Putting CENP-A in its place

Stellfox, Madison E.; Bailey, Aaron O.; Foltz, Daniel R.

doi:10.1007/s00018-012-1048-8

Cited by 76 publications

(60 citation statements)

References 154 publications

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“…Indeed, CENP-A levels were reduced in HeLa cells lacking RBBP7 and both RBBP7 and RBBP4, similar to cells downregulated for the CENP-A-specific histone chaperone HJURP (Dunleavy et al, 2009). Because CENP-A levels fluctuate through the cell cycle (Stellfox et al, 2013), we performed a similar experiment in cells synchronized at the G1/S transition by double thymidine block release (DTBR) treatment. In contrast to siRBBP4, siRBBP7 treatment was sufficient to reduce CENP-A and HJURP protein levels (Fig.…”

Section: Rbbp7 Is Required To Stabilize Cenp-a Protein Levelsmentioning

confidence: 96%

“…2C; supplementary material Fig. S2E), which corresponds to the cell stage when most of the CENP-A molecules have been loaded at centromeres , but have not yet been diluted during DNA replication (Stellfox et al, 2013). The cells were fixed 72 h after siRNA treatment to downregulate RBBP7, RBBP4 or HJURP (Fig.…”

Section: Rbbp7 Is Required To Stabilize Cenp-a Protein Levelsmentioning

confidence: 99%

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CRL4RBBP7 is required for efficient CENP-A deposition at centromeres

Mouysset¹,

Gilberto²,

Meier³

et al. 2015

Journal of Cell Science

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The mitotic spindle drives chromosome movement during mitosis and attaches to chromosomes at dedicated genomic loci named centromeres. Centromeres are epigenetically specified by their histone composition, namely the presence of the histone H3 variant CENP-A, which is regulated during the cell cycle by its dynamic expression and localization. Here, we combined biochemical methods and quantitative imaging approaches to investigate a new function of CUL4-RING E3 ubiquitin ligases (CRL4) in regulating CENP-A dynamics. We found that the core components CUL4 and DDB1 are required for centromeric loading of CENP-A, but do not influence CENP-A maintenance or pre-nucleosomal CENP-A levels. Interestingly, we identified RBBP7 as a substrate-specific CRL4 adaptor required for this process, in addition to its role in binding and stabilizing soluble CENP-A. Our data thus suggest that the CRL4 complex containing RBBP7 (CRL4 RBBP7 ) might regulate mitosis by promoting ubiquitin-dependent loading of newly synthesized CENP-A during the G1 phase of the cell cycle.

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Section: Rbbp7 Is Required To Stabilize Cenp-a Protein Levelsmentioning

confidence: 96%

Section: Rbbp7 Is Required To Stabilize Cenp-a Protein Levelsmentioning

confidence: 99%

CRL4RBBP7 is required for efficient CENP-A deposition at centromeres

Mouysset¹,

Gilberto²,

Meier³

et al. 2015

Journal of Cell Science

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“…5; Supplemental Table S4). Hjurp mediates the centromerespecific assembly of CENP-A nucleosomes, contributing to high-fidelity chromosome segregation during cell division (Stellfox et al 2013). The misregulation of Hjurp has been shown to affect chromosome stability in yeast and human cells (Mishra et al 2011), and expression levels in human cells influence senescence (Heo et al 2013).…”

Section: Cnv Genes Of Special Interestmentioning

confidence: 99%

Divergence patterns of genic copy number variation in natural populations of the house mouse (Mus musculus domesticus) reveal three conserved genes with major population-specific expansions

et al. 2015

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Copy number variation represents a major source of genetic divergence, yet the evolutionary dynamics of genic copy number variation in natural populations during differentiation and adaptation remain unclear. We applied a read depth approach to genome resequencing data to detect copy number variants (CNVs) ≥1 kb in wild-caught mice belonging to four populations of Mus musculus domesticus. We complemented the bioinformatics analyses with experimental validation using droplet digital PCR. The specific focus of our analysis is CNVs that include complete genes, as these CNVs could be expected to contribute most directly to evolutionary divergence. In total, 1863 transcription units appear to be completely encompassed within CNVs in at least one individual when compared to the reference assembly. Further, 179 of these CNVs show population-specific copy number differences, and 325 are subject to complete deletion in multiple individuals. Among the most copy-number variable genes are three highly conserved genes that encode the splicing factor CWC22, the spindle protein SFI1, and the Holliday junction recognition protein HJURP. These genes exhibit population-specific expansion patterns that suggest involvement in local adaptations. We found that genes that overlap with large segmental duplications are generally more copy-number variable. These genes encode proteins that are relevant for environmental and behavioral interactions, such as vomeronasal and olfactory receptors, as well as major urinary proteins and several proteins of unknown function. The overall analysis shows that genic CNVs contribute more to population differentiation in mice than in humans and may promote and speed up population divergence

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“…While it is clear that a specialized chromatin structure facilitates the assembly and function of .38 core kinetochore proteins and additional regulatory proteins (Stellfox et al 2012;Valente et al 2012), the key determinants of this chromatin structure have still not been fully elucidated. We therefore set out to identify histone H3 and H4 residues that contribute to chromosome segregation and kinetochore biorientation by performing two systematic genetic screens in budding yeast.…”

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confidence: 99%

Kinetochore Function and Chromosome Segregation Rely on Critical Residues in Histones H3 and H4 in Budding Yeast

Lenstra²,

Duggan

et al. 2013

Genetics

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Accurate chromosome segregation requires that sister kinetochores biorient and attach to microtubules from opposite poles. Kinetochore biorientation relies on the underlying centromeric chromatin, which provides a platform to assemble the kinetochore and to recruit the regulatory factors that ensure the high fidelity of this process. To identify the centromeric chromatin determinants that contribute to chromosome segregation, we performed two complementary unbiased genetic screens using a library of budding yeast mutants in every residue of histone H3 and H4. In one screen, we identified mutants that lead to increased loss of a nonessential chromosome. In the second screen, we isolated mutants whose viability depends on a key regulator of biorientation, the Aurora B protein kinase. Nine mutants were common to both screens and exhibited kinetochore biorientation defects. Four of the mutants map near the unstructured nucleosome entry site, and their genetic interaction with reduced IPL1 can be suppressed by increasing the dosage of SGO1, a key regulator of biorientation. In addition, the composition of purified kinetochores was altered in six of the mutants. Together, this work identifies previously unknown histone residues involved in chromosome segregation and lays the foundation for future studies on the role of the underlying chromatin structure in chromosome segregation.

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Putting CENP-A in its place

Cited by 76 publications

References 154 publications

CRL4RBBP7 is required for efficient CENP-A deposition at centromeres

CRL4RBBP7 is required for efficient CENP-A deposition at centromeres

Divergence patterns of genic copy number variation in natural populations of the house mouse (Mus musculus domesticus) reveal three conserved genes with major population-specific expansions

Kinetochore Function and Chromosome Segregation Rely on Critical Residues in Histones H3 and H4 in Budding Yeast

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