Telomeric Amplicons Of Sul1 And Y’ In Yeast Are Generated By Microhomology-Mediated Break Induced Replication Occurring In Cis
Gene amplification, the process where cells make extra copies of specific genes, is a powerful force in evolution and can contribute to diseases like cancer. Scientists have uncovered a new way this happens at the very ends of chromosomes, called telomeres, in yeast.
Imagine the ends of your shoelaces fraying; that’s similar to what happens to telomeres over time. This study shows that when these chromosome ends become unstable, or when certain genes involved in DNA maintenance are disrupted, a unique copying process kicks in. An unprotected telomere essentially “invades” a short, similar DNA sequence located further inside the same chromosome. This invasion, guided by tiny matching DNA stretches (called microhomology), creates a temporary circular structure. This structure then acts as a template, allowing the cell’s DNA copying machinery to repeatedly duplicate the chromosome end. The result is a chromosome with several identical copies of its end segment, arranged one after another.
This newly discovered mechanism, termed “pseudo-rolling circle microhomology-mediated break-induced replication,” not only explains how yeast cells can repair their eroding telomeres but also provides insights into how gene amplification, a process with implications for human health, might occur more broadly. The findings suggest that a similar process could be at play in human cells, particularly in situations of stress on our chromosomes.
Source: link to paper