Journal
CELL CYCLE
Volume 17, Issue 23, Pages 2520-2530Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2018.1553355
Keywords
Homologous recombination; dmc1; meiosis
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Funding
- Damon Runyon Cancer Research Foundation [DRG 2310-17]
- Directorate for Biological Sciences [MCB-1154511]
- National Cancer Institute [P01CA092584]
- National Institute of General Medical Sciences [R35GM118026]
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Meiosis is the basis for sexual reproduction and is marked by the sequential reduction of chromosome number during successive cell cycles, resulting in four haploid gametes. A central component of the meiotic program is the formation and repair of programmed double strand breaks. Recombination-driven repair of these meiotic breaks differs from recombination during mitosis in that meiotic breaks are preferentially repaired using the homologous chromosomes in a process known as homolog bias. Homolog bias allows for physical interactions between homologous chromosomes that are required for proper chromosome segregation, and the formation of crossover products ensuring genetic diversity in progeny. An important aspect of meiosis in the differential regulation of the two eukaryotic RecA homologs, Rad51 and Dmc1. In this review we will discuss the relationship between biological programs designed to regulate recombinase function.
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