Schizosaccharomyces kambucha
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ABSTRACT:
PROVIDER: PRJNA245261 | ENA |
REPOSITORIES: ENA
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Project description:Hybrid sterility is one of the earliest postzygotic isolating mechanisms to evolve between two recently diverged species. Uncovering the mechanisms of hybrid sterilitynot only provides insight into the origins of species but also potentially revealsnovel causes of intra-species infertility.Here we identify causes underlying hybrid infertilityofSchizosaccharomyces pombeand S. kambucha, two fission yeast species that are 99.5% identical at the nucleotide level.These yeasts mate to form viable diploids that efficiently complete meiosis. However,S. kambucha/S. pombe hybrids generate few viable gametes, most of which are either aneuploid or diploid.We find that chromosomal rearrangements and related recombination defectsare major causes of hybrid infertility. Surprisingly, using experiments in which we eliminate meiotic recombination, we find thatrecombination defects cannot completely explain the hybrid infertility. Instead, we find that a significant fraction of hybrid infertility is caused by the action of at least three distinct meiotic drive alleles, one on each S. kambucha chromosome,that M-bM-^@M-^\cheatM-bM-^@M-^] to be transmitted to more than half (up to 90%) of viable gametes.Two of these driving lociare linked by a chromosomal translocation and thus constitute a novel type of paired meiotic drive complex. We find that all three S. kambuchadrive loci independently contribute to hybrid infertility by causing nonrandom spore death. This study reveals how quickly multiple barriers to fertility can arise.In addition, it provides further support for models in which genetic conflicts, such as those caused by meiotic drive alleles, can drive speciation. Meiotic DNA double-strand break analysis of Schizosaccharomyces kambucha by immunoprecipitating accumulated Rec12-FLAG covalently linked to DNA (without exogenous crosslinking agent used) following nitrogen starvation .
2014-05-15 | E-GEOD-57039 | biostudies-arrayexpress
Project description:Hybrid sterility is one of the earliest postzygotic isolating mechanisms to evolve between two recently diverged species. Uncovering the mechanisms of hybrid sterilitynot only provides insight into the origins of species but also potentially revealsnovel causes of intra-species infertility.Here we identify causes underlying hybrid infertilityofSchizosaccharomyces pombeand S. kambucha, two fission yeast species that are 99.5% identical at the nucleotide level.These yeasts mate to form viable diploids that efficiently complete meiosis. However,S. kambucha/S. pombe hybrids generate few viable gametes, most of which are either aneuploid or diploid.We find that chromosomal rearrangements and related recombination defectsare major causes of hybrid infertility. Surprisingly, using experiments in which we eliminate meiotic recombination, we find thatrecombination defects cannot completely explain the hybrid infertility. Instead, we find that a significant fraction of hybrid infertility is caused by the action of at least three distinct meiotic drive alleles, one on each S. kambucha chromosome,that “cheat” to be transmitted to more than half (up to 90%) of viable gametes.Two of these driving lociare linked by a chromosomal translocation and thus constitute a novel type of paired meiotic drive complex. We find that all three S. kambuchadrive loci independently contribute to hybrid infertility by causing nonrandom spore death. This study reveals how quickly multiple barriers to fertility can arise.In addition, it provides further support for models in which genetic conflicts, such as those caused by meiotic drive alleles, can drive speciation.
2014-05-15 | GSE57039 | GEO
Project description:fission yeast meiotic drive recombination mapping
| PRJNA376152 | ENA
Project description:Meiotic cohesins modulate chromosome compaction during meiotic prophase in fission yeast
| PRJNA96393 | ENA
Project description:Meiosis is a specialized cell division that generates gametes, such as eggs and sperm. Errors in meiosis result in miscarriages and are the leading cause of birth defects, however the molecular origins of these defects remain unknown. Studies in model organisms are beginning to identify the genes and pathways important for meiosis, but the parts list is still poorly defined. Here we present a comprehensive catalogue of genes required for meiosis in the fission yeast, Schizosaccharomyces pombe. Our genome-wide functional screen surveyed all non-essential genes for roles in chromosome segregation and spore formation. Novel genes required at distinct stages of the meiotic chromosome segregation and differentiation programme were identified. Preliminary characterization implicated three of these genes in centrosome/spindle pole body function, centromere and cohesion function. Our findings represent a near-complete parts list of genes required for meiosis in fission yeast, providing a valuable resource to advance our molecular understanding of meiosis.
2018-01-04 | PXD008245 | Pride
Project description:We used CLIP-Seq to determine the RNAs bound specifically to RNA binding protein Mei2 in early meiosis in fission yeast. We added a TAP tag to the C-terminal ends of two meiotic RNA binding proteins, Mei2 and Msa1. We used an untagged fission yeast strain as a negative control. These strains were nitrogen starved and allowed to progress into meiosis, after which they were harvested, lyzed and crosslinking immunoprecipitaion was performed. The RNAs purified after CLIP were sequenced
2019-01-01 | GSE112117 | GEO
Project description:Nucleosomal organization of replication origins and meiotic recombination hotspots in fission yeast
| PRJNA140631 | ENA
Project description:Transcription profile of fission yeast
| PRJNA114859 | ENA
Project description:In most eukaryotes, meiotic crossovers are essential for error-free chromosome segregation but are specifically repressed near centromeres to prevent missegregation. Recognized for >85 years, the molecular mechanism of this repression has remained unknown. Meiotic chromosomes contain two distinct cohesin complexes: pericentric complex (for segregation) and chromosomal arm complex (for crossing-over). We show that the pericentric-specific complex also actively represses pericentric meiotic double-strand break (DSB) formation and, consequently, crossovers. The fission yeast pericentric regions contain heterochromatin, removal of which can result in derepression in double-strand break formation and recombination during meiosis. We uncover the mechanism by which fission yeast heterochromatin protein Swi6 (mammalian HP1-homolog) prevents recruitment of activators of meiotic DSB formation such as Rec10. Localizing these missing activators to wild-type pericentromeres bypasses repression and generates abundant crossovers but reduces gamete viability.The molecular mechanism elucidated here likely extends to other species including humans, where pericentric crossovers can result in disorders such as Down syndrome. These mechanistic insights provide new clues to understand the roles played by multiple cohesin complexes, especially in human infertility and birth defects.
2018-06-14 | GSE115726 | GEO
Project description:Meiotic recombination facilitates accurate pairing and faithful segregation of homologous chromosomes by forming physical connections (crossovers) between homologs. Developmentally programmed DNA double-strand breaks (DSBs) generated by Spo11 protein (Rec12 in fission yeast) initiate meiotic recombination. Until recently, attempts to address the basis of the highly non-random distribution of DSBs on a genome-wide scale have been limited to 0.1–1 kb resolution of DSB position. We have assessed individual DSB events across the Schizosaccharomyces pombe genome at near-nucleotide resolution by deep-sequencing the short oligonucleotides connected to Rec12 following DNA cleavage. The single oligonucleotide size-class generated by Rec12 allowed us to effectively analyze all break events. Our high-resolution DSB map shows that the influence of underlying nucleotide sequence and chromosomal architecture differs in multiple ways from that in budding yeast. Rec12 action is not strongly restricted to nucleosome-depleted regions but is nevertheless spatially biased with respect to chromatin structure. Furthermore, we find strong evidence across the genome for differential DSB repair previously predicted to account for crossover invariance (constant cM/kb in spite of DSB hotspots). Our genome-wide analyses demonstrate evolutionarily fluid factors contributing to crossover initiation and its regulation.
2014-06-25 | GSE49977 | GEO