In the last decade, the freshwater amphipod Gammarus fossarum proved to be a promising sentinel species in active biomonitoring programs to assess the effects of environmental contamination on nontarget organisms. In many vertebrates, xenobiotics cause deregulation of the retinoids (RETs) metabolism implicated in many crucial biological functions. The retinoid system, known in the crustaceans, is yet to be explored in G. fossarum. Therefore, we studied the implication of all-trans retinoic acid (atRA) in the reproduction (embryo, oocyte, and juvenile production) and development (success and delay of moulting) by exposing G. fossarum females to atRA and citral (CIT), a known inhibitor of RA synthesis to simulate an excess or a de ciency of RA, respectively. In parallel, we monitored the effects of methoprene (MET) and glyphosate (GLY), two pesticides suspected to interfere with atRA metabolism and signalling and frequently found in water systems. After 14 days of exposure, atRA, CIT, and MET reduced the number of oocytes, whereas only MET caused a reduced number of embryos. After 44 days, MET and GLY showed a tendency to decrease juvenile production. The duration of the moulting cycle increased following the exposures to atRA and MET, while the treatment with CIT caused a typical endocrine disruptive inverted Ushaped curve. The exposure to GLY led to increased duration of the moulting cycle at the lowest concentrations and lowered moulting success at the highest concentration tested. This study highlights for the rst time the implication of RA in the oogenesis and moulting of G. fossarum and suggests that it may be a potential mediator of MET-induced effects on these processes. This study adds to the comprehension of the reproductive and developmental control in G. fossarum and opens new research avenues to study the effects of xenobiotics on the RET system in this sentinel species. Ultimately, our study will drive the development of RET-based biomarkers for non-target aquatic invertebrates exposed to xenobiotics.

In the last decade, the freshwater amphipod Gammarus fossarum proved to be a promising sentinel species in active biomonitoring programs to assess the effects of environmental contamination on non-target organisms. In many vertebrates, xenobiotics cause deregulation of the retinoids (RETs) metabolism implicated in many crucial biological functions. The retinoid system, known in the crustaceans, is yet to be explored in G. fossarum. Therefore, we studied the implication of all­-trans­ retinoic acid (atRA) in the reproduction (embryo, oocyte, and juvenile production) and development (success and delay of moulting) by exposing G. fossarum females to atRA and citral (CIT), a known inhibitor of RA synthesis to simulate an excess or a deficiency of RA, respectively. In parallel, we monitored the effects of methoprene (MET) and glyphosate (GLY), two pesticides suspected to interfere with atRA metabolism and signalling and frequently found in water systems. After 14 days of exposure, atRA, CIT, and MET reduced the number of oocytes, whereas only MET caused a reduced number of embryos. After 44 days, MET and GLY showed a tendency to decrease juvenile production. The duration of the moulting cycle increased following the exposures to atRA and MET, while the treatment with CIT caused a typical endocrine disruptive inverted U-shaped curve. The exposure to GLY led to increased duration of the moulting cycle at the lowest concentrations and lowered moulting success at the highest concentration tested. This study highlights for the first time the implication of RA in the oogenesis and moulting of G. fossarum and suggests that it may be a potential mediator of MET-induced effects on these processes. This study adds to the comprehension of the reproductive and developmental control in G. fossarum and opens new research avenues to study the effects of xenobiotics on the RET system in this sentinel species. Ultimately, our study will drive the development of RET-based biomarkers for non-target aquatic invertebrates exposed to xenobiotics.