G
Graham C. Walker
Researcher at Massachusetts Institute of Technology
Publications - 386
Citations - 39252
Graham C. Walker is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Sinorhizobium meliloti & DNA polymerase. The author has an hindex of 93, co-authored 381 publications receiving 36875 citations. Previous affiliations of Graham C. Walker include Norwich Research Park & University of California, Santa Cruz.
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Journal ArticleDOI
umuDC-mediated cold sensitivity is a manifestation of functions of the UmuD(2)C complex involved in a DNA damage checkpoint control.
Mark D. Sutton,Graham C. Walker +1 more
TL;DR: It is shown that umuDC-mediated cold sensitivity can be genetically separated from the role of UmuD'(2)C in SOS mutagenesis, and genetic and biochemical characterizations ofUmuC derivatives bearing nested deletions of C-terminal sequences indicate that umUDC- mediated cold sensitivity is not due solely to the single-stranded DNA binding activity of UmUC.
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CbrA Is a Stationary-Phase Regulator of Cell Surface Physiology and Legume Symbiosis in Sinorhizobium meliloti
TL;DR: A putative two-component histidine kinase associated with a PAS sensory domain is identified, now designated CbrA (calcofluor-bright regulator A), which could play a role in regulating the lipopolysaccharide or lipoprotein components of the cell envelope.
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The Rhizobium meliloti ExoK and ExsH glycanases specifically depolymerize nascent succinoglycan chains
Gregory M. York,Graham C. Walker +1 more
TL;DR: It is resolved the apparent contradiction between the results of previous genetic analyses and depolymerization assays by determining that ExoK and ExsH can cleave high molecular weight succinoglycan that is being produced actively by R. meliloti, but not succinglycan that has accumulated in cultures, to yield LMW succ inoglycan.
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Replication is required for the RecA localization response to DNA damage in Bacillus subtilis.
TL;DR: It is determined that DNA replication is required for the cell to establish RecA-GFP foci after exposure to DNA-damaging agents and the model that existing RecA protein is recruited to ssDNA generated by the replisome at sites of DNA damage is supported.
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Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?
TL;DR: In this paper, the authors discuss the mechanisms underlying intrinsic and acquired drug resistance in cancer patients and the dual functions of mutagenic translesion synthesis (TLS) are discussed, which make these proteins very attractive potential targets for adjuvant therapy.