind of makes the question impossible to answer.

As @BryanKrause mentioned, if you intend 'unique' to signify "found only in humans/only inone of all other organisms", there will be very few. If you mean 'unique' to mean "different", we don't have that answer. We're still discovering new species almost every day!

@BryanKrause Protein redundancy is a fairly common method of allowing clusters of proteins to be represented by a single protein. This avoids biases introduced by overstudied systems or by large groups of very similar proteins masking distant proteins that would have different biochemistry. It's a scientific way of generating lists of "unique" proteins.

I see no reason it should be closed as unclear. It's a simple easy to understand the question. It's subjective indeed, but there are papers estimating these types of questions, so it's not completely a matter of opinion.

I'm voting to reopen this question since there have been scientific studies on exactly this question. See "Towards the completion of the earth's proteome" Perez-Iratxeta et al. 2007. This question can be quantified and objectively explored. On the other hand, the unclear votes appear to be from a miscommunication that single sequences can represent homologous clusters. I've edited the question to make this part of the question more clear.

To the close voters, what about this question is too broad? Potentially it could be answered with a number and a citation alone.

Current records
According to Uniprot, there are 85,381,808 protein records, and with the UniRef90 filter (i.e removing records that can be represented by an entry with at least 90% sequence similarity), there are 42,424,511. However, these databases are moving targets and will change over time. We will sequence more species, find novel splice isoforms, and various other methods will expand the databases. Indeed, the databases will be truncated also from time to time as some hypothetical proteins may be based on genes that turn out to not code for proteins after all.
In 2007, a study estimated that the earth's proteome would contain around 5 million sequences, and that the majority of these would be elucidated by 2012. I suspect this is a very thorough study, however, a lot has changed in the last 10 years. This estimate is actually less than the nearly 9 million species estimated in more recent studies.
Approximate estimate
So let's do some back of the envelope maths. Let's assume the article estimating nearly 9 million species is about right, and that we've only catalogued some 1.2 million. But UniProt isn't even close to this number.UniProt contains 25477 scientific names in it's controlled vocabulary. So for 25 thousand names, we have 85 million protein records. What if we had 8.75 million names?
Let's assume:
$\frac{Predicted~Proteins}{Predicted~Species}=\frac{Known~Proteins}{Known~Species}$
We can rearrange this to:
$\frac{Predicted~Species~\times~{Known~Proteins}}{Known~Species}= Predicted~Proteins$
Generous estimate (Uniprot, 335527 proteins per species):
$\frac{8750000\times{85381808}}{25477}=2.932413e^{+10}$
Conservative estimate (Swissprot, 41 proteins per species):
$\frac{8750000\times{554241}}{13408}=3.616952e^{+7}$
For the sake of completeness let's assume the number of <90% identical proteins will remain around half that value. We can say that there might be around $1.8e^{+7}$ to $1.5{e}^{+10}$ "unique" proteins, less than a trillion ($1e^{+12}$). Given the absurdly generous 335 thousand proteins and very stingy 41 proteins per species, we can be fairly certain that if there are indeed 8.75 million species, the number of proteins will fall between those estimates.
The biggest assumption here is that the proteins have a linear relationship with species which is unlikely to be the case, and at the generous estimate we are pretending that there are no proteins in UniProt that don't have species annotation. As for Swissprot, this only includes proteins that have been manually curated, so this ignores many proteins that are safe to assume exist and typically only covers proteins that are of interest to scientists.

A minor correction to your question, the UniProt lists ~20 thousand protein coding genes in the human proteome, not millions. Those protein coding genes are subject to various post translational modifications and isoform splicing, so there will be more final proteins than 20k.

The human proteome can contain millions of different proteins if we consider proteins with different post translational modifications (PTMs) to be different!

@JeppeNielsen I asked a similar question on this: Why does UniProt list 150,000 proteins in the human proteome?

Just because a database does not consider proteins with different PTMs to be different, does not mean that the proteins are identical. If you disregard PTMs you cannot explain the ABO bloodtypes as they are caused by differences in the glycosylation patterns.

Another good example would be the insulin receptor, which comes in many different variants.

@JeppeNielsen Yes, there are many PTMs, splice isoforms, and other variants that perform different functions. However, they are all from ~20,000 protein coding genes.

So you would say that the genome contains ~20,000 protein coding genes. The proteome is much larger.

@canadianer There isn't yet a strict definition of the proteome. UniProt has 20k records under the human proteome. After PTMs and isoform splicing, there are many more proteins. I've said this in the comments but since two people are not happy for some reason, I've edited the answer to be clearer.

Each UniProt record contains isoforms and modifications. That they choose to organize their database this way doesn't seem to me to have any bearing on the definition of the term proteome. Any definition I have heard refers to the entire complement of expressed proteins. See UniProt's, for example: A proteome is the set of protein sequences that can be derived by translation of all protein coding genes of a completely sequenced genome, including alternative products such as splice variants...

PS: I apologize if I seemed argumentative; that was not my intent. I think definitions are important but I  also realize that there aren't any real authorities on a lot of terminology.

Thank you canadianer, you previous comment highlight what I was trying to get across. Which namely is that the number of database entries is way lower than the possible number of proteins derived from those entries.

