J
John R. Lydeard
Researcher at Brandeis University
Publications - 4
Citations - 861
John R. Lydeard is an academic researcher from Brandeis University. The author has contributed to research in topics: DNA replication & Control of chromosome duplication. The author has an hindex of 4, co-authored 4 publications receiving 802 citations.
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Break-induced replication and telomerase-independent telomere maintenance require Pol32
TL;DR: It is shown that, in haploid budding yeast, Rad51-dependent BIR induced by HO endonuclease requires the lagging strand DNA Polα-primase complex as well as Polδ to initiate new DNA synthesis, and Pol32 is uniquely required for BIR.
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Break-induced replication requires all essential DNA replication factors except those specific for pre-RC assembly
John R. Lydeard,Zachary Lipkin-Moore,Yi-Jun Sheu,Bruce Stillman,Peter M. J. Burgers,James E. Haber +5 more
TL;DR: It is shown that BIR requires the replicative DNA helicase (Cdc45, the GINS, and Mcm2-7 proteins) as well as Cdt1, suggesting that origin-independent BIR involves cross-talk between normal DNA replication factors and PRR.
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A recombination execution checkpoint regulates the choice of homologous recombination pathway during DNA double-strand break repair
Suvi Jain,Neal Sugawara,John R. Lydeard,Moreshwar B. Vaze,Nicolas Tanguy Le Gac,James E. Haber +5 more
TL;DR: The data suggest that a "recombination execution checkpoint" (REC) regulates the choice of the homologous recombination pathway employed to repair a given DSB, and the RecQ family helicase Sgs1 plays a key role in regulating the choice.
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Sgs1 and exo1 redundantly inhibit break-induced replication and de novo telomere addition at broken chromosome ends.
TL;DR: The severe constraint on 5′ to 3′ resection, which also abrogates activation of the Mec1-dependent DNA damage checkpoint, permits an unprecedented level of new telomere addition in sgs1Δ exo 1Δ strains, where the level of BIR is not different from either single mutant.