The MAP kinase pathway coordinates crossover designation with disassembly of synaptonemal complex proteins during meiosis
- Harvard Medical School, United States
- Hebrew University of Jerusalem, Israel
- Imperial College London, United Kingdom
- London Research Institute, United Kingdom
- Barts Cancer Institute, United Kingdom
Abstract
Asymmetric disassembly of the synaptonemal complex (SC) is crucial for proper meiotic chromosome segregation. However, the signaling mechanisms that directly regulate this process are poorly understood. Here we show that the mammalian Rho GEF homolog, ECT-2, functions through the conserved RAS/ERK MAP kinase signaling pathway in the C. elegans germline to regulate the disassembly of SC proteins. We find that SYP-2, a SC central region component, is a potential target for MPK-1-mediated phosphorylation and that constitutively phosphorylated SYP-2 impairs the disassembly of SC proteins from chromosomal domains referred to as the long arms of the bivalents. Inactivation of MAP kinase at late pachytene is critical for timely disassembly of the SC proteins from the long arms, and is dependent on the crossover (CO) promoting factors ZHP-3/RNF212/Zip3 and COSA-1/CNTD1. We propose that the conserved MAP kinase pathway coordinates CO designation with the disassembly of SC proteins to ensure accurate chromosome segregation.
Article and author information
Author details
Reviewing Editor
- Bernard de Massy, Institute of Human Genetics, CNRS UPR 1142, France
Version history
- Received: October 2, 2015
- Accepted: February 26, 2016
- Accepted Manuscript published: February 27, 2016 (version 1)
- Version of Record published: March 14, 2016 (version 2)
Copyright
© 2016, Nadarajan et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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The MAP kinase pathway coordinates crossover designation with disassembly of synaptonemal complex proteins during meiosis
eLife 5:e12039.
https://doi.org/10.7554/eLife.12039
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