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Transcriptomic profiling of chemical exposure reveals roles of Yap1 in protecting yeast cells from oxidative and other types of stresses
Author(s) -
Zhang Chao,
Li Zhouquan,
Zhang Xiaohua,
Yuan Li,
Dai Heping,
Xiao Wei
Publication year - 2016
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/yea.3135
Subject(s) - yap1 , biology , transcriptome , mutant , downregulation and upregulation , gene , oxidative phosphorylation , biochemistry , genetics , microbiology and biotechnology , gene expression , transcription factor
Transcriptomic profiles are generated by comparing wild‐type and the yeast yap1 mutant to various chemicals in an attempt to establish a correlation between this gene mutation and chemical exposure. Test chemicals include ClonNAT as a non‐genotoxic agent, methyl methanesulphonate (MMS) as an alkylating agent, tert ‐butyl hydroperoxide ( t ‐BHP) as an oxidative agent and the mixture of t ‐BHP and MMS to reflect complex natural exposure. Differentially expressed genes (DEGs) were identified and specific DEGs were obtained by excluding overlapping DEGs with the control group. In the MMS exposure group, deoxyribonucleotide biosynthetic processes were upregulated, while oxidation–reduction processes were downregulated. In the t ‐BHP exposure group, metabolic processes were upregulated while peroxisome and ion transport pathways were downregulated. In the mixture exposure group, the proteasome pathway was upregulated, while the aerobic respiration was downregulated. Homologue analysis of DEGs related to human diseases showed that many of DEGs were linked to cancer, ageing and neuronal degeneration. These observations confirm that the yap1 mutant is more sensitive to chemicals than wild‐type cells and that the susceptible individuals carrying the YAP1 ‐like gene defect may enhance risk to chemical exposure. Hence, this study offers a novel approach to environmental risk assessment, based on the genetic backgrounds of susceptible individuals. Copyright © 2015 John Wiley & Sons, Ltd.