The role of pparγ in embryonic development of Xenopus tropicalis under triphenyltin-induced teratogenicity

Evidence has shown that triphenyltin (TPT) triggers severe malformations in Xenopus tropicalis embryos, partly due to activation of PPARγ (peroxisome proliferator activated receptor γ) protein. In the present study, we investigated how abundance of pparγ and TPT exposure interact and affect X. tropicalis embryonic development. We observed pparγ expression signals appeared in the neural crest and neural fold, as well as in the brain, eyes and spinal cord organs. Both pparγ overexpression and its Morpholino (MO) knockdown inhibited pax6 (paired box 6) expression, a marker of eye development, and significantly up- and down-regulated lipid and glucose homeostasis related genes, such as lpl (lipoprotein lipase), slc2a4 (solute carrier family 2 (facilitated glucose transporter), member 4) and pck1 (phosphoenolpyruvate carboxykinase 1, cytosolic), thus inducing eye phenotypes. Overexpression of pparγ induced small eye phenotype, while pparγ MO induced small eye plus turbid eye lens microencephaly and enlarged trunk. In contrast, 5–20 μg Sn/L (stannum/L) TPT exposure reversed some impacts induced by pparγ overexpression, i.e., no small eye, up-regulation of pax6 and down-regulation of pparγ lpl, slc2a4 and pck1. Meanwhile, microinjection of pparγ MO combined with exposure to 20 μg Sn/L TPT caused 85% mortality. In brief, our work clearly indicates that pparγ is essential to eye development and inhibition of its expression combined with TPT exposure can be extremely harmful to X. tropicalis embryo.