scholarly journals Whole genome screen reveals a novel relationship between Wolbachia levels and Drosophila host translation

2018 ◽  
Vol 14 (11) ◽  
pp. e1007445 ◽  
Author(s):  
Yolande Grobler ◽  
Chi Y. Yun ◽  
David J. Kahler ◽  
Casey M. Bergman ◽  
Hangnoh Lee ◽  
...  
Keyword(s):  
Whole Genome ◽  
Genome Screen

scholarly journals A whole-genome screen identifies Salmonella enterica serovar Typhi genes involved in fluoroquinolone susceptibility

2020 ◽  
Vol 75 (9) ◽  
pp. 2516-2525
Author(s):  
A Keith Turner ◽  
Sabine E Eckert ◽  
Daniel J Turner ◽  
Muhammud Yasir ◽  
Mark A Webber ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Insertion Site ◽  
Whole Genome ◽  
Genome Screen ◽  
Polysaccharide Biosynthesis ◽  
Salmonella Enterica Serovar Typhi ◽  
Transposon Insertion ◽  
Associated Functions ◽  
The Impact ◽  
Insertion Mutations

Abstract Objectives A whole-genome screen at sub-gene resolution was performed to identify candidate loci that contribute to enhanced or diminished ciprofloxacin susceptibility in Salmonella enterica serovar Typhi. Methods A pool of over 1 million transposon insertion mutants of an S. Typhi Ty2 derivative were grown in a sub-MIC concentration of ciprofloxacin, or without ciprofloxacin. Transposon-directed insertion site sequencing (TraDIS) identified relative differences between the mutants that grew following the ciprofloxacin treatment compared with the untreated mutant pool, thereby indicating which mutations contribute to gain or loss of ciprofloxacin susceptibility. Results Approximately 88% of the S. Typhi strain’s 4895 annotated genes were assayed, and at least 116 were identified as contributing to gain or loss of ciprofloxacin susceptibility. Many of the identified genes are known to influence susceptibility to ciprofloxacin, thereby providing method validation. Genes were identified that were not known previously to be involved in susceptibility, and some of these had no previously known phenotype. Susceptibility to ciprofloxacin was enhanced by insertion mutations in genes coding for efflux, other surface-associated functions, DNA repair and expression regulation, including phoP, barA and marA. Insertion mutations that diminished susceptibility were predominantly in genes coding for surface polysaccharide biosynthesis and regulatory genes, including slyA, emrR, envZ and cpxR. Conclusions A genomics approach has identified novel contributors to gain or loss of ciprofloxacin susceptibility in S. Typhi, expanding our understanding of the impact of fluoroquinolones on bacteria and of mechanisms that may contribute to resistance. The data also demonstrate the power of the TraDIS technology for antibacterial research.

A whole genome screen for association in Polish multiple sclerosis patients

2003 ◽  
Vol 143 (1-2) ◽  
pp. 107-111 ◽  
Author(s):  
Bartosz Bielecki ◽  
Marcin P. Mycko ◽  
Ewa Tronczyńska ◽  
Marek Bieniek ◽  
Stephen Sawcer ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Whole Genome ◽  
Genome Screen ◽  
Multiple Sclerosis Patients

scholarly journals A whole genome screen for HIV restriction factors

Retrovirology ◽  
2011 ◽  
Vol 8 (1) ◽  
pp. 94 ◽  
Author(s):  
Li Liu ◽  
Nidia MM Oliveira ◽  
Kelly M Cheney ◽  
Corinna Pade ◽  
Hanna Dreja ◽  
...  
Keyword(s):  
Whole Genome ◽  
Restriction Factors ◽  
Genome Screen

A whole genome screen for linkage in Turkish multiple sclerosis

2003 ◽  
Vol 143 (1-2) ◽  
pp. 17-24 ◽  
Author(s):  
M. Eraksoy ◽  
M. Kurtuncu ◽  
G. Akman-Demir ◽  
M. Kılınc ◽  
M. Gedizlioglu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Whole Genome ◽  
Genome Screen

scholarly journals A whole genome screen for association with multiple sclerosis in Portuguese patients

2003 ◽  
Vol 143 (1-2) ◽  
pp. 112-115 ◽  
Author(s):  
M. Santos ◽  
J. Pinto-Basto ◽  
M.E. Rio ◽  
M.J. Sá ◽  
A. Valença ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Whole Genome ◽  
Genome Screen

scholarly journals Whole-genome RNAi screen highlights components of the endoplasmic reticulum/Golgi as a source of resistance to immunotoxin-mediated cytotoxicity

2015 ◽  
Vol 112 (10) ◽  
pp. E1135-E1142 ◽  
Author(s):  
Matteo Pasetto ◽  
Antonella Antignani ◽  
Pinar Ormanoglu ◽  
Eugen Buehler ◽  
Rajarshi Guha ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Target Surface ◽  
Whole Genome ◽  
Gene Products ◽  
Genome Screen ◽  
Low Concentrations ◽  
Secretory System ◽  
Kdel Receptor ◽  
Per Gene

