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ATP synthase F1 subunits recruited to centromeres by CENP-A are required for male meiosis

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Show simple item record Collins, Catríona M. Malacrida, Beatrice Burke, Colin Kiely, Patrick A. Dunleavy, Elaine M. 2018-08-28T10:26:21Z 2018-08-28T10:26:21Z 2018
dc.description peer-reviewed en_US
dc.description.abstract The histone H3 variant CENP-A epigenetically defines the centromere and is critical for chromosome segregation. Here we report an interaction between CENP-A and subunits of the mitochondrial ATP synthase complex in the germline of male Drosophila. Furthermore, we report that knockdown of CENP-A, as well as subunits ATPsyn-α, -βlike (a testis-specific paralogue of ATPsyn-β) and -γ disrupts sister centromere cohesion in meiotic prophase I. We find that this disruption is likely independent of reduced ATP levels. We identify that ATPsyn- α and -βlike localise to meiotic centromeres and that this localisation is dependent on the presence of CENP-A. We show that ATPsyn-α directly interacts with the N-terminus of CENP-A in vitro and that truncation of its N terminus perturbs sister centromere cohesion in prophase I. We propose that the CENP-A N-terminus recruits ATPsyn-α and -βlike to centromeres to promote sister centromere cohesion in a nuclear function that is independent of oxidative phosphorylation. en_US
dc.language.iso eng en_US
dc.publisher Nature Publishing Group en_US
dc.relation.ispartofseries Nature Communications;9:2702
dc.subject CENP-A en_US
dc.subject chromosome segregation en_US
dc.title ATP synthase F1 subunits recruited to centromeres by CENP-A are required for male meiosis en_US
dc.type info:eu-repo/semantics/article en_US
dc.type.supercollection all_ul_research en_US
dc.type.supercollection ul_published_reviewed en_US
dc.identifier.doi 10.1038/s41467-018-05093-9
dc.contributor.sponsor SFI en_US
dc.relation.projectid 100105/Z/12/Z en_US
dc.relation.projectid 13/YI/2187 en_US
dc.relation.projectid 12/RI/2345 en_US
dc.relation.projectid 13/CDA/2228 en_US
dc.rights.accessrights info:eu-repo/semantics/openAccess en_US

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