Early-life exposure to methylmercury induces reversible behavioral impairments and gene expression modifications in one isogenic lineage of mangrove rivulus fish Kryptolebias marmoratus

Methylmercury (MeHg) is a ubiquitous bioaccumulative neurotoxicant present in aquatic ecosystems. It is known to alter behaviors, sensory functions and learning abilities in fish and other vertebrates. Developmental and early-life stages exposure to MeHg can lead to brain damage with immediate consequences on larvae behavior, but may also induce long term effects in adults after a detoxification period. However, very little is known about developmental origin of behavioral impairment in adults due to early exposure to MeHg. The aim of this study is to assess whether early-life MeHg exposure induces immediate and/or delayed effects on behaviors, related genes expression and DNA methylation (one of epigenetic mechanisms). To reach this goal, newly hatched larvae of mangrove rivulus fish, Kryptolebias marmoratus, were exposed to two sub-lethal concentrations of MeHg (90 mu g/L and 135 mu g/L) for 7 days, and immediate and delayed effects were assessed respectively in 7 dph (days post -hatching) and 90 dph fish. This species naturally produces isogenic lineages due to its self-fertilizing repro-duction system, which is unique among vertebrates. It allows to study how environment stressors can influence organism's phenotype while minimizing genetic variability. As results, both MeHg exposures are associated with a decreased foraging efficiency and thigmotaxis, and a dose-dependent reduction in larvae locomotor activity. Regarding molecular analysis in larvae whole bodies, both MeHg exposures induced significant decreased expression of DNMT3a, MAOA, MeCP2 and NIPBL, and significant increase of GSS, but none of those genes underwent methylation changes in targeted CpGs. None of significant behavioral and molecular impairments observed in 7-dph larvae were found in 90-dph adults, which highlight a distinction between immediate and delayed effects of developmental MeHg exposure. Our results suggest implications of aminergic system and its neurotransmitters, redox/methylation trade-off and possibly other epigenetic mechanisms in MeHg neurotoxicity underlying behavioral alterations in rivulus.

Automated summary

This study aims to assess the immediate and/or delayed effects of early-life methylmercury exposure on behaviors, related gene expression, and DNA methylation. The results showed that methylmercury exposure led to decreased foraging efficiency, increased thigmotaxis, and reduced locomotor activity in larvae. The expression of certain genes was also affected, but no methylation changes were found in targeted CpGs. The significant behavioral and molecular impairments observed in larvae were not found in adults, highlighting the distinction between immediate and delayed effects of developmental methylmercury exposure.