The researchers showed that this is a result of the defect in the genes encoding the BRCA1 and BRCA2 proteins. These proteins are responsible for repairing double-strand breaks and returning the DNA to its original state, and defects in them lead to the development of various types of cancer, including breast and ovarian cancer
Researchers at the Faculty of Biology at the Technion discovered a new mechanism that controls DNA damage repair. the research published in the journal Molecular cells Value Prof. Navia Ayoub and members of his research group - Inas Abu Zahya, Lila Beshara, Firas Mash'or, Alma Bar-Yitzchak and Bela Ben-Oz.
DNA is the hereditary material that contains the information necessary for the construction of all the cells in living things and their ongoing functioning. It is built from nucleic acids that form a ladder-like double helix, the two strands of which are connected to each other in transverse steps like a ladder. Along the length of the DNA molecule, according to the estimate, there are approximately 22,000 elements that make up the human genome. The information in the genome is transcribed from the DNA molecule to create an RNA molecule, which is then translated into the proteins necessary for the construction of the cell and the organism and their functioning.
Every day, hundreds of thousands of damages are caused to our DNA, originating both from external factors such as radiation, smoking and preservatives in food, and from by-products of cellular metabolism. Fortunately, in our body cells there are repair systems that scan the DNA, monitor it and constantly repair the damage that occurs in it. These systems include a wide variety of proteins that participate in identifying the damage and repairing it.
One of the most dangerous damages to DNA is double strand break which damages both DNA strands. A defect in one of the proteins involved in the repair of the double-stranded breaks causes the accumulation of mutations - DNA damage - that destabilize the genome and can cause a wide variety of diseases, including cancer.
One of the clearest examples illustrating the link between double-strand break repair failure and cancer development is the defect in the genes encoding the BRCA1 and BRCA2 proteins. These proteins are responsible for repairing double-stranded breaks and returning the DNA to its original state, and defects in them lead to the development of various types of cancer, including breast and ovarian cancer, similar to the famous case of the actress Angelina Jolie. Therefore, in-depth research into the repair mechanisms of DNA damage in general and double-strand breaks in particular is very important.
Prof. Navia Ayoub's research group in the Faculty of Biology investigates the connection between the repair of DNA damage, and especially double-strand breaks, and cancer. In recent years, the group's researchers have discovered several new genes involved in the repair of double-strand breaks in human cells. Today, after discovering the involvement of some specific genes in the repair of double-strand breaks, they are focusing on developing new therapeutic approaches toSelective eradication of cancer cells which originate from mutations in the same genes.
It is known that double-strand breaks in DNA cause a temporary silencing of gene expression in the vicinity of the resulting break - a silencing designed to prevent the formation of damaged proteins. In addition, it is known that not silencing the expression of the broken genes can cause cancer. Today, the popular opinion is that the silencing of gene expression is necessary for the effective repair of the broken genes, that is - without the activity of the silencing mechanism, the repair of the DNA damage will not be possible. Therefore, it is very important to understand the cellular mechanism that ensures the silencing of the broken genes.
In the article, the Technion researchers characterized the dual role of the CDYL1 protein in repairing double-strand breaks and silencing the expression of the broken genes. The researchers showed thatA few seconds after the formation of the double strand break, the protein CDYL1 Recruited to the fracture zone and contributes to its repair. In addition, they showed that the protein CDYL1 Lowers the crotonyl molecule (Kcr) from the histones (proteins that wrap the DNA and control its activity) in the damaged area, thereby silencing the broken gene. The researchers discovered that, contrary to popular belief, the silencing of gene activity is not required to repair the double-stranded breaks, and these processes occur independently.
These findings expand the understanding of the way gene expression control occurs following exposure to DNA damage. In addition, the research findings may have important implications in the discovery and refinement of cures for malignant diseases resulting from abnormal activity of the CDYL1 protein.
One response
Abby, how does this help someone who carries BRCA1-2.