L
Lindsey N. Williams
Researcher at University of Washington
Publications - 19
Citations - 686
Lindsey N. Williams is an academic researcher from University of Washington. The author has contributed to research in topics: DNA polymerase & DNA replication. The author has an hindex of 8, co-authored 18 publications receiving 556 citations. Previous affiliations of Lindsey N. Williams include Mayo Clinic.
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Journal ArticleDOI
Translation initiator EIF4G1 mutations in familial Parkinson disease
Marie-Christine Chartier-Harlin,Marie-Christine Chartier-Harlin,Justus C. Dachsel,Carles Vilariño-Güell,Sarah Lincoln,Frédéric Leprêtre,Frédéric Leprêtre,Mary M. Hulihan,Jennifer M. Kachergus,Austen J. Milnerwood,Lucia Tapia,Mee Sook Song,Emilie Le Rhun,Eugénie Mutez,Eugénie Mutez,Lydie Larvor,Lydie Larvor,A. Duflot,A. Duflot,Christel Vanbesien-Mailliot,Christel Vanbesien-Mailliot,Alexandre Kreisler,Alexandre Kreisler,Owen A. Ross,Kenya Nishioka,Alexandra I. Soto-Ortolaza,Stephanie A. Cobb,Heather L. Melrose,Bahareh Behrouz,Brett H. Keeling,Justin A. Bacon,Emna Hentati,Lindsey N. Williams,Akiko Yanagiya,Nahum Sonenberg,Paul J. Lockhart,Abba C. Zubair,Ryan J. Uitti,Jan O. Aasly,Anna Krygowska-Wajs,Grzegorz Opala,Zbigniew K. Wszolek,Roberta Frigerio,Demetrius M. Maraganore,David Gosal,Timothy Lynch,Michael Hutchinson,Anna Rita Bentivoglio,Enza Maria Valente,Enza Maria Valente,William C. Nichols,Nathan Pankratz,Tatiana Foroud,Rachel A. Gibson,Fayçal Hentati,Dennis W. Dickson,Alain Destée,Alain Destée,Matthew J. Farrer,Matthew J. Farrer +59 more
TL;DR: Genome-wide analysis of a multi-incident family with autosomal-dominant parkinsonism has implicated a locus on chromosomal region 3q26-q28 and highlighted a convergent pathway for monogenic, toxin and perhaps virally-induced Parkinson disease.
Journal ArticleDOI
Mutator Suppression and Escape from Replication Error–Induced Extinction in Yeast
Alan J. Herr,Masanori Ogawa,Nicole A. Lawrence,Lindsey N. Williams,Julie M. Eggington,Mallika Singh,Robert A. Smith,Bradley D. Preston +7 more
TL;DR: It is shown that populations tolerate mutation rates 1,000-fold above wild-type levels but collapse when the rate exceeds 10−3 inactivating mutations per gene per cell division and has implications for the role of mutator phenotypes in cancer.
Journal ArticleDOI
Ultra-Sensitive TP53 Sequencing for Cancer Detection Reveals Progressive Clonal Selection in Normal Tissue over a Century of Human Lifespan.
Jesse J. Salk,Kaitlyn Loubet-Senear,Elisabeth Maritschnegg,Charles C. Valentine,Lindsey N. Williams,Jacob Higgins,Reinhard Horvat,Adriaan Vanderstichele,Daniela Nachmanson,Kathryn T. Baker,Mary J. Emond,Emily Loter,Maria S. Tretiakova,Thierry Soussi,Thierry Soussi,Thierry Soussi,Lawrence A. Loeb,Robert Zeillinger,Paul Speiser,Rosa Ana Risques +19 more
TL;DR: It is shown that low-frequency TP53 mutations exist in multiple healthy tissues and progressively increase in abundance and pathogenicity with older age across tissue types, and great care must be taken to distinguish tumor-derived from age-associated mutations in high-sensitivity clinical cancer diagnostics.
Journal ArticleDOI
dNTP pool levels modulate mutator phenotypes of error-prone DNA polymerase ε variants
Lindsey N. Williams,Lisette Marjavaara,Gary Knowels,Eric M. Schultz,Edward J. Fox,Andrei Chabes,Alan J. Herr +6 more
TL;DR: DNTP pool levels correlate with Pol ε mutator severity, suggesting that treatments targeting dNTP pools could modulate mutator phenotypes for therapy.
Journal ArticleDOI
Emergence of DNA polymerase ε antimutators that escape error-induced extinction in yeast.
TL;DR: It is indicated that unrepaired leading- and lagging-strand polymerase errors drive extinction within a few cell divisions and suggest that there are polymerase-specific pathways of mutator suppression.