Journal
JOURNAL OF CELL BIOLOGY
Volume 217, Issue 2, Pages 555-570Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201707161
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Funding
- National Institutes of Health National Center for Research Resources
- Japan Society for the Promotion of Science
- Japan Society for the Promotion of Science KAKENHI [24687024, 15H04328, 15K18477, 17K15064]
- World Premier International Research Initiative of the Ministry of Education, Culture, Sports, Science and Technology, Japan
- Grants-in-Aid for Scientific Research [15K18477, 17K15064, 15H04328, 24687024] Funding Source: KAKEN
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Chromosomes that have undergone crossing over in meiotic prophase must maintain sister chromatid cohesion somewhere along their length between the first and second meiotic divisions. Although many eukaryotes use the centromere as a site to maintain cohesion, the holocentric organism Caenorhabditis elegans instead creates two chromosome domains of unequal length termed the short arm and long arm, which become the first and second site of cohesion loss at meiosis I and II. The mechanisms that confer distinct functions to the short and long arm domains remain poorly understood. Here, we show that phosphorylation of the synaptonemal complex protein SYP-1 is required to create these domains. Once crossover sites are designated, phosphorylated SYP-1 and PLK-2 become cooperatively confined to short arms and guide phosphorylated histone H3 and the chromosomal passenger complex to the site of meiosis I cohesion loss. Our results show that PLK-2 and phosphorylated SYP-1 ensure creation of the short arm subdomain, promoting disjunction of chromosomes in meiosis I.
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