Tags

Type your tag names separated by a space and hit enter

Regulator of G protein signaling-1 modulates paraquat-induced oxidative stress and longevity via the insulin like signaling pathway in Caenorhabditis elegans.
Toxicol Lett. 2017 May 05; 273:97-105.TL

Abstract

Insulin or insulin like signaling (IIS) pathway is a crucial pathway in Caenorhabditis elegans associated with mediating longevity, and stress resistance. Regulators of G protein signaling (RGS) also modulate stress resistance and longevity in multiple in vitro and in vivo models. However, the mechanism underlying RGS mediating stress resistance and longevity remains largely unclear. Here we report that rgs-1, an important member of rgs family, is a novel modulator of IIS pathway in C. elegans. We found that the loss of rgs-1 dramatically promoted paraquat resistance in C. elegans. Further genetic analyses demonstrated that rgs-1 acted downstream of daf-2 and upstream of age-1, pdk-1, daf-16. Instead of affecting those IIS-associated genes in transcriptional process, loss of rgs-1 promoted DAF-16's nucleus translocation and subset genes' expression in paraquat-induced oxidative status. By this way, rgs-1 mutant worms exhibited lower ROS damage and longer survival time than wild type worms when both exposed to paraquat. Other than paraquat exposure, rgs-1 mutant also promoted lifespan and cadmium resistance relying on daf-16. As rgs is evolutionarily conserved, our findings open a new insight into rgs family and its role in paraquat-induced oxidative stress and longevity in C. elegans or even mammals.

Authors+Show Affiliations

Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China; Department of Biomedical Engineering, University of Houston, Houston, TX 77204, USA. Electronic address: cmohan@Central.UH.EDU.Center for Nephrology and Metabolomics, Division of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China. Electronic address: pengai@tongji.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28366735

Citation

Wu, Mingyu, et al. "Regulator of G Protein Signaling-1 Modulates Paraquat-induced Oxidative Stress and Longevity Via the Insulin Like Signaling Pathway in Caenorhabditis Elegans." Toxicology Letters, vol. 273, 2017, pp. 97-105.
Wu M, Kang X, Wang Q, et al. Regulator of G protein signaling-1 modulates paraquat-induced oxidative stress and longevity via the insulin like signaling pathway in Caenorhabditis elegans. Toxicol Lett. 2017;273:97-105.
Wu, M., Kang, X., Wang, Q., Zhou, C., Mohan, C., & Peng, A. (2017). Regulator of G protein signaling-1 modulates paraquat-induced oxidative stress and longevity via the insulin like signaling pathway in Caenorhabditis elegans. Toxicology Letters, 273, 97-105. https://doi.org/10.1016/j.toxlet.2017.03.027
Wu M, et al. Regulator of G Protein Signaling-1 Modulates Paraquat-induced Oxidative Stress and Longevity Via the Insulin Like Signaling Pathway in Caenorhabditis Elegans. Toxicol Lett. 2017 May 5;273:97-105. PubMed PMID: 28366735.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulator of G protein signaling-1 modulates paraquat-induced oxidative stress and longevity via the insulin like signaling pathway in Caenorhabditis elegans. AU - Wu,Mingyu, AU - Kang,Xin, AU - Wang,Qiang, AU - Zhou,Chunyu, AU - Mohan,Chandra, AU - Peng,Ai, Y1 - 2017/03/31/ PY - 2017/02/23/received PY - 2017/03/25/revised PY - 2017/03/29/accepted PY - 2017/4/4/pubmed PY - 2017/7/5/medline PY - 2017/4/4/entrez KW - Insulin signaling KW - Longevity KW - Oxidative stress KW - Paraquat KW - rgs-1 SP - 97 EP - 105 JF - Toxicology letters JO - Toxicol. Lett. VL - 273 N2 - Insulin or insulin like signaling (IIS) pathway is a crucial pathway in Caenorhabditis elegans associated with mediating longevity, and stress resistance. Regulators of G protein signaling (RGS) also modulate stress resistance and longevity in multiple in vitro and in vivo models. However, the mechanism underlying RGS mediating stress resistance and longevity remains largely unclear. Here we report that rgs-1, an important member of rgs family, is a novel modulator of IIS pathway in C. elegans. We found that the loss of rgs-1 dramatically promoted paraquat resistance in C. elegans. Further genetic analyses demonstrated that rgs-1 acted downstream of daf-2 and upstream of age-1, pdk-1, daf-16. Instead of affecting those IIS-associated genes in transcriptional process, loss of rgs-1 promoted DAF-16's nucleus translocation and subset genes' expression in paraquat-induced oxidative status. By this way, rgs-1 mutant worms exhibited lower ROS damage and longer survival time than wild type worms when both exposed to paraquat. Other than paraquat exposure, rgs-1 mutant also promoted lifespan and cadmium resistance relying on daf-16. As rgs is evolutionarily conserved, our findings open a new insight into rgs family and its role in paraquat-induced oxidative stress and longevity in C. elegans or even mammals. SN - 1879-3169 UR - https://www.unboundmedicine.com/medline/citation/28366735/Regulator_of_G_protein_signaling_1_modulates_paraquat_induced_oxidative_stress_and_longevity_via_the_insulin_like_signaling_pathway_in_Caenorhabditis_elegans_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4274(17)30141-8 DB - PRIME DP - Unbound Medicine ER -