@JeppeNielsen Yes, I see your point. But even if each record had an average 10 splice and PTM isoforms, these errors are nothing compared to the other error causing assumptions that seem to generate several orders of magnitude of variance in estimation.


text:
What species is this aromatic plant found in a mountainous region of Greece?
This plant was found in the Taygetos mountains, Greece, and had a lemony smell.
Small plant about a foot high.
The shiny recurved leaves are reminiscent of rosemary, and the dry seed-heads seem rather distinctive.
Any ideas of Genus or species most welcome!

The seed pods look like delphinium or a weird dwarf lilium species. Perhaps it is a mountain Lilly species. google lens said lilium and perhaps a weird heather variant. http://www.flora.dempstercountry.org/V.B.28.Ericaceae/Phyllo.empe/Phyllo.empe.pic1.jpg

@LifeInTheTrees - neither of the plants you mentioned are aromatic.

@anongoodnurse I had another look at this and now I'm pretty sure it's a Hypericum..

After taking another look at this, I think it's almost certainly a Hypericum species. Compare with Hypericum empetrifolium.
The fruit of Hypericum are very distinctive:
https://www.inaturalist.org/observations/104581263

The narrow revolute leaves of H. empetrifolium are also unlike other Hypericum species:
https://www.inaturalist.org/observations/69680320

Geographic distribution seems right:
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:433403-1

A type of greek lavender with no blossoms anymore?
https://www.florealpes.com/photos/lavandulastoechias_5.jpg?PHPSESSID=0a72039f5036d91c7df80dd406b795b0

The desiccated seed heads seem like nothing that would come from a lavender flower though..


text:
What is the outcome of a human population starting with only 2 individuals?

Starting with a human population N = 2, is there any way the genetic variability seen today could have come about? I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents? Without a population to start with, wouldn't the lineage eventually turn into clones of each other like the cheetahs are now?
Are there any known mechanisms besides mutation that replenish the variability in alleles?

Once again a first-time poster with a "Please help me respond to a creationist" question.

I am not sure we have to be so categorical with creationist question. It is indeed good to close creationist question when the answer has nothing to do with biology but with the philosophy of knowledge or philosophy of logic. This question clearly concerned evolutionary biology (except the first question that had to do with the definition of information).

I agree that creationist motivated questions are a bit too common on this site and often ask for very long answers mixing philosophy and biology. In the meantime research level questions are very uncommon and we ave to accept more introductory questions. Opinions still vary in the Meta site

@Remi.b: Introductory questions are fine I think. But the low-rep creationist questions are IMO not worth the trouble, notwithstanding your good answers. The questions are not motivated by curiosity but by a desire to convert, which in context strikes me as inappropriate for this or any science forum.

@daniel I'm referencing a past discussion that I came across. I never intended to debate anyone (including the creationist in question). If I had left out the reference, you would probably think I was a creationist troll, when in reality I simply wanted to know the biological reasons why the argument was nonsense.

@scubadude22: I don't doubt this and you are probably not the only one. But I think the answers to very general evolution questions are available elsewhere and so on balance the site should avoid them. As Remi.b notes, not everyone agrees with me.

Indeed natural selection decrease variability and therefore decrease information and mutation recreate this information. You can think of a bunch of pens of different colors. If you select
for the red pens you will decrease the variability in pen colors as the other colors will slowly disappear. If you allow for mutation to occur you will recreate blue and black and purple and yellow pens to occur again in your population of pens.
Is it an accurate statement that less variability means less total information?
Yes, less variability means less information. Information is a concept that increases as predictability decreases. If no variability exist, you can predict at 100% what allele a given individual is carrying. You may want to have a look to shannon's theory of information here on Khan academy. Note: this has not much to do with biology but it has to the mathematical definition has to do with mathematics, probability and computer science.
Are there any known mechanisms besides mutation that replenish the variability in alleles?
No, there is nothing else than mutations that creates new alleles. "Mutation" means any kind of structural change of DNA. So by definition any change in the DNA is due to mutations, therefore only mutations creates new alleles. Note: that some people may use the word mutation in a more narrow sense including some kind of DNA change such as indels but excluding chromosome rearrangement for example. I used here the word mutation in the broad sense.
Segregation and Recombination
Two other concepts may interest you though: Segregation (See Mendelian inheritance) and recombination(also called crossing over).
For example if 2 individuals $AB$ (Allele $A$ on one chromosome and allele $B$ on the other chromosome) reproduce they can create the individuals $AA$, $AB$ or $BB$ thanks to segregation.
Two Genes set on chromosomes and if two genes are on the same chromosome, one might think that these two genes cannot segregate independently one from the other, they are linked! For example imagine an individual has the alleles $A_1$ and $B_1$ on two loci of one chromsome and alleles $A_2$ and $B_2$ on the two same loci but of the homologous chromosome. If this individual transmit the allele $A_2$ it must necessarily transmit the allele $B_2$ and can't transmit $B_1$ if recombination does not occur. But recombination does occur and allows for partially independent segregation of these two genes.
You will find more information about these two concepts on wikipedia. I don't want to go too much into details but in short these processes can in some conditions increase the phenotypic variance but in any case these phenomenon do not create new alleles. New alleles are created by mutations only.
Can 2 individuals carry as much genetic information than today's world population?
No! As a very simple argument, two individuals can only have 4 different alleles. But we know several loci (sing: locus, position on a chromosome) where there exist more than 4 different alleles. Therefore, mutations must have happened at some time.
And only to enjoy some further arguments: if these two individuals had together 4 alleles at all loci, it would be extraordinary unlikely that their variation would have remained in today's population. Let's imagine two heterozygote (=who has two different alleles on their two chromosomes for a given locus) individuals are $AB$ and $CD$ that have two offsprings. The probability that their 4 alleles are present in the two offsprings is $1/4$. I don't when Adam and Eve were supposed to exist but it very sound like their variability would have not been maintained through times. This random process which diminish variability is called genetic drift. To be a bit more accurate, in a population that do not change in size, the expected loss of alleles due to genetic drift at each generation $1/2N$, where $N$ is the population size. So the bigger is the population size, the lower is the loss of alleles due to genetic drift. In the above example $N=2$ and therefore the expected loss is $1/4$.
I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents?
Yes, as said above, one individual can only have two alleles at a given loci and can therefore not transmit more than two different alleles.
Without a population to start with, wouldn't the lineage eventually turn into clones of each other[..]?
Yes, because in absence of mutations (and in absence of different special types of selection such as overdominance) the variability is slowly lost due to the randomness of segregation. This process is called genetic drift.

