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Spo11-oligo mapping in Saccharomyces species (S. paradoxus, S. mikatae, S. kudriavzevii) and wild-derived S. cerevisiae strains (YPS128, UWOPS03-461.4)

ABSTRACT: Spo11-oligo mapping in Saccharomyces species (S. paradoxus, S. mikatae, S. kudriavzevii) and wild-derived S. cerevisiae strains (YPS128, UWOPS03-461.4)

PROVIDER: PRJNA292494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2154270_1.fastq.gz	Fastqsanger.gz
	SRR2154270_2.fastq.gz	Fastqsanger.gz
	SRR2154271_1.fastq.gz	Fastqsanger.gz
	SRR2154271_2.fastq.gz	Fastqsanger.gz
	SRR2154272_1.fastq.gz	Fastqsanger.gz

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Spo11-oligo mapping in Saccharomyces species (S. paradoxus, S. mikatae, S. kudriavzevii) and wild-derived S. cerevisiae strains (YPS128, UWOPS03-461.4)

Project description:The nonrandom distribution of meiotic recombination shapes heredity and genetic diversification. A widely held view is that individual hotspots - favored sites of recombination initiation - are always ephemeral because they evolve rapidly toward extinction. An alternative view, often ignored or dismissed as implausible, predicts conservation of the positions of hotspots if they are chromosomal features under selective constraint, such as gene promoters. Here we empirically test opposite predictions of these theories by comparing genome-wide maps of meiotic recombination initiation from widely divergent species in the Saccharomyces clade. We find that the frequent overlap of hotspots with promoters is true of the species tested and, consequently, hotspot positions are well conserved. Remarkably, however, the relative strength of individual hotspots is also highly conserved, as are larger-scale features of the distribution of recombination initiation. This stability, not predicted by prior models, suggests that the particular shape of the yeast recombination landscape is adaptive, and helps in understanding evolutionary dynamics of recombination in other species.

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Spo11-oligo mapping in wild type S. cerevisiae strain

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Project description:Meiotic recombination promotes genetic diversification as well as pairing and segregation of homologous chromosomes, but the double-strand breaks (DSBs) that initiate recombination are dangerous lesions that can cause mutation or meiotic failure. How cells control DSBs to balance between beneficial and deleterious outcomes is not well understood. This study tests the hypothesis that DSB control involves a network of intersecting regulatory circuits. We show that DSBs form in greater numbers in Saccharomyces cerevisiae cells lacking ZMM proteins, a suite of recombination-promoting factors traditionally regarded as acting strictly downstream of DSB formation. This counterintuitive result suggests that homologous chromosomes that have successfully engaged one another stop making DSBs, and provides new insight into phenotypes of zmm and other recombination-defective mutants. A genetically distinct pathway ties DSB formation to meiotic progression through the Ndt80 transcription factor. High-resolution genome-wide DSB maps generated by sequencing short oligonucleotides covalently bound to Spo11 (Spo11 oligos) demonstrate that feedback tied to ZMM function contributes in unexpected ways to spatial patterning of the recombination landscape.

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