Like, I’m assuming you mean it happened but died out, but because what we’re talking about is insanely small, if it happens once, it’s happens all around it at roughly the same time. And it’s not a question of if it’s more efficient than alone, it will be more efficient and out co.oete it’s separate components.
That’s not the barrier to entry. The barrier is two compatible things finding each other. An extreme change like this can’t be selected for.
It’s literally a freak chance that it can even happen. Which is why it’s so infrequent
I think you mean that the initial bit - where the smaller bacterium is swallowed but stays alive in its host - is the “can’t be selected for”. After this, if the chimera survives, then most definitely the natural selection process is in action and selection is taking place.
What I really want to know is how it produces offspring that also has both parts. Neither one’s DNA has code for the other. And even if both reproduce asexually with plain old binary fission cell division, how do you get both to divide at the same time, and give each cell one of the new organelles?
with plain old binary fission cell division, how do you get both to divide at the same time, and give each cell one of the new organelles?
An excellent question! Luckily it was answered in the paper. The researchers actually had a high resolution soft x-ray movie of cell division (ok, an exaggeration, they had a few micrographs showing the sequence). In the sequence, it showed how the organelles (including the novel N2 fixation one) undergoing division and each ‘child’ organelle ending up in different halves.
Cell division is controlled in the cell by an amazing process:
2 centres are created on opposite sides of the cell
Structures like tethers are built that connect each centre to each of the organelles (the nucleus, mitochondria and the N2 fixators). These are called microtubules
The microtubules then start shortening, pulling the organelles in two directions, separating them.
The x-ray micrographs show that the N2 fixators are already integrated into this mitosis mechanism - my guess is that the N2 fixators already ‘understand’ the parent cell’s mitosis signaling.
The authors also say that the organelles have lost a number of genes for essential cellular functions, relying on the parent cell to provide those capabilities. By comparison, mitochondria have only 37 genes left, and chloroplasts weren’t known for having any DNA when I was at school, but are now known to have about 110 genes.
In other words, a lot of evolution has already occurred and they are well on the way to being ‘proper’ organelles.
That’s not exactly how this works…
Like, I’m assuming you mean it happened but died out, but because what we’re talking about is insanely small, if it happens once, it’s happens all around it at roughly the same time. And it’s not a question of if it’s more efficient than alone, it will be more efficient and out co.oete it’s separate components.
That’s not the barrier to entry. The barrier is two compatible things finding each other. An extreme change like this can’t be selected for.
It’s literally a freak chance that it can even happen. Which is why it’s so infrequent
I think you mean that the initial bit - where the smaller bacterium is swallowed but stays alive in its host - is the “can’t be selected for”. After this, if the chimera survives, then most definitely the natural selection process is in action and selection is taking place.
What I really want to know is how it produces offspring that also has both parts. Neither one’s DNA has code for the other. And even if both reproduce asexually with plain old binary fission cell division, how do you get both to divide at the same time, and give each cell one of the new organelles?
Sorry for taking a long time to reply.
An excellent question! Luckily it was answered in the paper. The researchers actually had a high resolution soft x-ray movie of cell division (ok, an exaggeration, they had a few micrographs showing the sequence). In the sequence, it showed how the organelles (including the novel N2 fixation one) undergoing division and each ‘child’ organelle ending up in different halves.
Cell division is controlled in the cell by an amazing process:
The x-ray micrographs show that the N2 fixators are already integrated into this mitosis mechanism - my guess is that the N2 fixators already ‘understand’ the parent cell’s mitosis signaling.
The authors also say that the organelles have lost a number of genes for essential cellular functions, relying on the parent cell to provide those capabilities. By comparison, mitochondria have only 37 genes left, and chloroplasts weren’t known for having any DNA when I was at school, but are now known to have about 110 genes.
In other words, a lot of evolution has already occurred and they are well on the way to being ‘proper’ organelles.