Yin Zhai

ORCID: 0000-0001-8878-4353
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About
Contact & Profiles
Research Areas
  • Bacterial Genetics and Biotechnology
  • DNA Repair Mechanisms
  • Gene Regulatory Network Analysis
  • Evolution and Genetic Dynamics
  • Antibiotic Resistance in Bacteria
  • CRISPR and Genetic Engineering
  • DNA and Nucleic Acid Chemistry
  • Microbial Natural Products and Biosynthesis
  • Genomics and Phylogenetic Studies
  • Bacillus and Francisella bacterial research
  • Glycosylation and Glycoproteins Research
  • Misinformation and Its Impacts
  • Bioinformatics and Genomic Networks
  • Biochemical and Structural Characterization
  • RNA and protein synthesis mechanisms
  • Protein Structure and Dynamics
  • Soybean genetics and cultivation

Baylor College of Medicine
2018-2025

Dan L Duncan Comprehensive Cancer Center
2018

Heilongjiang Institute of Wood Science
2015

Wuhan University
2015

Evolution of antibiotic resistance is a world health crisis, fueled by new mutations. Drugs to slow mutagenesis could, as cotherapies, prolong the shelf-life antibiotics, yet evolution-slowing drugs and drug targets have been underexplored ineffective. Here, we used network-based strategy identify that block hubs fluoroquinolone antibiotic-induced mutagenesis. We U.S. Food Drug Administration– European Medicines Agency–approved drug, dequalinium chloride (DEQ), inhibits activation...

10.1126/sciadv.adg0188 article EN cc-by-nc Science Advances 2023-06-23

In this paper we describe the identification of a new linaridin RiPP, legonaridin, from soil bacterium <italic>Streptomyces</italic> sp. CT34.

10.1039/c5ob01269d article EN Organic & Biomolecular Chemistry 2015-01-01

Caught in the act, DNA reaction intermediates bacterial genomes may illuminate disease-driving regions human chromosomes.

10.1126/sciadv.abe2846 article EN cc-by-nc Science Advances 2021-06-18

SUMMARY DNA damage provokes mutations and cancer, results from external carcinogens or endogenous cellular processes. Yet, the intrinsic instigators of are poorly understood. Here we identify proteins that promote when overproduced: DNA-damaging (DDPs). We discover a large network DDPs in Escherichia coli deconvolute them into six DNA-damage-causing function clusters, demonstrating DDP mechanisms three: reactive-oxygen increase by transmembrane transporters, chromosome loss replisome...

10.1101/354589 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-06-26

Presented here is a draft genome sequence of Streptomyces sp. strain CT34, which produces novel ribosomally synthesized and posttranslationally modified peptide (RiPP). Analysis the deduced open reading frame set identified putative RiPP biosynthesis gene cluster, as well other secondary metabolite clusters.

10.1128/genomea.01508-14 article EN Genome Announcements 2015-02-06

The N protein of phage Mu was indicated from studies in Escherichia coli to hold linear chromosomes a circular conformation by non-covalent association, and thus suggested potentially bind DNA double-stranded ends. Because its role association with DNA, we tested whether fluorescent-protein fusions might provide useful tool for labeling damage including double-strand break (DSB) ends single cells. We compared N-GFP biochemically well documented DSB-end binding protein, the Gam Mu, also fused...

10.1016/j.dnarep.2018.09.005 article EN cc-by-nc-nd DNA repair 2018-09-14

SUMMARY Antibiotics can induce mutations that cause antibiotic resistance. Yet, despite their importance, mechanisms of antibiotic-promoted mutagenesis remain elusive. We report the fluoroquinolone ciprofloxacin (cipro) induces drug resistance by triggering differentiation a mutant-generating cell subpopulation, using reactive oxygen species (ROS) to signal sigma-S (σ S ) general-stress response. Cipro-generated DNA breaks activate SOS DNA-damage response and error-prone polymerases in all...

10.1101/493015 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-12-11

SUMMARY Antibiotics can induce mutations that cause antibiotic resistance, triggered by stress responses. The identities of the stress-response activators reveal environmental cues elicit mutagenesis, and are weak links in mutagenesis networks, inhibition which could slow evolution resistance during therapies. Despite pivotal importance, few fewer functions responses clear. Here, we identify stringent starvation response fluoroquinolone-antibiotic ciprofloxacin (stress)-induced mutagenesis....

10.1101/2022.07.06.499071 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-07-07
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