I removed the unrelated part about information theory from my original question. Thanks

authors: Улжан Кошкарова


text:
Has a new functional structure ever been observed arising spontaneously?
Have we ever observed a new functional biological structure arising spontaneously such as a new functional organ (sensory or otherwise. such as tracing some creature in the past few hundred years which had no electroreception organ and now has evolved this organ)
Or has what we observed been limited to changes in existing structures.
(Lenski's E. coli bacteria is not what i am looking for since it is a change in an existing metabolic system (not a new functional structure) and furthermore e-coli already had some ability to use citrate as an energy source )
Looking for a completely new functional organ (such as a new sensory organ) that we have actually observed - not deduced from fossil record.
Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect.

Can you define "functional biological structure"? As it is now, this is a good question which is not very clearly defined. For example, would a single new enzyme count as a "new function"?

@MarchHo looking for a new organ, such as an electroreception probe or a poison gland with delivery system. i.e. a new working functional system of non trivial complexity

@MarchHo new enzyme is not a sensor or organ. looking for a new functional system like a new organ or a new sense. I updated the question to reflect your point. thanks

how about story of epigenetic inheritance of fear? http://www.nature.com/news/fearful-memories-haunt-mouse-descendants-1.14272 Although it wasn't spontaneous

@aandreev what new organ arose there? thnx

organ in form of memory about never-encountered before adorant.

@aandreev new memory is not a new organ. memory infrastructure is already there. that's obviously not the question here. interesting article on epigenetics though. it seems that our understanding of DNA could change dramatically

What do you mean with "spontaneously" (without human influence? in a short period of time/instantaneously?)? The reason why I'm asking is that creationists often formulate questions in a similar way, from the perspective of doubting evolution as a whole (we haven't "seen" this/that happen), misunderstanding the evolutionary process (e.g. mutation -> new function) and their artifical boundary between macro and microevolution. I'm not saying that you believe in this, and I'm just asking for clarifications, since the current framing of your question might lead to misunderstandings.

correct. spontaneously means without human influence. time means since human recorded history.

Would an organelle do?

@WYSIWYG need a limb or organ in something the size of an insect or bigger. dont want to waste this question on trivial complexity arguments. could be a new functional limb or antenna or eye. something non trivial complexity. thnx

could even be a duplicated eye or antenna and this was advantageous and spread into the population. i.e. some species which had 2 eyes and now has 3

@r2d2 And what do you exactly mean by "trivial complexity arguments"?

@WYSIWYG exactly what it says. not some trivial change or strucutre. this is why i asked for new limb or organ, etc. in size of insect or bigger. or even a duplicated antena, etc.if you dont have. thnx

@r2d2 and you think changes that do not lead to a new limb formation are trivial? Please get the concepts right.

no. but at least those that lead to a new limb,etc in an insect, are usually not trivial. have to set some kind of bar. otherwise, will get some trivial organelles or enzyme molecule and the question is wasted

It is hard to know what examples would be satisfying to you. How about the classical case of human lactose digestion (see this answer)?

It seems like you are attempting to frame this as a question about current evolutionary theory. However, current evolutionary theory doesn't expect anything as complex as an organ to arise spontaneously without any precursors. You suggest a new claw in an insect would be something "spontaneous" enough for you. This again shows that your question and the answer you are looking for are not related to evolutionary theory. The insect organs you are talking about are all modified appendages. This includes claws, mandibles, antennae, legs, fangs. These appendages all share a common genetic and developmental framework that has been slightly modified over long periods of time to give raise to the variety of insect appendages that we see today.
The idea that evolutionary theory supports the spontaneous creation of organs is a willful ignorance of evolutionary theory. The molecular mechanisms that generate novelty (e.g. genome duplication, gene duplication, de novo genes, mutation, gene regulation) for natural selection to work on are relatively well understood. Since we have an understanding of how novelty is created it is known that spontaneous organ generation has never happened or is expected to happen under evolutionary theory.
Here is link to the University of California, Berkeley's webpage designed to teach the public about evolution.

