Induction of germline apoptosis by cobalt and relevant signal transduction pathways in Caenorhabditis elegans

Abstract

Many investigations showed that cobalt exposure could induce apoptosis both in cells and tissues. However, appropriate in vivo animal models to assess the underlying mechanisms of cobalt-induced apoptosis are currently unavailable. The model organism, Caenorhabditis elegans, has been shown to be a good model for evaluating many biological processes. This study detected significant cobalt induced germline cell apoptosis after 12-h exposure; thus demonstrating that C. elegans could be a mammalian in vivo substitute model to study mechanisms of apoptosis. Then knockout gene C. elegans strains were utilized to investigate the relationship between cobalt-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 cobalt-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 JNK and p38 MAPK signaling cascades suppressed cobalt-induced germline apoptosis, while ERK signaling cascades have no effect on the cobalt-induced germline apoptosis.