Thread by @jessdiscala

UV-ray DNA damage repair
[thread]

Here I will go over:
⁃DNA Pol Eta (translesion synthesis)
⁃Nucleotide Excision Repair

These are two mechanisms that work proficiently to prevent skin cancer, & are part of why I believe the sun does not cause it.

UV rays can cause a wide variety of damage to DNA. They most commonly break the backbone of DNA which causes single & double stranded breaks.

They can also cause thymine dimers:

Thymine dimers are when two thymines that are next to each other on a strand get covalently bonded together, which contorts them into a shape where they are not able to form H-bonds with their base pair.

DNA Pol Eta is a eukaryotic polymerase involved in translesion synthesis.

Translesion synthesis is a DNA repair mechanism where polymerases, other than the main polymerase III, are needed to repair a mistake or mutation.

If DNA Pol III is stuck at a mutation, a different Pol for repair will come in to replace Pol III & insert mismatched nucleotides so that Pol III can hop back on & finish its job.

Eta is a polymerase that specializes in fixing thymine dimers.

It will replace Pol III & insert two adenines to complement the two thymines in the thymine dimer. Then it will jump back off to allow Pol III to come back.

DNA Pol Eta is important for fixing thymine dimers in Eukaryotic cells & a deficiency in the enzyme causes Xeroderma Pigmentosum.

Pol Eta was evolved to replace Photolyase, which turned into a pseudogene in mammals.

Photolyase is an enzyme that uses energy from the sun to repair thymine dimers. It breaks the covalent bond between the thymines & restores the H-bonds with the complimentary adenines.

So even though we don’t have photolyase to repair sun damage, we have a very efficient DNA Pol Eta to repair a large chunk of UV ray DNA damage.

Another mechanism cells use to repair UV damage is Nucleotide Excision Repair(NER)

This mechanism finds a mutation, removes it & the nucleotides surrounding it & brings in polymerase for repair

NER is able to fix most problems, including dimers & oxidative damage from UV rays

There are 4 subunits of NER:
⁃Uvr A
⁃Uvr B
⁃Uvr C
⁃Uvr D

How it works:

Once the mutated DNA is identified by Uvr A & B, two Uvr C proteins attach on both sides of the strand & create nicks (small single stranded cuts).

The helicase Uvr D can then remove the single strand of DNA, exposing a 3’ OH group which DNA polymerase needs to start synthesis of the gap.

Lastly, DNA ligase comes in to seal the last bond & the repair is then completed.

Nucleotide Excision Repair is thought to be at least as old as Archaea, which evolved about 2.7 billion years ago.

DNA Pol Eta evolved when mammals diverged about 200-250 million years ago.

My point is that these UV damage repair mechanisms have been fine tuned to be highly efficient & have stood the test of millions/ billions of years of evolving with UV rays.

Humans evolved in the sun, without sunscreen, & without industrialized chemicals & processed food & seed oils.

The list goes on & on of how modern living is extremely different than what we evolved in.

The first documented cases of skin cancer were in the 1800s, I’m not saying it didn’t exist before then, it definitely did.

I simply need more evidence than is currently provided for me to believe something that, to me, goes against human evolution.