Welcome to Biology. Great answer to a controversial question. +1. If you could add a reference to the evolutionary theory to allow people to read about it more that would really help.

nice dodge. of course it is not expected to happen because then random evolution would need to be observable and that would be the end of theory. and we cant allow that to happen, right

@r2d2 You may continue your efforts to associate these false hypotheses with Evolutionary Theory. However, I believe your time will be better spent reading and understanding Evolutionary Theory than parroting old and disproved creationist miseducation literature. At the very least, a better understanding of evolution will allow you to form coherent arguments against it.

this "answer" should be changed to a comment. show me please some real empirical evidence or admit that none exists. i dont want to waste this question on pitiful dodges whose stregnth of argument is only that the creationist alternative cannot be true

can even be duplicated structure such as some insect species which had 2 eyes and now has 3. or 2 antenna and now has 3 and this was advantageous and spread into the population. please, i'm begging you show me at least this

@r2d2 You should check your condescending attitude. "i dont want to waste this question": really!!? Stop behaving as if you are some kind of supreme being. Provide details in your question if you expect an answer with "empirical evidence".

How about the Italian wall lizards that evolved new muscles around their intestines after being introduced to an island? (other article, actual paper). The paper reports that these cecal valves are "a structure previously unreported for this species and rare in this family and scleroglossan lizards in general"; indeed, "The fact that <1% of all currently known species of squamates have cecal valves ... illustrates the unusual nature of these structures in this population.".
It is possible that these values are an ancestral structure that was reactivated by natural selection; however, we know that natural selection can act very quickly to change the size of morphological structures, so it's also possible that existing muscles quickly changed size in response to selective pressure. Figuring out the developmental mechanism of cecal valves would sort that out.

comment there: "I’m assuming this is a predominance of one possible phenotype, not a change in the genetic structure of the lizards, and that the genes for this phenotype were already present in these lizards..." answered there: "it’s still just the phenotypic expression of a bunch of stupid base pairs... There are other herbivorous lizards with cecal valves" makes sense given that took only 30 generations. i.e. sounds like this was already built into the lizards and was waiting to come out when needed

Do you have EVIDENCE that it was "built into the lizards"?  Or did you just make that up so you can deny that the example you asked for was given to you?  Why ask the question if you are prepared to say that EVERY possible answer "was always built in" with no evidence to support your claim?

@r2d2 I've updated my answer to reflect your point. Don't forget that for most (all?) animals, every individual starts as a single cell, so everything is "just the phenotypic expression of a bunch of stupid base pairs", plus whatever else was contained in that cell.

morphological changes not what i am asking. the "new valve" they found between the small and large intestine is simply an enlargement of muscles already present in the gut wall at this juncture. looking for completely new functional structure. like a new primitive claw in insects or new antenna. also, just curious how do you know the changes were from random mutations/NS? given that 30 generations is nothing for genetic algorithms (have worked with some) it seems far more likely those changes were built in responses/activations of existing DNA - not new genetic info from random mutations

@swbarnes2 a simple test. If we compare the full genome of the lizards on the original island to those on the new island, the genomes should be essentially the same. However, if the cecal valves are the result of new genes (or significantly modified old genes) that were produced by mutation and natural selection, the genomes should be noticeably different. No one has done this comparison, however, as it is not easy. They did do the easy comparison, looking at mitochondrial DNA in each population of lizard. They found the two populations indistinguishable. from http://blog.drwile.com/?p=7699

Again, do you HAVE the results of that test, or are you just jumping from "the evidence could theoretically show this" to "I conclude that this is what is happening" without having the evidence in hand?

@swbarnes2 you are the one jumping to conclusions here without evidence. arent you a scientist? given that it was <30 generations. it was either a very lucky dice roll or pre-existing phenotype expression. let's wait and see. secondly, it was not a new organ or limb as that link explains

What is your point in asking this?  If you are so sure that novel 'organs' can't evolve in a century, when evidence did you expect people to come up with?  Surely you are aware the the genetic evidence we can see TODAY shows the homology between flagella and type III secretory systems, why isn't THAT good enough evidence of the evolution of a novel structure?

To be sure a new trait actually evolved before our very eyes and wasn't simply mistaken for a wild trait we never noticed, you probably want to look at domestic animals. We have directly observed, through animal husbandry, the evolution of new fingers in cats, new ribs in pigs (wild pigs have 14, some breeds now have 17), new fins in fish (here I'm talking about the double tail mutation in golfish).
These new structures act, for the most part, like the old ones. I assume because of this you might be interested too, in the observed evolution of completely new functions from old parts:
The Norwegian Lundehund (dog breed) has evolved the ability to seal its ears shut with muscles that other dogs/wolves use to simply move their ears.
As someone else mentioned,  In an island population of Podarcis sicula (lizard species), muscles in the digestive tract which normally function to squeeze food through the intestines, have bunched up to form a new valve, thus creating a fermentation chamber.
Off the top of my head, I can't think of other directly observed changes in function but there are MANY super solid inferred changes in function:
Bee stingers are modified ovipositors (egg-laying organ). We know this because they are nearly identical to the ovipositors of other insects, and because the queen uses hers as a stinger and as an ovipostor.
Snake venom is modified saliva and snake fangs are simply a merger of tooth and saliva duct.
Bird wings are modified arms with 3 fingered claws. I could go on but I'll call that good.

just curious is there any evidence that these changes occurred by random mutations? i could think of other possibilities such as inherent mechanism within the organism which changes itself. after all, we are far from fully understanding even the most simple bacteria

There are two main issues in your question that make it hard or fundamentally impossible to answer. The two issues are

What you would accept being an 'observation'
What you would accept being significant enough to be an example of interest.

