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The transcription factor Prdm12 exerts important influences on the development of nociceptors, peripheral touch and pain-sensing neurons, and has been implicated in human pain sensation disorders. We examined the consequences of exposing developing Xenopus laevis embryos to the commonly used pesticide malathion on Prdm12 expression. Using qPCR and western blot analysis we observed that malathion treatment for the first six days of tadpole development significantly increased both prdm12 mRNA levels and Prdm12 protein levels compared to controls. Consequently, early exposure to this pesticide has potential to alter nociceptor development.
Figure 1. The pesticide malathion enhances prdm12 mRNA and Prdm12 protein expression:
Tadpoles were raised in two concentrations of the pesticide malathion (0.5 and 2.0 mg/L) for six days until stage 47 (a) then prdm12 mRNA (b) and Prdm12 protein (c,d) levels were assessed in comparison to vehicle controls (0 mg/L). Both concentrations of the pesticide caused noticeable gross morphological alterations in tadpole axes with more severely bent phenotypes observed in the higher concentration (a). Malathion at 0.5 mg/L did not significantly alter prdm12 mRNA expression levels as assessed by qPCR though 2.0 mg/L malathion caused a significant 99-fold increase in prdm12 mRNA expression levels (b). Both concentrations of malathion significantly increased Prdm12 protein levels (d) as assessed by western blot with anti-PRDM12 (c, lower panel) as normalized to total protein per lane (c, upper panel). *p=0.01; **p=0.0026; ****p<0.0001. Scale bar = 1 mm.
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