Molecular mechanisms of resistance to human pathogenic bacteria in Caenorhabditis elegans by MEV-1 mediated oxidative stress.
Both mutation and knockdown in mev-1 gene render Caenorhabditis elegans susceptibility to Enterococcus faecalis infection. However, the mechanisms by which of MEV-1 defects pathogen resistance remain unclear. Here we show that mev-1RNAi causes a dramatic decrease in oxidative stress and antioxidant enzyme expressions, thereby leading to increased E. faecalis accumulation in nematode intestine. Mitochondrial superoxide change after infection induced these oxidative responses through DAF-16 activity. All together, this highlights MEV-1 as a key regulatory component for determining genetic responsiveness to oxidant/antioxidant imbalance that is associated with innate immunity.
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China.
Na
N
Feng
Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
Dejuan
D
Zhi
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China.
Liyun
L
Zhang
Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
Jing
J
Tian
Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
Hui
H
Ren
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China.
Chanhe
C
Li
Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
Hongmei
H
Zhu
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China; Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China. Electronic address: lihy@lzu.edu.cn.
Hongyu
H
Li
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology*; D029742:Caenorhabditis elegans Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D045303:Cytochromes b; D013293:Enterococcus faecalis / Q000276:immunology / Q000472:pathogenicity*; D051858:Forkhead Transcription Factors; D017238:Genes, Helminth; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics / Q000502:physiology; D008062:Lipofuscin / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation; D018384:Oxidative Stress; D034622:RNA Interference; D013385:Succinate Dehydrogenase / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism; D015533:Transcriptional Activation
D029742:Caenorhabditis elegans Proteins; D051858:Forkhead Transcription Factors; D008062:Lipofuscin; C472666:MEV-1 protein, C elegans; D014157:Transcription Factors; C108831:daf-16 protein, C elegans; D045303:Cytochromes b; D013385:Succinate Dehydrogenase
DAF-16; Infection; Mitochondrial superoxide; Oxidative stress; mev-1