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Xuan Zhu

Researcher at Memorial Sloan Kettering Cancer Center

Publications -  12
Citations -  1097

Xuan Zhu is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Homologous recombination & Genetic recombination. The author has an hindex of 6, co-authored 9 publications receiving 934 citations. Previous affiliations of Xuan Zhu include Cornell University & Amazon.com.

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Journal ArticleDOI

A hierarchical combination of factors shapes the genome-wide topography of yeast meiotic recombination initiation.

TL;DR: This analysis offers mechanistic insight into DSB formation and early processing steps, supporting the view that the recombination terrain is molded by combinatorial and hierarchical interaction of factors that work on widely different size scales.
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The Landscape of Mouse Meiotic Double-Strand Break Formation, Processing, and Repair.

TL;DR: These results paint a comprehensive picture of features governing successive steps in mammalian meiotic recombination, including a stereotyped hotspot structure and relationships between SPO11, chromatin, and the histone methyltransferase PRDM9.
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Homologue engagement controls meiotic DNA break number and distribution

TL;DR: It is shown that DSBs form in greater numbers in Saccharomyces cerevisiae cells lacking ZMM proteins, and feedback tied to ZMM function contributes in unexpected ways to spatial patterning of recombination.
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Mechanistic View and Genetic Control of DNA Recombination during Meiosis

TL;DR: By combining genome-wide meiotic heteroduplex DNA patterns with meiotic DNA double-strand break sites, it is shown that part of this complexity results from frequent template switching during synthesis-dependent strand annealing that yields noncrossovers and from branch migration of double Holliday junction (dHJ)-containing intermediates that mainly yield crossovers.
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High-Resolution Global Analysis of the Influences of Bas1 and Ino4 Transcription Factors on Meiotic DNA Break Distributions in Saccharomyces cerevisiae.

TL;DR: R roles of these TFs on DSB hotspot strength cannot be simply explained via chromatin “openness,” histone modification, or compensatory interactions between adjacent hotspots, counter to prevailing models.