A big issue in your question is based upon what you call an observation!
When you say

observed - not deduced

, you highlight the whole issue of what you would consider being an observation.
In science, observations often take complex form. It is not only direct visual observation recorded on a standard camera. It is like asking for, recorded-on-camera evidence that quartz exist. Such evidence don't exist (and cannot exist), yet we know of their existence through other means of observation. It would make no sense for someone to only consider camera recording as valid mean of observation.
Of course, We have never recorded on a camera the evolution of an entire new organ because it takes a lot of time. Yet, evidences are numerous.
This technic of limiting arbitrarily the field of methods that one accepts to recognize as bringing evidence and call "observation" is a common technic from science denier (e.g. flat earth society, creationist). I made a similar point as the one I made here on this post if you want.
How to solve this "What is an observation" problem?
There is only one way to go. It will be for you to be able to understand the forms that observation can take. For this, you will have to learn a little bit about evolutionary biology and evolutionary genetics. For a very short introduction to evolutionary biology, you can have a look at Evo101 by UC Berkeley.
You may have hoped for someone to give an entire course on evolutionary biology to fill up this gap of knowledge of yours but I am afraid it would be way too much work for a single post. If this was your position, then it would be like refusing to accept that earth is a sphere without having yourself explain how GPS data work. We just can't give you an entire course here.
So you have two solutions; rely on authority or understand by yourself. If you rely on authority you have two main options; Rely on those that rely on evidence (science) or those that don't rely on evidence and either rely on other forms of justification (justification theory;such as a religious book for example). (either those that work through observations, scientists). You second solution is to understand the field by yourself and therefore start studying for it.
A second issue is that it is unclear to know what you would accept being "not trivial"
When you say

Also not looking for something trivial such as a new/modified enzyme or protein molecule but rather a new organ in a species at least the size of an insect

It is hard to know what you would call a significant enough evolutionary event to be accepted. The risk is that you may define it large enough so that it fundamentally cannot be observed by a mean that you would accept.
For your curiosity, this post talks about evolution of lactose digestion in humans and this post about the evolution of cardio-vascular system.
Somewhat related post
You might want to have a look at post Is evolution a fact? and the link posts in the top voted answer.
Just another comment

random evolution

In the scientific literature, "evolution" is never said to be "random". The fact that you're using this expression shows what kind of literature you are used to.
For all reasons explained above, the question cannot be answered, not by lack of evidence, but because the question is unclear. I am therefore voting to close as unclear. Good luck in your investigation of the question.

listen to your words. then it sounds like the whole area is not at all scientific. yet it is taught as science

My answer is more of an explanation for the philosophical difficulties behind the question. My answer is more of a long comment to explain why I think the question is unclear and deserves to be closed as such.

its not my question thats unclear. its the whole theory of random evolution thats unclear

@r2d2 I am quite convince there is no way to change your mind, so I won't try too hard. If you wanted to learn something you would have by the time (and would have stopped to stop to call this field of knowledge the "theory of random evolution" as creationist do; nobody call it that way in science). I am a researcher in the field of evolutionary biology and I know a thing or two about this theory and it is always a bit funny to face someone who knows nothing about it but thinks he knows best.

that was not me. it was a random computer glitch. i;ve studied the theory extensively. but it boils down to taking seriously something which is foolish and stupid. the scientists cannot reject it though, because it's the only explanation that "fits" the way they view the world

i've studied the theory extensively Really? Let's make a test. Here are a number of questions that one could find in an exam to a course of evolutionary biology. 1) In a population of constant size $N$, what is the expected coalescent time? 2) Why does the average $F_{ST}$ decreases with the effective population size? 3) Is the change in allele frequency at a bi-allelic locus faster when the deleterious allele that is a low frequency is dominant and recessive? 4) Is there a positive or negative correlation between recombination rate and heterozygosity in the D. melanogaster genome and why?

How can you estimate recombination rate from linkage disequilibrium and genetic diveristy patterns? 6) What is the shifting balance theory? 7) How does the methods of contrasts is helpful in comparative genomics? 8) What is a monophyletic group? 9) What is the concept of antagonist pleiotropy and how does it help us understand the evolution of ageing? 10) What is incomplete lineage sorting?

all your building of foolishness collapses once you realize random processes only result in nonsense. but that will never happen. i know

@r2d2 Anyway. I shall not feed the troll more than that. I hope your inability to answer or even understand these small questions will allow you to realize that you don't know much about evolution. Cheers!


