Genome complexity: DNA repair molecule (Introduction)

by David Turell , Monday, July 22, 2019, 18:49 (1733 days ago) @ David Turell

A new one is fund and described in its function:

https://phys.org/news/2019-07-molecular-sensor-scouts-dna.html

"In the time it takes you to read this sentence, every cell in your body suffers some form of DNA damage. Without vigilant repair, cancer would run rampant, and now scientists at the University of Pittsburgh have gotten a glimpse of how one protein in particular keeps DNA damage in check.

"According to a study published today in Nature Structural and Molecular Biology, a protein called UV-DDB—which stands for ultraviolet-damaged DNA-binding—is useful beyond safeguarding against the sun. This new evidence points to UV-DDB being a scout for general DNA damage and an overseer of the molecular repair crew that fixes it.

"'If you're going to fix a pothole, you have to find it first. That's what UV-DDB does. It identifies DNA damage so that another crew can come in and patch and seal it," said study senior author Bennett Van Houten, Ph.D., professor of pharmacology and chemical biology at the Pitt School of Medicine and UPMC Hillman Cancer Center.

***

"'UV-DDB is like a helicopter that can land and then roll for a couple blocks," Van Houten said. "It also has the ability to find damage buried in chromosomes and help DNA repair molecules go places they otherwise couldn't, the way a helicopter can navigate really hilly areas."

"When UV-DDB finds damage, it acts like a foreman to help the DNA repair crew get in, fix the faulty bases and detach quickly.

"For the first time, Van Houten's team witnessed this molecular tango along a "tightrope" of DNA slung between two silica beads, using real-time, single-molecule imaging.

"To show that UV-DDB performs the same functions in living cells, Van Houten recruited the help of Marcel Bruchez, Ph.D., of Carnegie Mellon University, and Patricia Opresko, Ph.D., of Pitt. Together they inflicted oxidative damage to the chromosomes' protective endcaps—called telomeres. As in the DNA tightrope experiment, UV-DDB rushed to the scene, and when it wasn't available, cells were more sensitive to oxidative stress.

***

"'It's clear this protein is involved in a very fundamental problem," Van Houten said. "We could not have evolved out of the slime if we didn't have good DNA repair.'" (my bold)

Comment: Note the final bolded statement, which points out the obvious reason why this is a designed system. It had to be present with the first living cells.