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Status |
Public on Apr 16, 2015 |
Title |
The N-terminal Tail of CENP-A Confers Epigenetic Stability to Centromeres via the CENP-T Branch of the CCAN in Fission Yeast |
Organism |
Schizosaccharomyces pombe |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
We employ the well-studied fission yeast centromere to investigate the function of the CENP-A (Cnp1) N-tail. We show that alteration of the N-tail did not affect Cnp1 loading at centromeres, outer kinetochore formation, or spindle checkpoint signaling, but nevertheless elevated chromosome loss. N-Tail mutants exhibited synthetic lethality with an altered centromeric DNA sequence, with rare survivors harboring chromosomal fusions in which the altered centromere was epigenetically inactivated. Elevated centromere inactivation was also observed for N-tail mutants with unaltered centromeric DNA sequences. N-tail mutants specifically reduced localization of the CCAN proteins Cnp20/CENP-T and Mis6/CENP-I, but not Cnp3/CENP-C. Overexpression of Cnp20/CENP-T suppressed defects in an N-tail mutant, suggesting a causal link between reduced CENP-T recruitment and the observed centromere inactivation phenotype. Thus, the Cnp1 N-tail promotes epigenetic stability of centromeres via recruitment of the CENP-T branch of the CCAN.
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Overall design |
Genome-wide localization of GFP-tagged N-tail Cnp1 variant tailswap versus wt control in cnp1 deletion background
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Contributor(s) |
Folco HD, Espinoza CA, Desai AB |
Citation(s) |
25619765 |
Submission date |
Nov 17, 2014 |
Last update date |
May 15, 2019 |
Contact name |
Arshad Desai |
E-mail(s) |
abdesai@ucsd.edu
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Organization name |
UCSD/LICR
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Department |
Cellular & Molecular Medicine
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Lab |
Desai laboratory
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Street address |
9500 Gilman Dr
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City |
La Jolla |
State/province |
CA |
ZIP/Postal code |
92093 |
Country |
USA |
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Platforms (1) |
GPL9854 |
Illumina Genome Analyzer (Schizosaccharomyces pombe) |
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Samples (4)
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Relations |
BioProject |
PRJNA267552 |
SRA |
SRP049949 |