Publications by authors named "M Jasin"
Maintaining genome integrity is an essential and challenging process. RAD51 recombinase, the central player of several crucial processes in repairing DNA and protecting genome integrity, forms filaments on DNA, which are tightly regulated. One of these RAD51 regulators is FIGNL1, that prevents persistent RAD51 foci without or after DNA damage and genotoxic chromatin association in cells.
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- Harnessing DNA double-strand breaks (DSBs) for gene editing can lead to loss of heterozygosity (LOH), which is a potential risk factor for cancer development.
- A new flow cytometry system called Flo-LOH was developed to detect LOH in about 5% of cells after a DSB, revealing that while LOH cells initially decrease in number due to competition, they can stably grow if isolated.
- The study found that LOH can extend over large regions of DNA and is significantly increased when certain DNA repair pathways are inhibited, emphasizing the need to cautiously consider the implications of using DSBs for gene editing.
Article Synopsis
- Pathogenic variants in the RAD51C gene increase the risk for breast and ovarian cancer, and certain homozygous variants can lead to Fanconi anemia.
- Researchers used saturation genome editing to analyze a large number of genetic variants, identifying 3,094 as disruptive, with high accuracy in variant classification.
- The study found significant links between specific variants depleted via genome editing and cancer diagnoses, contributing to a better understanding of RAD51C's role in cancer susceptibility.
Maintaining genome integrity is an essential and challenging process. RAD51 recombinase, the central player of several crucial processes in repairing and protecting genome integrity, forms filaments on DNA. RAD51 filaments are tightly regulated.
View Article and Find Full Text PDFReprogramming to pluripotency is associated with DNA damage and requires the functions of the BRCA1 tumor suppressor. Here, we leverage separation-of-function mutations in BRCA1/2 as well as the physical and/or genetic interactions between BRCA1 and its associated repair proteins to ascertain the relevance of homology-directed repair (HDR), stalled fork protection (SFP), and replication gap suppression (RGS) in somatic cell reprogramming. Surprisingly, loss of SFP and RGS is inconsequential for the transition to pluripotency.
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