It has been reported that a basic helix-loop-helix transcription factor MXL-3 (Max-like 3) represses the expression of the lysosomal lipases in the presence of nutrients. On the other hand, under starvation conditions, MXL-3 is down-regulated and the expression of the lysosomal lipases are induced. Consequently, fats are broken down by inducing lipophagy. Moreover, it has been reported that the transcription factor SKN-1, a homolog of mammalian Nrf proteins, binds to MXL-3 which is involved in oxidative stress response. These studies suggest that MXL-3 may be involved oxidative stress response. We have previously shown that X-ray irradiation extends lifespan and up-regulates the expression of
mxl-3 at a dauer larval stage of the nematode Caenorhabditis elegans. It is well known that the radiation generates reactive oxygen species in response to water in vivo. To investigate the role of MXL-3 in oxidative stress response, we examined, 1)
mxl-3 expression levels in wild-type animals exposed to paraquat, 2) the lifespan of a
mxl-3 (
ok1947) mutant under high oxygen levels, 3) paraquat sensitivity of the
mxl-3 mutant. Our results showed that
mxl-3 mRNA levels was up-regulated in wild type worms exposed to 30mM paraquat for 4 hours and longer. The
mxl-3 mutant was hypersensitive to paraquat. Moreover, under 90% oxygen, the mean lifespan of the
mxl-3 mutant was relatively more decreased in comparison to wild type. It has been reported that
mxl-3 mutant is long lived in abundant food conditions. On the other hand, we observed
mxl-3 mutant is short lived under high oxidative stress. In addition,
mxl-3 was up-regulated in wild type animals. Our result raise the possibility that MXL-3 is not involved in response to low oxidative stress such as normoxia s but in response to hyperoxia.