6533b7d0fe1ef96bd125afee
RESEARCH PRODUCT
Phosphorylation of CENP-A on serine 7 does not control centromere function.
Glennis A. LogsdonGlennis A. LogsdonAaron AslanianDon W. ClevelandBen E. BlackDaniele FachinettiSolène HervéAndrea ScelfoYael Nechemia-arbelyYael Nechemia-arbelyViviana BarraViviana BarraSebastian Hoffmannsubject
0301 basic medicine1.1 Normal biological development and functioningScience[SDV]Life Sciences [q-bio]CentromereGeneral Physics and Astronomy02 engineering and technology[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleSerineChromosome segregation03 medical and health sciencesHistone H3Underpinning researchCentromereGeneticsHumansViability assayPhosphorylationlcsh:ScienceComputingMilieux_MISCELLANEOUSCancerGene EditingMultidisciplinaryQGene targetingGeneral Chemistry021001 nanoscience & nanotechnologyCell biologySettore BIO/18 - Genetica030104 developmental biologyChromosome segragationHela CellsPhosphorylationEpigeneticslcsh:QGeneric health relevance0210 nano-technologyFunction (biology)Centromere Protein AHumanHeLa Cellsdescription
CENP-A is the histone H3 variant necessary to specify the location of all eukaryotic centromeres via its CENP-A targeting domain and either one of its terminal regions. In humans, several post-translational modifications occur on CENP-A, but their role in centromere function remains controversial. One of these modifications of CENP-A, phosphorylation on serine 7, has been proposed to control centromere assembly and function. Here, using gene targeting at both endogenous CENP-A alleles and gene replacement in human cells, we demonstrate that a CENP-A variant that cannot be phosphorylated at serine 7 maintains correct CENP-C recruitment, faithful chromosome segregation and long-term cell viability. Thus, we conclude that phosphorylation of CENP-A on serine 7 is dispensable to maintain correct centromere dynamics and function.
year | journal | country | edition | language |
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2019-12-01 | Nature communications |