Ontology highlight
ABSTRACT:
PROVIDER: PRJNA844054 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19458400.fastq.gz | Fastqsanger.gz | |||
| SRR19458500.fastq.gz | Fastqsanger.gz | |||
| SRR19458600.fastq.gz | Fastqsanger.gz | |||
| SRR19458700.fastq.gz | Fastqsanger.gz | |||
| SRR19458800.fastq.gz | Fastqsanger.gz |
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Project description:Nuclear chromosome locations dictate segregation error frequencies
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Project description:Meiosis produces gametes through a specialised, two-step cell division, which is highly error-prone in humans. Reductional meiosis I, where maternal and paternal chromosomes (homologs) segregate, is followed by equational meiosis II, where sister chromatids separate. Uniquely during meiosis I, sister kinetochores are monooriented and pericentromeric cohesin is protected. Here, we demonstrate that these key adaptations for reductional chromosome segregation are achieved through separable control of multiple kinases by the meiosis I-specific budding yeast Spo13 protein. Recruitment of Polo kinase to kinetochores directs monoorientation, while, independently, cohesin protection is achieved by controlling the effects of cohesin kinases. Therefore, reductional chromosome segregation, the defining feature of meiosis, is established by multifaceted kinase control by a master regulator. The recent identification of Spo13 orthologs, fission yeast Moa1 and mouse MEIKIN, suggests that kinase coordination by a master meiosis I regulator may be a general feature in the establishment of reductional chromosome segregation.
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Project description:The conserved Mps1 kinase corrects improper kinetochore-microtubule attachments, thereby ensuring chromosome biorientation. Yet, its critical targets in this process remain elusive. Mps1 is also involved in the spindle assembly checkpoint (SAC), the surveillance mechanism halting chromosome segregation until biorientation is attained. Its role in SAC activation is antagonized by the PP1 phosphatase and involves phosphorylation of Knl1/Spc105, which recruits Bub1 to kinetochores to promote assembly of SAC effector complexes. A crucial question is whether error correction and SAC activation are part of a single device or separable pathways. Here we characterise a novel yeast mutant, mps1-3, defective in chromosome biorientation and SAC activation. Through an unbiased screen for suppressors, we found that mutations lowering PP1 levels at Spc105 or forced association of Bub1 with Spc105 reinstate both chromosome biorientation and SAC signalling in mps1-3 cells. Our data strongly argue that Mps1-dependent phosphorylation of the Knl1/Spc105 kinetochore scaffold is critical for Mps1 function in both chromosome biorientation and SAC activation, thus supporting the idea that a common sensory apparatus simultaneously elicits error correction and SAC signalling.
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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.
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Project description:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation. Genome-wide distributions of condensin and Pol III factors in fission yeast.
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Project description:Eukaryotic cell proliferation requires chromosome replication and precise segregation to ensure daughter cells have identical genomic copies. The genus Plasmodium, the causative agent of malaria, has developed remarkable characteristic of nuclear division throughout its lifecycle to meet some peculiar and unique challenges of DNA replication and chromosome segregation. The parasite undergoes atypical endomitosis and endoreduplication with an intact nuclear membrane and intranuclear mitotic spindle. To understand diverse modes of cell division in Plasmodium we have studied the behaviour and composition of a key part of the mitotic apparatus, the outer kinetochore Ndc80 complex that attaches the centromere of chromosomes to the microtubules of the mitotic spindle. Using Ndc80 live-cell imaging in Plasmodium berghei we observe dynamic changes throughout proliferative life-stages including highly unusual kinetochore arrangements in sexual stages of the parasite. Furthermore, we identify a divergent Spc24 component of Ndc80 complex, previously thought to be missing, and completing a canonical, albeit unusual, Ndc80 complex structure. Altogether our studies reveal the kinetochore as an ideal starting point towards understanding non-canonical modes of chromosome segregation and cell division in Plasmodium.
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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. Two experiments: Experiment A: Sgo1 is required for condensin localization in the pericentromere. Sample 1: Wild type input DNA Sample 2: Wild type Brn1-6HA ChIP DNA, Sample 3 sgo1D input DNA, Sample 4 sgo1D Brn1-6HA ChIP DNA; Experiment B: Sgo1 is not required for cohesin localization in the periecentromere: Sample 5: wild type input DNA, Sample 6 Wild type Scc1-6HA ChIP DNA, Sample 7, sgo1D input DNA, Sample 8 sgo1D Scc1-6HA ChIP DNA. 1 replicate of each repeat
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Project description:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation.
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