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Mesoporous silica particles as anti cancer drug delivery method
If this question is a little off topic for Biology, I'm sorry. I've recently read a lot about mesoporous silica nanoparticles as a promising drug delivery method. The huge range of customizability of the particles, coatings, contents, etc. can pretty much tailor them to be effective in delivering most drugs to most target locations in the body (or to specific cells). The research is not new, and all the articles hail the method as a very promising way to treat for example cancer. However, as far as I know, these methods are not widely used today. Why? Is there some catch that I don't see?
I'm no biology expert, but if this is so promising, and the research is at least a decade old, some companies would have produced this (they already produce the particles) in terms of drug delivery. So why not? Is it a case of null-findings not being published? Is it actually used and I'm blind?
Thanks for your help!
edit: for those interested, here is a good review

It's Nice question. But mostly Nanotechnology is not into health industry is because of side effects(and may be the cost of research) or toxicity. http://guardianlv.com/2014/07/nanoparticles-that-deliver-medicines-have-problems-that-may-be-solved/

Those are good points, but given the amount of research done, and the huge (I would believe) interest of the pharmaceutical industry, those problems are easily rectified. Negative surface charge (when considering targeting the brain), size to prevent endocytosis. It can target specific cells via antibody coatings. It can be used in MRI. You can control content release. I mean, whats not to like. Still we go on with systemic drugs and therapies (looking at you chemotherapy). The materials used can alse be designed to be biodegrable and non toxic.

I work in the pharma/biotech industry. Nanotechnology in general is a very active field of research. The issues with any new delivery system are two-fold - the first is being able to prove safety and efficacy, which is no small task, and the second is development time. It can take 10-15 years or more for a novel therapeutic to reach the market, and that's with a "standard" delivery system like a pill or infusion. Developing and getting approval for something entirely new like this would add even more time to the pipeline, which is why you haven't seen it on the market yet.

I think that pretty much answers the question. I would guess that this form of delivery method is indeed surging forward to the markets as we speak? Do you perchance have links or information about any specific solutions that are on their way to market, or nearing a point where they can be put to market?

Though I totally agree with your views towards nanotechnology, There is always two sides of a coin.
According to this article THE BAD (of Nanotechnology):

Health:
Nanoparticles have been shown to be absorbed in the livers of research
  animals and even cause brain damage in fish exposed to them after just
  48 hours.   If they can be taken up by cells, then they can enter our
  food chain through bacteria and pose a health threat like mercury in
  fish, pesticides in vegetables or hormones in meat.  The
  increasingly-popular carbon nanotube (20x stronger and lighter than
  steel) looks very much like an asbestos fiber – what happens if they
  get released into the air?  Being carbon-based, they wouldn’t set off
  the usual alarms in our bodies, making them difficult to detect.
Environmental:
If nanomaterials really are as strong as diamonds, how decomposable or
  persistent are they?  Will they litter our environment further or
  present another disposal problem like nuclear waste or space litter?
  In the distant future, will self-replicating nanobots – necessary to
  create the trillions of nanoassemblers needed to build any kind of
  product – run amok, spreading as quickly as a virus, in the infamous
  “gray goo” scenario?

Not only that Each country have a different point of view on the topic of nanotechnology in Health(or nano-medicine).
Government Response on Nanotechnology:
United Kingdom
In its seminal 2004 report Nanoscience and Nanotechnologies: Opportunities and Uncertainties, the United Kingdom's Royal Society concluded that:

Many nanotechnologies pose no new risks to health and almost all the
  concerns relate to the potential impacts of deliberately manufactured
  nanoparticles and nanotubes that are free rather than fixed to or
  within a material.

They want to change the existing regulation to be modified on a precautionary basis because they expect that the toxicity of chemicals in the form of free nanoparticles cannot be predicted from their toxicity in a larger form.
United States
Rather than adopt a new nano-specific regulatory framework, FDA convenes an 'interest group' each quarter with representatives of FDA centers that have responsibility for assessment and regulation of different substances and products. This interest group ensures coordination and communication. A September 2009 FDA document called for identifying sources of nanomaterials, how they move in the environment, the problems they might cause for people, animals and plants, and how these problems could be avoided or mitigated.
Berkeley, CA is currently the only city in the United States to regulate nanotechnology, which is still being opposed.
European Union
The European Union has formed a group to study the implications of nanotechnology called the Scientific Committee on Emerging and Newly Identified Health Risks which has published a list of risks associated with nanoparticles.
Consequently, manufacturers and importers of carbon products, including carbon nano-tubes will have to submit full health and safety data within a year or so in order to comply with REACH.
According to REACH(from Page 22, 4.2 Pharmaceutical regulation, PhD Thesis of Steffen Foss Hansen, DTU):
The application of engineered nanoparticles for medical use offers immense benefits
within areas like diagnosis, targeted drug delivery, and drug development and have been
marketed for more than 17 years (NanoRoad SME 2006, EGE 2007, Gaspar 2007).
Well-described and understood medicinal products containing nanoparticles in the form
of liposomes, polymer protein conjugates, polymeric substances or suspensions have
been given Marketing Authorizations within the EU under the existing regulatory
framework e.g. Regulation 726/2004 on authorization and supervision of medicinal
products for human and veterinary use, Directive 2001/83/EC on medicinal products for
human use, Directive 93/42/EEC concerning medical devices, Directive 90/385/EEC
relating to active implantable medical devices, and Directive 98/79/EC on in vitro
diagnostic medical devices (EP & CEU 2004, Council of the European Communities
1990, 1993, 1998, 2001).
There is no specific mentioning of nanomedicine in the EU legislation on medicinal
products and devices, tissue engineering and other advanced therapies. None of these
regulations or directives was written with nanomedicinal applications in mind and
although their scope covers nanomedicine they have been accused for being general and
non-specific and fraught with concerns and difficulties when it comes to dealing with
drugs more complex than traditional ones (Editorial 2007, D'Silva and Van Calster
2008).
The use of nanoparticles in nanomedicine has not been subject to much regulatory
scrutiny since existing laws and regulatory instruments are believed also to cover
medical products based on nanotechnology. The extensive testing requirements prior to
marketing of medicine may also contribute to the notion that the potentially negative
effects will be discovered prior to marketing, that patients are adequately informed
about negative side-effects, and that benefits outweigh the risks or the adverse effects,
should such be found to occur (EGE 2007, N&ET Working Group 2007) .


