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Nickel-induced apoptosis and relevant signal transduction pathways in Caenorhabditis elegans
Cai Kezhou1, Ren Chong, Yu Zengliang
1Biology and Food Industrial College, Hefei University of Technology, Hefei, People's Republic of China, Key Laboratory of Ion Beam Bioengineering, Chinese Academy of Sciences, Hefei, People's Republic of China.
Abstract:
Many investigations have shown that nickel exposure can induce micronuclei generation, inhibit DNA repair and induce cell apoptosis, both in cells and tissues. However, there is a lack of appropriate in vivo animal models to study the underlying mechanisms of nickel-induced apoptosis. The model organism, Caenorhabditis elegans, has been shown to be a good model for investigating many biological processes. In the present study, we detected 0.01 mM nickel induced significantly germline cell apoptosis after treatment for 12 hours, which demonstrated that C. elegans could be a mammalian in vivo substitute model to study the mechanisms of apoptosis. Then gene knockout C. elegans strains were utilized to investigate the relationship between nickel-induced apoptosis and relevant signal pathways, which were involved in DNA damage and repair, apoptosis regulation and damage signal transduction. The results presented here demonstrated that nickel-induced apoptosis was independent of the DNA damage response gene, such as hus-1, p53/cep-1 and egl-1. The loss-of-function of the genes that related to Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPK) signaling cascades suppressed nickel-induced germline apoptosis, while ERK signaling cascades have no effects on the nickel-induced germline apoptosis.
Insights
Nickel exposure induces apoptosis in Caenorhabditis elegans germline cells. This study reveals nickel-induced apoptosis is independent of DNA damage response genes but relies on Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPK) signaling pathways.
Area of Science:
- Toxicology
- Cell Biology
- Genetics
Background:
- Nickel exposure is known to cause DNA damage and cell apoptosis.
- There is a need for suitable in vivo models to study nickel-induced apoptosis mechanisms.
- Caenorhabditis elegans (C. elegans) is a versatile model organism for biological studies.
Purpose of the Study:
- To establish C. elegans as an in vivo model for studying nickel-induced apoptosis.
- To investigate the molecular pathways involved in nickel-induced germline apoptosis.
- To determine the role of DNA damage response and mitogen-activated protein kinase (MAPK) pathways.
Main Methods:
- Treatment of wild-type C. elegans with nickel chloride.
- Utilizing gene knockout C. elegans strains for pathway analysis.
- Assessing germline cell apoptosis and analyzing gene function related to DNA damage and signaling cascades.
Main Results:
- Nickel exposure (0.01 mM for 12 hours) significantly induced germline cell apoptosis in C. elegans.
- Nickel-induced apoptosis was independent of DNA damage response genes (hus-1, p53/cep-1, egl-1).
- Inhibition of Jun N-terminal kinase (JNK) and p38 MAPK signaling pathways suppressed nickel-induced apoptosis, while ERK signaling had no effect.
Conclusions:
- C. elegans serves as a viable in vivo model for studying nickel-induced apoptosis.
- Nickel-induced apoptosis in C. elegans germline is mediated by JNK and p38 MAPK signaling pathways.
- The DNA damage response pathway is not involved in nickel-induced germline apoptosis in this model.
