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Mapping of cohesion factor association sites in S. cerevisiae - Meiosis I chromosome segregation is established through regulation of microtubule-kinetochore interactions.

ABSTRACT: During meiosis, a single round of DNA replication is followed by two consecutive rounds of nuclear divisions called meiosis I and meiosis II. In meiosis I, homologous chromosomes segregate, while sister chromatids remain together. Determining how this unusual chromosome segregation behavior is established is central to understanding germ cell development. Here we show that preventing microtubule-kinetochore interactions during premeiotic S phase and prophase I is essential for establishing the meiosis I chromosome segregation pattern. Premature interactions of kinetochores with microtubules transform meiosis I into a mitosis-like division by disrupting two key meiosis I events: coorientation of sister kinetochores and protection of centromeric cohesin removal from chromosomes. Furthermore we find that restricting outer kinetochore assembly contributes to preventing premature engagement of microtubules with kinetochores. We propose that inhibition of microtubule-kinetochore interactions during premeiotic S phase and prophase I is central to establishing the unique meiosis I chromosome segregation pattern. The association of the cohesion factors Rec8, Pds5, and Sgo1 were measured by ChIP-chip analysis in wild-type and CUP-CLB3 strains.

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Elcin Unal

PROVIDER: E-GEOD-41339 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mapping of cohesion factor association sites in S. cerevisiae - Meiosis I chromosome segregation is established through regulation of microtubule-kinetochore interactions.

Project description:During meiosis, a single round of DNA replication is followed by two consecutive rounds of nuclear divisions called meiosis I and meiosis II. In meiosis I, homologous chromosomes segregate, while sister chromatids remain together. Determining how this unusual chromosome segregation behavior is established is central to understanding germ cell development. Here we show that preventing microtubule-kinetochore interactions during premeiotic S phase and prophase I is essential for establishing the meiosis I chromosome segregation pattern. Premature interactions of kinetochores with microtubules transform meiosis I into a mitosis-like division by disrupting two key meiosis I events: coorientation of sister kinetochores and protection of centromeric cohesin removal from chromosomes. Furthermore we find that restricting outer kinetochore assembly contributes to preventing premature engagement of microtubules with kinetochores. We propose that inhibition of microtubule-kinetochore interactions during premeiotic S phase and prophase I is central to establishing the unique meiosis I chromosome segregation pattern.

2012-10-05 | GSE41339 | GEO

Pcs1 and Mde4 are inner centromere proteins required to prevent merotelic kinetochore orientation

Project description:Chromosome segregation depends on proper attachment of sister kinetochores to microtubules. Merotelic kinetochore orientation is an error which occurs when a single kinetochore is attached to microtubules emanating form opposite poles. Mechanisms preventing or correcting the merotelic attachment must operate to avoid chromosome missegregation. Pcs1 has been implicated in preventing merotelic attachment in mitosis and meiosis II. We describe here the identification of Mde4 protein which forms a complex with the Pcs1. Both Mde4 and Pcs1 localize to the central core of the centromere. Similarly to the pcs1 mutant, in the absence of mde4 lagging chromosomes are frequently observed during mitosis and meiosis II . We provide the first evidence that the lagging chromosomes in pcs1 and mde4 mutants are due to merotelic kinetochore orientation. Keywords: ChIP-chip analysis ChIP-chip analysis: In all cases, hybridization data for ChIP fraction was compared with that of SUP (supernatant) fraction. Pombe whole chromosome array was used.

2010-06-10 | E-GEOD-5257 | biostudies-arrayexpress

Pcs1 and Mde4 are inner centromere proteins required to prevent merotelic kinetochore orientation

2007-06-18 | GSE5257 | GEO

The proteomic landscape of centromeric chromatin reveals an essential role for the Ctf19 complex in meiotic kinetochore assembly.

Project description:Faithful gamete formation during meiosis requires that kinetochores take on new functions that impact homolog pairing/recombination and their attachments to microtubules. We used a proteomics pipeline to determine the global composition of centromeric chromatin and kinetochores at distinct meiotic stages. Our datasets uncover an unanticipated role for the Ctf19CCAN inner kinetochore sub-complex in gametogenesis. We show that components of the Ctf19 complex that are dispensable for mitotic growth become critical for assembly of a functional kinetochore upon meiotic entry. Consequently, in the absence of these factors, chromosomes fail to attach to meiotic spindles and produce inviable gametes due to gross segregation errors. Our evidence suggests that functional kinetochore assembly is driven by Ctf19CCAN complex-dependent Ipl1AURORA B positioning at the inner kinetochore. Thus, our global view of kinetochore composition in meiosis reveals the extent of kinetochore remodelling during gametogenesis and uncovers a kinetochore assembly pathway that becomes critical in meiosis.

