Centromeric SMC1 promotes centromere clustering and stabilizes meiotic homolog pairing

During meiosis, each chromosome must selectively pair and synapse with its own unique homolog to enable crossover formation and subsequent segregation. How homolog pairing is maintained in early meiosis to ensure synapsis occurs exclusively between homologs is unknown. We aimed to further understand...

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Bibliographic Details
Published in:PLoS genetics 2019-10, Vol.15 (10), p.e1008412-e1008412
Main Authors: Hatkevich, Talia, Boudreau, Vincent, Rubin, Thomas, Maddox, Paul S, Huynh, Jean-René, Sekelsky, Jeff
Format: Article
Language:English
Subjects:
Animals
Biology and Life Sciences
Cell Cycle Proteins - genetics
Centromere - genetics
Chromosomal Proteins, Non-Histone - genetics
Chromosome Pairing - genetics
Chromosome Segregation - genetics
Chromosomes
Curricula
Cysts
Drosophila
Drosophila - genetics
Funding
Genetics
Genomes
Homologous Recombination - genetics
Insects
Life Sciences
Medicine and Health Sciences
Meiosis
Meiosis - genetics
Molecular biology
Proteins
Research and Analysis Methods
Synapses
Synaptonemal Complex
Telomere - genetics
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Summary:During meiosis, each chromosome must selectively pair and synapse with its own unique homolog to enable crossover formation and subsequent segregation. How homolog pairing is maintained in early meiosis to ensure synapsis occurs exclusively between homologs is unknown. We aimed to further understand this process by examining the meiotic defects of a unique Drosophila mutant, Mcm5A7. We found that Mcm5A7 mutants are proficient in homolog pairing at meiotic onset yet fail to maintain pairing as meiotic synapsis ensues, causing seemingly normal synapsis between non-homologous loci. This pairing defect corresponds with a reduction of SMC1-dependent centromere clustering at meiotic onset. Overexpressing SMC1 in this mutant significantly restores centromere clustering, homolog pairing, and crossover formation. These data indicate that the initial meiotic pairing of homologs is not sufficient to yield synapsis exclusively between homologs and provide a model in which meiotic homolog pairing must be stabilized by centromeric SMC1 to ensure proper synapsis.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1008412