What is it about?
Biparental reproduction, in which an offspring receives half their genetic material, or DNA, from one parent, and half from the other parent, occurs in nearly all eukaryotes. To ensure that exactly half of an individual’s DNA comes from each parent, eukaryotes have developed a specialized process to divide up this DNA called meiosis. The central enzyme responsible for this segregation of genetic material is called Dmc1. Dmc1 has several key partner proteins that regulate its function and improve its accuracy. Herein, we uncovered a mutant version of the Dmc1 protein that can function without one of these normally essential partner proteins. We conclude that this partner protein, Mei5-Sae3, affects how stably Dmc1 interacts with DNA, and show that the Dmc1 mutant has serious defects in its activity as a result of loss of regulation by Mei5-Sae3.
Photo by Amit Rana on Unsplash
Why is it important?
Errors made during meiosis can lead to abnormalities that cause miscarriage or birth defects, such as trisomy 21. Dmc1 has a very similar structure and function in all eukaryotes, from single-celled organisms such as budding yeast all the way up to humans. By improving our understanding of how Dmc1 functions and the proteins that enhance its activity, we can potentially gain insight into errors in meiosis that have consequences for human reproduction.
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This page is a summary of: A mutant form of Dmc1 that bypasses the requirement for accessory protein Mei5-Sae3 reveals independent activities of Mei5-Sae3 and Rad51 in Dmc1 filament stability, PLoS Genetics, December 2019, PLOS, DOI: 10.1371/journal.pgen.1008217.
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