Even on a good day, DNA is constantly getting damaged.

Nicks, scratches, breaks: the delicate strands that carry life's genetic code take a beating as they jumble about in the course of their work. If left untreated, errors accumulate, with fatal consequences -- such as cancerous tumors -- for the cell and the organism.

This is where two key proteins come to the rescue: PARP -- or poly ADP ribose polymerase -- acts as a marker for a trouble spot, allowing XRCC1 -- or X-ray repair cross-complementing protein 1 -- to zoom in and begin a repair.

This much has been known for some time and was even recognized in the 2015 Nobel prizes for chemistry, resulting in the development of anti-cancer drugs known as PARP inhibitors that work to disrupt the growth of certain types of tumors.

But while these actors had been identified, their precise roles were not clear. Now a team of scientists at Tokyo Metropolitan University, the University of Sussex, and Kyoto University have revealed exactly how XRCC1 does its work.

"PARP turns out to be something of a villain," explains Kouji Hirota at Tokyo Metropolitan. "The spots it marks become 'PARP traps', which left un-repaired lead to disfunction and cell death."

XRCC1 therefore isn't simply repairing DNA, it is disarming PARP traps.

The scientists compared cells lacking the XRCC1 gene with those lacking PARP as well as with still others lacking both proteins. The team discovered that without XRCC1 on patrol, PARP traps accumulate like landmines.

"PARP exerts toxic effects in the cell and XRCC1 suppresses this toxicity," Hirota elaborates.

The team next seeks to delve even further into these processes, aiming to aid in the development of future cancer treatments.

KyotoU's Shunichi Takeda says: "These results indicate that XRCC1 is a critical factor in the resolution of PARP traps and may be a determinant of the therapeutic effect of PARP inhibitors used in the treatment of hereditary breast and ovarian cancer syndromes."

The genetic code is the set of rules by which information encoded in genetic material (DNA or RNA sequences) is translated into proteins (amino acid sequences) by living cells.

Specifically, the code defines a mapping between tri-nucleotide sequences called codons and amino acids; every triplet of nucleotides in a nucleic acid sequence specifies a single amino acid.

Because the vast majority of genes are encoded with exactly the same code, this particular code is often referred to as the canonical or standard genetic code, or simply the genetic code, though in fact there are many variant codes; thus, the canonical genetic code is not universal. For example, in humans, protein synthesis in mitochondria relies on a genetic code that varies from the canonical code. The genome of an organism is inscribed in DNA, or in some viruses RNA. The portion of the genome that codes for a protein or an RNA is referred to as a gene.

Those genes that code for proteins are composed of tri-nucleotide units called codons, each coding for a single amino acid. Each nucleotide sub-unit consists of a phosphate, deoxyribose sugar and one of the 4 nitrogenous nucleotide bases. The purine bases adenine (A) and guanine (G) are larger and consist of two aromatic rings. The pyrimidine bases cytosine (C) and thymine (T) are smaller and consist of only one aromatic ring.

In the double-helix configuration, two strands of DNA are joined to each other by hydrogen bonds in an arrangement known as base pairing. These bonds almost always form between an adenine base on one strand and a thymine on the other strand and between a cytosine base on one strand and a guanine base on the other. This means that the number of A and T residues will be the same in a given double helix as will the number of G and C residues.

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Archives in Cancer Research