Phys.Org has a new summary about a new finding regarding heterochromatin repair in the nucleus which involves the nuclear membrane. In their discussion, they make some interesting points:
Previously, the nuclear membrane was thought to be mostly just a protective bubble around the nuclear material, with pores acting as channels to transport molecules in and out. But in a study published on October 26 in Nature Cell Biology, a research team led by Irene Chiolo documents how broken strands of a portion of DNA known as heterochromatin are dragged to the nuclear membrane for repair.
The reason why we don’t experience thousands of cancers every day in our body is because we have incredibly efficient molecular mechanisms that repair the frequent damages occurring in our DNA. But those that work in heterochromatin are quite extraordinary.
So, let’s reflect here a little bit. If the repair mechanism is not in place, an organism will die of cancer, and leave no offspring. So, how did this system “evolve” in the first place? Actually, isn’t this more like IC, “irreducible complexity”?
The bacterial cell, IIRC, has no nucleus, and has a much smaller genome which is circular. So, to deal with a larger genome, you need something to tidy the chromosomes up. So you break them into smaller units, and come up with a way of condensing the nucleotide string of bases, which is the job of chromatin. But now, if chromatin fails, then what?
Lo and behold: a repair mechanism that utilizes the nuclear membrane to segregate the chromsomes from getting stuck together with other portions of the cell, and then you use to nuclear membrane for repair so that until the heterochromatin is repaired, it won’t get gummed up with something else and cause greater problems.
Working with the fruit fly Drosophila melanogaster, the team observed that breaks in heterochromatin are repaired after damaged sequences move away from the rest of the chromosome to the inner wall of the nuclear membrane. There, a trio of proteins mends the break in a safe environment, where it cannot accidentally get tangled up with incorrect chromosomes.
I tell you, it functions like a machine! Oops. I’m sorry. We know it looks designed, and acts designed, but everything came about in a random fashion. As Dawkins tells us to keep doing, I have to repeat to myself, “It isn’t designed. It isn’t designed…,” or else I risk getting confused.
More seriously, we’ve come a long way since Darwin’s time, a time when the cell was thought to be no more than “protoplasm,” some gel that filled the ovum. Egg white, if you will.
In the same way, the nuclear membrane is just a bunch of lipids that spontaneously configured themselves. You know—a bubble.
With each passing month, as techonology improves, more and more complexity is found. And, according to the strictly materialist view that underpins much of Darwinism, this is brought about by “random” mutations.
The rise of complexity is hitting the scientific community like a tidal wave; and yet it just digs in its heels and says: “No big thing. We’ve known about that for a long time.”
Here’s the abstract from Nature Cell Biology:
Heterochromatin mostly comprises repeated sequences prone to harmful ectopic recombination during double-strand break (DSB) repair. In Drosophila cells, ‘safe’ homologous recombination (HR) repair of heterochromatic breaks relies on a specialized pathway that relocalizes damaged sequences away from the heterochromatin domain before strand invasion. Here we show that heterochromatic DSBs move to the nuclear periphery to continue HR repair. Relocalization depends on nuclear pores and inner nuclear membrane proteins (INMPs) that anchor repair sites to the nuclear periphery through the Smc5/6-interacting proteins STUbL/RENi. Both the initial block to HR progression inside the heterochromatin domain, and the targeting of repair sites to the nuclear periphery, rely on SUMO and SUMO E3 ligases. This study reveals a critical role for SUMOylation in the spatial and temporal regulation of HR repair in heterochromatin, and identifies the nuclear periphery as a specialized site for heterochromatin repair in a multicellular eukaryote.