2021-02-23 | PXD019754 | Pride

Shugoshin biases chromosomes for biorientation through condensin recruitment to the pericentromere

Project description:To protect against aneuploidy, chromosomes must attach to microtubules from opposite poles (“biorientation”) prior to their segregation during mitosis. Biorientation relies on the correction of erroneous attachments by the aurora B kinase, which destabilizes kinetochore-microtubule attachments that lack tension. Incorrect attachments are also avoided because sister kinetochores are intrinsically biased towards capture by microtubules from opposite poles. Here we show that shugoshin acts as a pericentromeric adaptor that plays dual roles in biorientation in budding yeast. Shugoshin maintains the aurora B kinase at kinetochores that lack tension, thereby engaging the error correction machinery. Shugoshin also recruits the chromosome-organising complex, condensin, to the pericentromere. Pericentromeric condensin biases sister kinetochores towards capture by microtubules from opposite poles. Overall, shugoshin integrates a bias to sister kinetochore capture with error correction to enable chromosome biorientation. Our findings uncover the molecular basis of the bias to sister kinetochore capture and expose shugoshin as a pericentromeric hub controlling chromosome biorientation.

2014-01-08 | GSE53856 | GEO

Shugoshin biases chromosomes for biorientation through condensin recruitment to the pericentromere

2014-01-08 | E-GEOD-53856 | biostudies-arrayexpress

Monopolar attachment of sister kinetochores at meiosis I requires casein kinase 1.

Project description:The segregation of maternal centromeres away from the paternal ones during the first division of meiosis depends on the attachment of sister kinetochores to microtubules emanating from the same spindle pole. In budding yeast monopolar attachment requires the recruitment to kinetochores of a protein complex called monopolin. The biochemical function of monopolin was unknown. Here, we have identified the casein kinase I Hrr25 as a hitherto unknown subunit of monopolin. Hrr25 differs from other monopolin components by its enzymatic activity and strong evolutionary conservation. We demonstrate that Hrr25’s kinase activity and its interaction with monopolin are both required for monopolar attachment. Accordingly, Hrr25 is associated with centromeres in meiosis I. Our results revealed a surprising new role for casein kinases and provide a hypothesis for the mechanism of monopolar attachment during meiosis I in sexually reproducing organisms: casein kinase I-dependent phosphorylation of kinetochore proteins. Keywords: ChIP-chip, Meiosis, Cell cycle, Saccharomyces cerevisiae, Chromosome VI tiling array, Hrr25, Mam1

2006-09-23 | GSE4792 | GEO

Centromere-Like Regions in Budding Yeast

Project description:Accurate chromosome segregation requires centromeres (CENs), the chromosomal sites where kinetochores form, to bridge DNA and attach to microtubules. In contrast to most eukaryotes, Saccharomyces cerevisiae possesses sequence-defined point centromeres. Chromatin immunoprecipitation followed by sequencing (ChIP-Seq) of four kinetochore components reveals regions of overlapping, extra-centromeric protein localization upon overproduction of the centromeric histone, Cse4 (CENP-A or CenH3). These identified sequences enhance proper plasmid and chromosome segregation, and are termed Centromere-like Regions (CLRs). CLRs form in close proximity to S. cerevisiae CENs and share characteristics typical of point and regional centromeres. CLR sequences are conserved among related budding yeasts, suggesting a role in vivo. These studies provide new insights into the origin and evolution of centromeres. ChIP-Seq analysis of the kinetochore components Cse4, Mif2, Ndc10 and Ndc80 in budding yeast strains (Saccharomyces cerevisiae) with normal and elevated levels of Cse4

2013-01-18 | E-GEOD-31466 | biostudies-arrayexpress

Expression profiles of histone point mutants

Project description: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 mutants in every residue of histone H3 and H4. In one screen, we identified mutants that lead to increased loss of a non-essential chromosome. In the second screen, we isolated mutants whose viability depends on a key regulator of biorientation, the Aurora B protein kinase. Nine mutations, H3 Q5A, H3 R40A, H3 G44A, H3 R53A, H3 N108A, H3 L109A, H4 K44A, H4 V81A, and H4 Y98A, were common to both screens and exhibited kinetochore biorientation defects. Five of the mutants map near the unstructured nucleosome entry site and their genetic interaction with decreased Ipl1 function can be suppressed by increasing the dosage of the Sgo1 protein. In addition, the composition of purified kinetochores was altered in five of the mutants. Together, this work identifies previously unknown histone residues involved in chromosome segregation and lays the foundation for future studies of the role of the underlying chromatin structure in segregation.

2013-12-04 | GSE39903 | GEO

Functional dissection of human mitotic proteins using CRISPR-Cas9 tiling screens

Project description:Kinetochores are large protein assemblies that mark the centromere and bind to mitotic spindle microtubules to ensure accurate chromosome segregation. Like most protein-coding genes, the full multifunctional nature of kinetochore factors remains uncharacterized due to the limited experimental tools for unbiased dissection of human protein sequences. Here, we develop a method that leverages CRISPR-Cas9 induced mutations to comprehensively identify key functional regions within protein sequences that are required for cellular outgrowth. Our analysis of 48 human kinetochore genes revealed hundreds of regions required for cell proliferation, corresponding to known and uncharacterized protein domains. We biologically validated 15 of these regions, including amino acids 387-402 of Mad1, which when deleted compromise Mad1 kinetochore localization and chromosome segregation fidelity. Altogether, we demonstrate that CRISPR-Cas9-based tiling mutagenesis enables de novo identification of key functional domains in protein-coding genes, which elucidates separation of function mutants and allows functional annotation across the human proteome

2023-01-26 | GSE179188 | GEO

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