Cobalt is widespread in the environment and excess dietary Co exposure can result in toxic effects in many organisms. However, whether the multi-biological toxicities caused by Co exposure can be transferred from parents to progeny has not been clarified. In the present study, we analyzed the multiple toxicities of Co to the nematode Caenorhabditis elegans and its progeny. Endpoints of life span, body size, vulva development, brood size, generation time, body bend, head thrash, and chemotaxis plasticity were used for toxicity testing. Our results indicate that Co induced multi-biological defects by affecting the life span, development, reproduction, behavior, and behavioral plasticity. Moreover, we found that most of these multi-biological defects could be transferred from parents to the filial generation (F1 and F2) progenies, and that this transmission could only be partially recovered. Certain specific phenotypes in the progeny exhibited even more severe defects than in the parents, such as chemotaxis plasticity. We classified the defects caused by Co exposure into four groups according to their transferable properties. Furthermore, the stress responses were investigated in embryos using a stable transgenic line, hsp16-2-gfp. Our data suggest that the multi-biological defects caused by Co exposure can be transferred from parents to progeny, and that Co toxicity might be accumulated in the eggs of nematodes.

Significance Functional plasticity of the nociceptive circuit is a remarkable feature and is of clinical relevance. As an example, nociceptors lower their threshold upon tissue injury, a process known as allodynia that would facilitate healing by guarding the injured areas. However, long-lasting hypersensitivity could lead to chronic pain, a debilitating disease not effectively treated. Therefore, it is crucial to dissect the mechanisms underlying basal nociception and nociceptive hypersensitivity. In both vertebrate and invertebrate species, conserved transient receptor potential (Trp) channels are the primary transducers of noxious stimuli. Here, we provide a precedent that in Drosophila larvae, heat sensing in the nociception and hypersensitivity states is mediated by distinct heat-sensitive neurons and TrpA1 alternative isoforms.

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<p>Figure S6 shows anti-MET VHH pool significantly inducing MET degradation.</p>