Immunotoxins (antibody–toxin fusion proteins) target surface antigens on cancer cells and kill these cells via toxin-mediated inhibition of protein synthesis. To identify genes controlling this process, an RNAi whole-genome screen (∼22,000 genes at three siRNAs per gene) was conducted via monitoring the cytotoxicity of the mesothelin-directed immunotoxin SS1P. SS1P, aPseudomonasexotoxin-based immunotoxin, was chosen because it is now in clinical trials and has produced objective tumor regressions in patients. High and low concentrations of SS1P were chosen to allow for the identification of both mitigators and sensitizers. As expected, silencing known essential genes in the immunotoxin pathway, such as mesothelin, furin, KDEL receptor 2, or members of the diphthamide pathway, protected cells. Of greater interest was the observation that many RNAi targets increased immunotoxin sensitivity, indicating that these gene products normally contribute to inefficiencies in the killing pathway. Of the top sensitizers, many genes encode proteins that locate to either the endoplasmic reticulum (ER) or Golgi and are annotated as part of the secretory system. Genes related to the ER-associated degradation system were not among high-ranking mitigator or sensitizer candidates. However, the p97 inhibitor eeyarestatin 1 enhanced immunotoxin killing. Our results highlight potential targets for chemical intervention that could increase immunotoxin killing of cancer cells and enhance our understanding of toxin trafficking.

scholarly journals Linkage to nodal osteoarthritis: quantitative and qualitative analyses of data from a whole-genome screen identify trait-dependent susceptibility loci

2006 ◽  
Vol 65 (9) ◽  
pp. 1131-1138 ◽  
Author(s):  
C Greig ◽  
K Spreckley ◽  
R Aspinwall ◽  
E Gillaspy ◽  
M Grant ◽  
...  
Keyword(s):  
Whole Genome ◽  
Susceptibility Loci ◽  
Genome Screen ◽  
Qualitative Analyses

Abstract 487: Whole genome screen to identify genes targeting MYCN-driven embryonal tumors

2015 ◽  
Author(s):  
Carol J. Thiele ◽  
Zhihui Liu ◽  
Veronica Veschi ◽  
Eugene Buehler ◽  
Scott Martin
Keyword(s):  
Whole Genome ◽  
Embryonal Tumors ◽  
Genome Screen

scholarly journals A whole genome screen for linkage disequilibrium in multiple sclerosis confirms disease associations with regions previously linked to susceptibility

Brain ◽  
2002 ◽  
Vol 125 (6) ◽  
pp. 1337-1347 ◽  
Author(s):  
Stephen Sawcer ◽  
Mel Maranian ◽  
Efrosini Setakis ◽  
Val Curwen ◽  
Eva Akesson ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Linkage Disequilibrium ◽  
Whole Genome ◽  
Genome Screen ◽  
Disease Associations

scholarly journals Chaperone Control of the Activity and Specificity of the Histone H3 Acetyltransferase Rtt109

2008 ◽  
Vol 28 (13) ◽  
pp. 4342-4353 ◽  
Author(s):  
Jeffrey Fillingham ◽  
Judith Recht ◽  
Andrea C. Silva ◽  
Bernhard Suter ◽  
Andrew Emili ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Histone Acetyltransferase ◽  
Histone H3 ◽  
Histone Chaperone ◽  
Genetic Interactions ◽  
Whole Genome ◽  
Genome Screen ◽  
Associated Lesions

ABSTRACT Acetylation of Saccharomyces cerevisiae histone H3 on K56 by the histone acetyltransferase (HAT) Rtt109 is important for repairing replication-associated lesions. Rtt109 purifies from yeast in complex with the histone chaperone Vps75, which stabilizes the HAT in vivo. A whole-genome screen to identify genes whose deletions have synthetic genetic interactions with rtt109Δ suggests Rtt109 has functions in addition to DNA repair. We show that in addition to its known H3-K56 acetylation activity, Rtt109 is also an H3-K9 HAT, and we show that Rtt109 and Gcn5 are the only H3-K9 HATs in vivo. Rtt109's H3-K9 acetylation activity in vitro is enhanced strongly by Vps75. Another histone chaperone, Asf1, and Vps75 are both required for acetylation of lysine 9 on H3 (H3-K9ac) in vivo by Rtt109, whereas H3-K56ac in vivo requires only Asf1. Asf1 also physically interacts with the nuclear Hat1/Hat2/Hif1 complex that acetylates H4-K5 and H4-K12. We suggest Asf1 is capable of assembling into chromatin H3-H4 dimers diacetylated on both H4-K5/12 and H3-K9/56.

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