Abstract
SummaryMeiotic chromosome movement is important for the pairwise alignment of homologous chromosomes, which is required for correct chromosome segregation. Movement is driven by cytoplasmic forces, transmitted to chromosome ends by nuclear membrane-spanning proteins. In animal cells, lamins form a prominent scaffold at the nuclear periphery, yet the role lamins play in meiotic chromosome movement is unclear. We show that chromosome movement correlates with reduced lamin association with the nuclear rim, which requires lamin phosphorylation at sites analogous to those that open lamina network crosslinks in mitosis. Failure to remodel the lamina results in delayed meiotic entry, altered chromatin organization, unpaired or interlocked chromosomes, and slowed chromosome movement. The remodeling kinases are delivered to lamins via chromosome ends coupled to the nuclear envelope, potentially enabling crosstalk between the lamina and chromosomal events. Thus, opening the lamina network plays a role in modulating contacts between chromosomes and the nuclear periphery during meiosis.
Highlights
To ensure faithful chromosome segregation at the first meiotic division, a physical tether needs to be established between parental chromosomes via crossover formation
Nuclear Lamina Characteristics Change after Meiotic Entry To investigate whether characteristics of the meiotic lamina network change upon meiotic entry, we constructed C. elegans strains expressing functional GFP::LMN-1 from a MosSCI (Mos1-mediated single copy insertion) defined chromosomal insertion site in the lmn-1 deletion mutant and tagged the endogenous locus by CRISPR
Extruded C. elegans gonads recapitulate the stages of meiotic prophase I in a temporal order (Hillers et al, 2017)
Summary
To ensure faithful chromosome segregation at the first meiotic division, a physical tether needs to be established between parental chromosomes via crossover formation This is achieved by repairing induced DNA double-strand breaks (DSBs) through homologous recombination, using a sister chromatid of the parental homolog as the repair template. Chromosome movement within the nucleus is driven by cytoskeletal forces generated in the cytoplasm and transmitted through the nuclear membranes via a conserved mechanism involving SUN (Sad1p, UNC-84) and KASH (Klarsicht, ANC-1, Syne Homology) domain proteins (Caenorhabditis elegans SUN-1 and ZYG-12 [Penkner et al, 2009; Sato et al, 2009]). SUN-1 becomes hyperphosphorylated and concentrated at chromosome ends, which is
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
