I have 2 questions about evolution:

Also, I now see why you brought my question straight to the non existence of god. You are clearly sent from the devil
>666

user, it's Richard Dawkins explaining the evolution of the eye.

>1- how does it explain creatures like pic related?

Outliers who were once considered the abnormal in their population (let's assume original population was just some shade of brown or black) end up surviving better because all it's predators were brainlets that couldn't tell them apart from leaves. Thus allowing them to spread their abnormal traits on more frequently.

Alternatively they could have also been among the last surviving members of their species to repopulate their native population due to a given near extinction level event.

>2- if life exists for another billion years but still remain 100% the same on a macro level, would it disprove evolution?

No, because that would mean the questioned ecosystems remained very stable for that period of time. Meaning there was no reason to shift adaptation strategies for life.

The Nautilus have pinhole eyes.

Thank you. They look cool.

>Richard Dawkins

He's a moron making money off of angsty teenage atheists.

The 'how' of macroscopic structure change is always an interesting one, as there are many molecular pathways that are taken. However, if you're talking about simple evolution by allele change, a classic example is to look at the curious case of beak length of birds in tropical islands that are roughly insulated. Depending on the climate and weather, birds of the same species but differing beak size will be more successful, with longer ones being able to reach further into trees and the like. If you can imagine a case where it was so much more advantageous for the long beaked birds to survive, then a scenario where the tiny beaked ones don't even live til reproduction becomes a natural conclusion.

Going back to how the differences or mutations arise, it's a well-documented molecular phenomenon. In the process of gamete creation, or making the sperm/egg, there's a cellular process called meiosis where DNA recombination occurs. I suppose I'll make a second post going into that and explaining exactly HOW an error might happen, but errors do happen, which are actually fairly simple to recognize.
1) A segment of DNA is replicated.
2) A segment of DNA is inverted- essentially turned so that it's the opposite end first when put back into sequence.
3) A segment is deleted
4) A single nucleotide is changed
And then a sort of a weird one
5) Transposition/retroviral mechanism occurs.

All of those add up over time to create new features, which then through sheer chance might end up with some 'function'. As soon as a feature becomes a function, then it can undergo pressure-based selection.

The simplistic nature of how there are many pathways to reach some kind of effect is demonstrated well on the molecular level by this. (Pic attached), The way the active site of hemoglobin and chlorophyll are similar in chemical construction lends itself to the notion of radically different origins for similar processes, which is an incredibly interesting field of study.

To add;

So, a single DNA pair strand coiled up is called a chromosome. You may know that we all have 23 unique sequence pairs of chromosomes, but that's actually 46, with two copies of each. In the attached picture is both phases of meiosis. What happens is that each chromosome duplicates itself- and this is usually a perfect copy, but this stage itself could replicate imperfectly, usually leading to issues like 3 or 4, where some part is missing, or a single nucleotide is incorrectly put in place. You have probably seen chromosomes look like two sort of stubby looking appendages and then one area where they get narrow and connect, and that narrow area is the centromere- it's just sort of a non-coding mechanistic region of DNA that a protein complex called the kinetocore latches on to.
In the first action packed stage of Meiosis, the pairs that are being split are the non-identical mom and dad versions, not the identically copied ones (those are for part 2).

Now, at the opposite poles of a cell, are things called 'spindles', which have microtubules, like tenticles that lash around at this stage of meiosis. Once they latch on to the kinetocore, they tug a bit. If the kinetocore undergoes tension, it stops releasing a signal that stops the cell from moving through meiosis by breaking down the cohesins (basically molecular glue) between the DNA pairs.

In meiosis 1, the tension across the kinetocore is created by actually physically breaking the DNA of all 4 strands, and then fusing them all together. It creates bridges, called chiasma, which will then make them intertwined so the tension is generated. Once the cohesins are gone, the DNA is violently ripped, leaving some strands with sections from the other, and offering plenty of opportunities when the DNA is being repaired to either flip around, go missing, change nucleotide, etc.

Meosis 2 is boring, it's just the separation of the 2 copies, so you end up with sperm/egg w/1 copy of each chromosome.

God I'm retarded, I didn't add the picture. At any rate, these mutations occur at different rates dependent on the species- some species have protein variants that are much more delicate than their homologs in other species, which will then create fewer mutations. Some purposefully have more mutations because they are in environments that require the addition of new variants that can then be selected for. It's on a weird sort of meta level that's hard to examine- after all, evolution doesn't plan for the future, but faster adapting lineages will often have greater reproductive success.

To talk about OP's example of the bug which looks like a leaf, let's think of some novel example of a bug, let's say a cockroach or any other model bug. In one generation, there's a crapshoot of offspring, one of which has a mutation in the gene that controls for pigment that causes the pigment to not be expressed as much because it's a broken protein. Then, instead of being dark brown, the bugs with this mutation are light brown. They are more successful because the animals that eat the bugs can't see them as well against the trees. Then, let's say that there's a few amino acid changes to a pigment protein that, when they do their biomolecular production, they end up synthesizing molecules that contain different resonant patterns than the one it's used to, and it absorbs a different wavelength of visible light- this time, reflecting green. Those have such a higher chance of survival that eventually, all of the ones that are brown can't compete- of course they would have reproductive success at first, but if each generation they end up not being able to get the resources because they're outcompeted by the green ones, their lineage will die off. From there, the rest of the structures that are leaf-like aren't too difficult to imagine.