Sublethal perfluorooctanoic acid and perfluorooctanesulfonic acid delay C. elegans larval development and population growth but do not alter egg hatching.

Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are polyfluoroalkyl substances (PFAS) used as surface coatings in manufacturing. Exposure to PFAS was shown to be correlated with infertility, low birth weight, and delayed aspects of pubertal development in mammals. Despite many correlational studies, there have been few direct investigations examining the link between PFAS exposure and early animal development. The aim of this study was to (1) examine the effects of PFOA on development and reproduction using the roundworm Caenorhabditis elegans, a model with a high predictive value for human reproductive toxicity and (2) compare observations to exposure to PFOS. PFAS exposure did not markedly alter egg hatching but delayed population growth, in part due to slower larval development. PFAS-exposed worms took longer to progress through larval stages to reach reproductive maturity, and this was not attributed to PFOA-induced toxicity to their food. Our results provide a robust benchmark for testing developmental and reproductive toxicity for other PFAS and PFAS-alternatives which continue to be used in manufacturing and released into the environment.

The Doublesex/Mab-3 domain transcription factor DMD-10 regulates ASH-dependent behavioral responses.

The Doublesex/Mab-3 Domain transcription factor DMD-10 is expressed in several cell types in C. elegans, including in the nervous system. We sought to investigate whether DMD-10 is required for normal neuronal function using behavioral assays. We found that mutation of dmd-10 did not broadly affect behavior. dmd-10 mutants were normal in several behavioral assays including a body bends assay for locomotion, egg laying, chemotaxis and response to gentle touch to the body. dmd-10 mutants did have defects in nose-touch responsiveness, which requires the glutamate receptor GLR-1. However, using quantitative fluorescence microscopy to measure levels of a GLR-1::GFP fusion protein in the ventral nerve cord, we found no evidence supporting a difference in the number of GLR-1 synapses or in the amount of GLR-1 present in dmd-10 mutants. dmd-10 mutants did have decreased responsiveness to high osmolarity, which, along with nose-touch, is sensed by the polymodal sensory neuron ASH. Furthermore, mutation of dmd-10 impaired behavioral response to optogenetic activation of ASH, suggesting that dmd-10 promotes neuronal signaling in ASH downstream of sensory receptor activation. Together our results suggest that DMD-10 is important in regulating the frequency of multiple ASH-dependent behavioral responses.