Genome-wide gene-deletion screening identifies mutations that significantly enhance explosives vapor detection by a microbial sensor

2020 ◽  
Vol 59 ◽  
pp. 65-73 ◽  
Author(s):  
Benjamin Shemer ◽  
Etai Shpigel ◽  
Anat Glozman ◽  
Sharon Yagur-Kroll ◽  
Yosssef Kabessa ◽  
...  
Keyword(s):  
Gene Deletion ◽  
Vapor Detection ◽  
Microbial Sensor ◽  
Genome Wide

Pleiotropic drug-resistance attenuated genomic library improves elucidation of drug mechanisms

2015 ◽  
Vol 11 (11) ◽  
pp. 3129-3136 ◽  
Author(s):  
Namal V. C. Coorey ◽  
James H. Matthews ◽  
David S. Bellows ◽  
Paul H. Atkinson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Mechanism Of Action ◽  
Gene Deletion ◽  
Genomic Library ◽  
Deletion Mutants ◽  
Pleiotropic Drug Resistance ◽  
Genome Wide

Identifying Saccharomyces cerevisiae genome-wide gene deletion mutants that confer hypersensitivity to a xenobiotic aids the elucidation of its mechanism of action (MoA).

scholarly journals Towards a Systems Approach in the Genetic Analysis of Archaea: Accelerating Mutant Construction and Phenotypic Analysis inHaloferax volcanii

Archaea ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Ian K. Blaby ◽  
Gabriela Phillips ◽  
Crysten E. Blaby-Haas ◽  
Kevin S. Gulig ◽  
Basma El Yacoubi ◽  
...  
Keyword(s):  
High Throughput ◽  
Gene Deletion ◽  
Systems Approach ◽  
Essential Gene ◽  
Gene Knockout ◽  
Deletion Mutants ◽  
Mutant Library ◽  
Phenotypic Analysis ◽  
Genome Wide ◽  
A Genome

With the availability of a genome sequence and increasingly sophisticated genetic tools,Haloferax volcaniiis becoming a model for both Archaea and halophiles. In order forH. volcaniito reach a status equivalent toEscherichia coli, Bacillus subtilis, orSaccharomyces cerevisiae, a gene knockout collection needs to be constructed in order to identify the archaeal essential gene set and enable systematic phenotype screens. A streamlined gene-deletion protocol adapted for potential automation was implemented and used to generate 22H. volcaniideletion strains and identify several potentially essential genes. These gene deletion mutants, generated in this and previous studies, were then analyzed in a high-throughput fashion to measure growth rates in different media and temperature conditions. We conclude that these high-throughput methods are suitable for a rapid investigation of anH. volcaniimutant library and suggest that they should form the basis of a larger genome-wide experiment.

scholarly journals Copy Number Variation of UGT 2B Genes in Indian Families Using Whole Genome Scans

2016 ◽  
Vol 2016 ◽  
pp. 1-7
Author(s):  
Avinash M. Veerappa ◽  
Prakash Padakannaya ◽  
Nallur B. Ramachandra
Keyword(s):  
Copy Number ◽  
Gene Deletion ◽  
Indian Population ◽  
Snp Array ◽  
Copy Number Variations ◽  
Genome Scans ◽  
Genome Wide ◽  
Disease Associations ◽  
Number Variation

Background and Objectives. Uridine diphospho-glucuronosyltransferase 2B (UGT2B) is a family of genes involved in metabolizing steroid hormones and several other xenobiotics. These UGT2B genes are highly polymorphic in nature and have distinct polymorphisms associated with specific regions around the globe. Copy number variations (CNVs) status of UGT2B17 in Indian population is not known and their disease associations have been inconclusive. It was therefore of interest to investigate the CNV profile of UGT2B genes.Methods. We investigated the presence of CNVs in UGT2B genes in 31 members from eight Indian families using Affymetrix Genome-Wide Human SNP Array 6.0 chip.Results. Our data revealed >50% of the study members carried CNVs in UGT2B genes, of which 76% showed deletion polymorphism. CNVs were observed more in UGT2B17 (76.4%) than in UGT2B15 (17.6%). Molecular network and pathway analysis found enrichment related to steroid metabolic process, carboxylesterase activity, and sequence specific DNA binding.Interpretation and Conclusion. We report the presence of UGT2B gene deletion and duplication polymorphisms in Indian families. Network analysis indicates the substitutive role of other possible genes in the UGT activity. The CNVs of UGT2B genes are very common in individuals indicating that the effect is neutral in causing any suspected diseases.

