Drosophila Met and Gce are partially redundant in transducing juvenile hormone action

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 gce null single mutants are fully viable, but the Met gce double mutant, Met27 gce2.5k, dies during the larval–pupal transition. Precocious and enhanced caspase-dependent programmed cell death (PCD) appears in fat body cells of Met27 gce2.5k 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 Met27 gce2.5k during larval molts. Consequently, expression of br occurs precociously in Met27 gce2.5k, which m ay cause precocious caspase-dependent PCD during the early larval stages. Defective phenotypes and gene expression changes in Met27 gce2.5k 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 Met27 gce2.5k 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.

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► Both Met and gce null mutants are viable, but the Met gce double mutant dies during the larval–pupal transition.
► Lethality of Met gce double mutant can be rescued by either a Met transgene or overexpression of gce.
► Precocious and enhanced apoptosis appears in the fat body cells of the Met gce double mutant larvae.
► Kr-h1 expression is totally blocked and br expression is precociously activated in the Met gce double mutant larvae.