text:
Which are the best programs to analyze circular RNA?
Hello I'm just started with bioinformatics and I would like to know which programs are best for the task of finding circRNA (circular RNA) in sequences of tissues and different cellular types. I have heard about circRNA finder, find circ, CIRCexplorer, CIRI, and MapSplice which all are different programs to find circRNA, but I really don't know which one is the most used and easy to use, and which one is most accurate for finding circRNA.

Welcome to SE Biology. Just to let you know why I changed "algorithm" to "program". An algorithm is the strategy by which a problem can be solved computationally, a program is its implementation in code. You would ask about the best algorithm if you wanted to write your own implementation or you knew which algorithms the different programs you mention used and wished to choose from those using the best algorithm. I assume that in fact you just want recommendations from the programs named.

According to the most recent paper (https://doi.org/10.1093/bib/bbx014), CIRI2 shows a balanced performance on sensitivity and FDR.
"Computational detection methods have been widely used in studies on the biogenesis and the function of circular RNAs (circRNAs). However, all of the existing tools showed disadvantages on certain aspects of circRNA detection. Here, we propose an improved multithreading detection tool, CIRI2, which used an adapted maximum likelihood estimation based on multiple seed matching to identify back-spliced junction reads and to filter false positives derived from repetitive sequences and mapping errors. We established objective assessment criteria based on real data from RNase R-treated samples and systematically compared 10 circular detection tools, which demonstrated that CIRI2 outperformed its previous version CIRI and all other widely used tools, featured with remarkably balanced sensitivity, reliability, duration and RAM usage."


text:
Where do the four ADPs come from in the second stage of glycolysis?
In the first stage of glycolysis, the two molecules of ATP are broken down into 2 ADPs + 2 Pi through hydrolysis, then in the second stage of glycolysis they are phosphorilazed to obtain 2 ATPs. How can this process happen twice to yield 4 molecules of ATP if we only have 2 ADPs to begin with?
Note: I'm not asking why the process happens twice, since it's easy to see that the Fructose-1,6-biphosphate is being broken down into two Glyceraldehyde phosphate molecules. I'm asking how can the process of producing two ATPs happen twice if we only broke down two ATP molecules into ADP.

There are many other sources of ADP in the cell: various proteins that use ATP as an energy source hydrolyze it to form ADP + phosphate, thereby extracting energy. This ADP can then be re-phosphorylated by glycolysis to form ATP again. If glycolysis did not produce a net yield of ATP it would be pointless, so it really should be unbalanced in this sense.

This idea was my best guess, however most of the sources I checked out on glycolysis omitted this information. So, to be clear, what you're saying is that ADP doesn't have to come directly from the previous steps of glycolysis, but it usually comes from other sources in the cell?

Yes. The whole point of producing ATP is that it serves as a common source of energy for various energy-demanding reactions in the cell. And those reactions turn ATP back into ADP.

I think I understand your question, and stumbled upon it because i was wondering the same thing while studying for my Microbio test. I know its a year late, but someday someone else might need this info...so here it is.
To put it simply: there is a second pair of phosphates added to the two 3-carbon molecules cleaved from the preparatory stage before the 4 ATP are finally formed. These get added by an enzyme while reducing the NAD+ molecules.
In depth: The first pair of phosphates the cell uses to synthesize ATP come from the initial 2 ATP invested during the prep stage, but an additional 2 phosphates are added when the cell oxidizes the two Glyceraldehyde, 3 Phosphate (G3P) molecules to form NADH. In this step, two electrons are taken away from the G3Ps and an available inorganic phosphate is added to the "1" position, forming "1,3 Biphosphoglyceric Acid " (1,3BPG). Afterwards, the molecules each have 2 phosphates for a total of 4 phosphates available to get oxidized and used to synthesize 4 ATPs.
This step, (the addition of an inorganic phosphate as an intermediary step) is SO overlooked by regular textbooks that its not even funny. mine doesnt even list the enzyme; I had to look it up.
but yeah, that's the source of the additional phosphates available for forming the 4 ATP molecules of glycolysis, and possibly why you didnt see it from the diagram in your textbook (you're not alone!).
Hope that helps!
Sources, as of 4/18/17:

