The Drosophila Methoprene-tolerant (Met) and Germ cell-expressed (Gce) bHLH-PAS transcription factors are products of two paralogous genes. Both proteins potentially mediate the effect of juvenile hormone (JH) as candidate JH receptors. Here we report that Met and Gce are partially redundant in transducing JH action. Both Met and g. ce null single mutants are fully viable, but the Met gce double mutant, Met 27 gce 2.5k, dies during the larval-pupal transition. Precocious and enhanced caspase-dependent programmed cell death (PCD) appears in fat body cells of Met 27 gce 2.5k during the early larval stages. Expression of Kr-h1, a JH response gene that inhibits 20-hydroxyecdysone (20E)-induced broad (br) expression, is abolished in Met 27 gce 2.5k during larval molts. Consequently, expression of br occurs precociously in Met 27 gce 2.5k, which m ay cause precocious caspase-dependent PCD during the early larval stages. Defective phenotypes and gene expression changes in Met 27 gce 2.5k double mutants are similar to those found in JH-deficient animals. Importantly, exogenous application of JH agonists rescued the JH-deficient animals but not the Met 27 gce 2.5k mutants. Our data suggest a model in which Drosophila Met and Gce redundantly transduce JH action to prevent 20E-induced caspase-dependent PCD during larval molts by induction of Kr-h1 expression and inhibition of br expression.
- JH signaling pathway
- Programmed cell death