Genome-wide analysis of barcoded Saccharomyces cerevisiae gene-deletion mutants in pooled cultures

2007 ◽  
Vol 2 (11) ◽  
pp. 2958-2974 ◽  
Author(s):  
Sarah E Pierce ◽  
Ron W Davis ◽  
Corey Nislow ◽  
Guri Giaever
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Deletion ◽  
Deletion Mutants ◽  
Genome Wide Analysis ◽  
Genome Wide

A genome-wide association meta-analysis and mouse gene deletion identify WNT16 as a regulator of cortical bone thickness

Bone ◽  
2012 ◽  
Vol 50 ◽  
pp. S33
Author(s):  
J. Tobias ◽  
C. Ohlsson ◽  
L. Paternoster ◽  
T. Lehtimaki ◽  
O. Raitakari ◽  
...  
Keyword(s):  
Cortical Bone ◽  
Gene Deletion ◽  
Meta Analysis ◽  
Mouse Gene ◽  
Genome Wide Association ◽  
Bone Thickness ◽  
Cortical Bone Thickness ◽  
Genome Wide ◽  
A Genome

scholarly journals Genome-Wide Analysis of Syntenic Gene Deletion in the Grasses

2012 ◽  
Vol 4 (3) ◽  
pp. 265-277 ◽  
Author(s):  
James C. Schnable ◽  
Michael Freeling ◽  
Eric Lyons
Keyword(s):  
Gene Deletion ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Syntenic Gene

scholarly journals Combined gene deletion of dihydrofolate reductase-thymidylate synthase and pteridine reductase in Leishmania infantum

2021 ◽  
Vol 15 (4) ◽  
pp. e0009377
Author(s):  
Arijit Bhattacharya ◽  
Philippe Leprohon ◽  
Marc Ouellette
Keyword(s):  
Dihydrofolate Reductase ◽  
Thymidylate Synthase ◽  
Culture Medium ◽  
Gene Deletion ◽  
Folate Metabolism ◽  
Nucleoside Transporter ◽  
Null Mutant ◽  
Hypothetical Gene ◽  
Intracellular Parasites ◽  
Genome Wide

Our understanding of folate metabolism in Leishmania has greatly benefited from studies of resistance to the inhibitor methotrexate (MTX). Folates are reduced in Leishmania by the bifunctional dihydrofolate reductase thymidylate synthase (DHFR-TS) and by pteridine reductase (PTR1). To further our understanding of folate metabolism in Leishmania, a Cos-seq genome-wide gain of function screen was performed against MTX and against the two thymidylate synthase (TS) inhibitors 5-fluorouracil and pemetrexed. The screen revealed DHFR-TS and PTR1 but also the nucleoside transporter NT1 and one hypothetical gene derived from chromosome 31. For MTX, the concentration of folate in the culture medium affected the enrichment pattern for genes retrieved by Cos-seq. We generated a L. infantum DHFR-TS null mutant that was thymidine auxotroph, a phenotype that could be rescued by the addition of thymidine or by transfection of the flavin dependent bacterial TS gene ThyX. In these DHFR-TS null mutants it was impossible to obtain a chromosomal null mutant of PTR1 except if DHFR-TS or PTR1 were provided episomally. The transfection of ThyX however did not allow the elimination of PTR1 in a DHFR-TS null mutant. Leishmania can survive without copies of either DHFR-TS or PTR1 but not without both. Provided that our results observed with the insect stage parasites are also replicated with intracellular parasites, it would suggest that antifolate therapy in Leishmania would only work if both DHFR-TS and PTR1 would be targeted simultaneously.

scholarly journals Analysis of Genetic Variants Associated with Levels of Immune Modulating Proteins for Impact on Alzheimer’s Disease Risk Reveal a Potential Role for SIGLEC14

Genes ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 1008
Author(s):  
Benjamin C. Shaw ◽  
Yuriko Katsumata ◽  
James F. Simpson ◽  
David W. Fardo ◽  
Steven Estus
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Copy Number ◽  
Gene Deletion ◽  
Association Studies ◽  
Family Members ◽  
Genome Wide Association Studies ◽  
Complex Genetics ◽  
Genome Wide

Genome-wide association studies (GWAS) have identified immune-related genes as risk factors for Alzheimer’s disease (AD), including TREM2 and CD33, frequently passing a stringent false-discovery rate. These genes either encode or signal through immunomodulatory tyrosine-phosphorylated inhibitory motifs (ITIMs) or activation motifs (ITAMs) and govern processes critical to AD pathology, such as inflammation and amyloid phagocytosis. To investigate whether additional ITIM and ITAM-containing family members may contribute to AD risk and be overlooked due to the stringent multiple testing in GWAS, we combined protein quantitative trait loci (pQTL) data from a recent plasma proteomics study with AD associations in a recent GWAS. We found that pQTLs for genes encoding ITIM/ITAM family members were more frequently associated with AD than those for non-ITIM/ITAM genes. Further testing of one family member, SIGLEC14 which encodes an ITAM, uncovered substantial copy number variations, identified an SNP as a proxy for gene deletion, and found that gene expression correlates significantly with gene deletion. We also found that SIGLEC14 deletion increases the expression of SIGLEC5, an ITIM. We conclude that many genes in this ITIM/ITAM family likely impact AD risk, and that complex genetics including copy number variation, opposing function of encoded proteins, and coupled gene expression may mask these AD risk associations at the genome-wide level.

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