https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/glycolysis/a/glycolysis
https://en.wikipedia.org/wiki/1,3-Bisphosphoglyceric_acid

i know that is simple because if you can just look at the first step there were 2ATP only and the energy in this molecule is used to phosphorylate the glucose molecule  to give fructose biphosphate and 2ADP and 2pi is left this to molecule may reorganize by the substrate level phosphoryalation to give 4ATP molecules as you know the enery is come from the chamical energy from the GP(glyceraldehyde 3 phosphate ) as initially we have 2ADP and 2Pi but finally we have 4ATP because  the energy is enough to reconstract  additional 2ADP and 2Pi which comes from other non glycolisis reactions

It may help if I suggest two ways of looking at the situation.

The first way, which tries to reflect your line of thinking (as I understand it), looks at the situation as two reactions being needed to maintain ADP in the cell. The first reaction produces ATP:

Glycolysis: ADP + Pi → ATP

Whereas the second reaction regenerates ADP by using the ATP

Biosynthesis / Movement / Electrochemical work etc: ATP → ADP + Pi

If the second reaction doesn’t occur, the first one will stop too, but that is OK as the cell has no need to produce ATP if there is plenty.

A second (perhaps more sophisticated) way is to regard the situation as an equilibrium:

ADP + Pi ⇋ ATP

The position of this equilibrium (and hence the relative concentrations of ADP and ATP) will vary depending on the situation in the cell. The concentrations of ADP and ATP will effect glycolysis (and other aspects of metabolism) both by simple mass action, and also be something you may not have yet met, the regulation of certain key enzymes (allosteric regulation). (An equilibrium between ATP, ADP and AMP also exists.)
Finally, there are both open systems and (semi-) closed systems in biological chemistry. The conversion of foodstuffs into chemical energy and the structural components of a cell is obviously an open system — the substrates for glycolysis ultimately come from outside the organism. The interconversion of ATP and ADP (and NAD+/NADH) can be regarded as (semi-) closed, as the main part of the chemical moiety is being conserved. However one should not forget that, initially, when the organism is growing and cells are dividing, the adenosine backbone has to be synthesized, and it requires energy to do this and more energy to add phosphates (also from the diet) to the ribose.


text:
Could life protect itself from ultraviolet radiation?
I have heard it argued that life as we know it (DNA-, RNA- and protein-based) could not have evolved without the ozone layer to protect it from UV radiations.
It seems to me that mechanisms to deal with this would have evolved. Is there any scientific evidence on this point?

Life on earth predates the ozone layer by over a billion years.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. I suggest starting with a search like "UV protection plant" — you will find a lot of information showing that this has happened (obviating you post). Please see the [tour] and [help] starting with [ask] for details.

Donno, maybe intelligent design shouldn't play with UV to start with. Or leap seconds.

If you're interested in hypothetical questions, perhaps relating to a fictional world you are thinking about creating, then [worldbuilding.se] is a splendid resource for that.

Preamble
The original question asked about fair assumptions, but addressed conviction rather than scientific evidence. This site primarily exists to address biological questions that can be answered or at least approached objectively. It certainly does not exit to rehearse people for arguments against those who have already made up their minds on a topic because of religious convictions. So I changed the question to restrict it to UV-resistance of living organisms.
Answer
It is already known that organisms currently exist that are resistant to ultraviolet radiation. The bacterium, Deinococcus radiodurans, an extremophile which is also resistant to other radiation, is a prime example.
In addition, organisms, including higher organisms, have mechanisms for repairing DNA damaged by ultraviolet light, as summarized in this brief Nature Scitable article.
Hence, even without knowing that the ozone layer postdated the origin of life by a billion years (as @canadianer pointed out), there is ample evidence that life would have managed to deal with ultraviolet light.


text:
Unbounded synaptic weight in Hebb’s rule
I am new to neuroscience and apologies in advance if this is a very trivial question. I want to model the synaptic weights of neurons and using the discrete Hebb’s update rule
$$w_{n+1}=w_n(1+c)$$
That is whenever two neurons fire in succession the synaptic weight is increased by a factor c. But here the synaptic weights are unbounded and grow to infinity. Is there any other simple discrete update rule which takes care of this. I came across Oja’s rule but it seems to depend on postsynaptic and presynaptic activity

Are you looking for a rule based on a biological mechanism, or simply one suitable for simulating biologically-motivated network activity? Oja's rule certainly seems like it would be an answer, but it's not clear to me why you suggest it depends on "postsynaptic and presynaptic activity", or why that would be a problem, per se.

Actually, in my model there are only two states of the neuron. Either it fires or it doesn't.  So I don't have a measure of the post or presynaptic activity. Do you think I can use Ojas rule in this setting?

My understanding is the only difference between Oja and Hebb is Oja scales the weight vector to have length 1.

Do you have a reference for this?

https://en.wikipedia.org/wiki/Oja%27s_rule perhaps as a start? Or go right to the source: https://link.springer.com/content/pdf/10.1007/BF00275687.pdf