Scott Keeney

The paper develops hypercleavage TOP2 mutants in yeast, human, and mouse to study TOP2-mediated DNA damage and toxicity, showing their utility in genetic screens and in vivo models.

The paper investigates how MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice by analyzing the effects of DSB processing and end joining.

The paper analyzes evolutionary divergence in meiotic recombination proteins across four taxa, identifying regions under positive selection and functional constraints using structural and functional data.

This study shows TRIP13 is involved in transcription suppression and DSB repair during meiosis, with distinct roles in spermatocytes and oocytes.

This study reconstitutes SPO11-dependent DNA double-strand break formation in vitro, revealing dimerization-dependent cleavage and topoisomerase activity.

This study identifies Fun30 as essential for meiotic DNA break resection, showing it works with MRX and Exo1 to generate resection tracts necessary for recombination.

This study shows the MRN complex is essential for both initiating and extending DNA end resection in mouse meiosis, with defects leading to spermatogenic failure.

The paper optimizes S1-seq for mapping meiotic DSBs and resection tracts in mouse spermatocytes and evaluates quantitative features of resection.

This study investigates the role of the ANKRD31-REC114 interaction in meiotic recombination and spermatogenesis, showing its critical importance for DSB formation, repair, and location in mice.

This study uses S1-seq to evaluate H-DNA triplex-forming potential in the mouse genome, identifying motifs and structural features associated with DNA secondary structure.

This study shows YTHDC2 is essential for meiotic pachytene progression by maintaining a meiotic transcriptome and preventing microtubule-driven telomere clustering.

The paper identifies deletion and duplication events caused by double cuts at recombination hotspots in mouse germlines, revealing their role in meiotic mutagenesis.

The paper shows that DNA double-strand breaks (DSBs) during meiosis often occur in clusters with periodic spacing, challenging the idea that DSBs are isolated events.

The paper identifies a mutation in Mov10l1 that disrupts piRNA biogenesis and causes male sterility by affecting retrotransposon silencing.

This study characterizes the structure and function of the Spo11 core complex in S. cerevisiae, revealing its monomeric structure and DNA-binding properties related to meiotic DSB formation.

The paper shows that chromosome-autonomous feedback reduces meiotic DSBs when homologs engage, using yeast mutants with chromosomal abnormalities.

The paper identifies the role of the MutLγ-Exo1 complex in meiotic crossover formation by showing Exo1 recruits Cdc5 to activate MutLγ and highlights its spatial regulation near DSB hotspots.

The paper identifies cis- and trans-acting factors that drive meiotic DNA break formation in the mouse pseudoautosomal region, revealing structural and molecular mechanisms essential for recombination and segregation.

This study identifies a mutation in mouse Spata22 that disrupts splicing, leading to impaired meiotic recombination and sterility.

This study shows that Saccharomyces cerevisiae uses multiple mechanisms to control DSB formation on short chromosomes to prevent meiotic missegregation.

The paper investigates meiotic crossover mechanisms in mice by analyzing heteroduplex DNA in Msh2-/- mutants, finding MSH2-independent correction and biased crossover resolution.

This study investigates how DNA-dependent macromolecular condensation facilitates the self-assembly of the meiotic DNA break machinery in yeast.

The paper defines resected DSB structures in mouse spermatocytes, identifies ATM as a key regulator of resection, and shows PRDM9-dependent chromatin remodeling at recombination sites.

This study shows that cyclin B3 is not required for male meiosis despite its meiosis-specific expression, as male mice lacking cyclin B3 are fertile with normal spermatogenesis.

This study identifies ANKRD31 as a regulator of meiotic DNA break formation in mice, showing its role in controlling DSB number, timing, and location, and linking its dysfunction to infertility.

The paper identifies privileged end-adjacent regions near telomeres that maintain DSBs and contribute to higher recombination rates on short chromosomes in yeast.

The paper shows MEIOB and SPATA22 interact with RPA to support meiotic recombination by modifying RPA-coated ssDNA and stabilizing recombination intermediates.

This paper reviews ATM's role in regulating meiotic DSB numbers and distribution, discussing its evolutionary conservation and future research directions.

The paper identifies YTHDC2 as essential for meiotic progression in mice, showing its role in gene expression transitions and its evolutionary conservation.

The paper introduces S1-seq, a next-generation sequencing assay to study DNA end resection during yeast meiosis, and describes its experimental and computational methods.