@article {6393, title = {Met and gce are functionally redundant in transducing the {\textquotedblleft}status quo{\textquotedblright} action of juvenile hormone in Drosophila.}, journal = {Insect Biochemistry and Molecular Biology}, volume = {41}, year = {2011}, month = {2011 Dec}, pages = {938-45}, abstract = {

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, 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 may 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.

}, issn = {1879-0240}, doi = {10.1016/j.ibmb.2011.09.003}, author = {Abdou, M and He, Q and Wen, D and Zyaan, O and Wang, J and Xu, J and Baumann, Aaron and Joseph, J and WIlson, TG and Li, S and Wang, J} } @inbook {6395, title = {Molecular evolution of juvenile hormone signaling.}, booktitle = {Gene Duplication: Book 2}, year = {2011}, chapter = {18}, author = {Baumann, Aaron and WIlson, TG}, editor = {Friedberg, F} } @article {6391, title = {Evolutionary divergence of the paralogs Methoprene tolerant (Met) and germ cell expressed (gce) within the genus Drosophila.}, journal = {Journal of Insect Physiology}, volume = {56}, year = {2010}, month = {2010 Oct}, pages = {1445-55}, abstract = {

Juvenile hormone (JH) signaling underpins both regulatory and developmental pathways in insects. However, the JH receptor is poorly understood. Methoprene tolerant (Met) and germ cell expressed (gce) have been implicated in JH signaling in Drosophila. We investigated the evolution of Met and gce across 12 Drosophila species and found that these paralogs are conserved across at least 63 million years of dipteran evolution. Distinct patterns of selection found using estimates of dN/dS ratios across Drosophila Met and gce coding sequences, along with their incongruent temporal expression profiles in embryonic Drosophila melanogaster, illustrate avenues through which these genes have diverged within the Diptera. Additionally, we demonstrate that the annotated gene CG15032 is the 5{\textquoteright} terminus of gce. In mosquitoes and beetles, a single Met-like homolog displays structural similarity to both Met and gce, and the intron locations are conserved with those of gce. We found that Tribolium and mosquito Met orthologs are assembled from Met- and gce-specific domains in a modular fashion. Our results suggest that Drosophila Met and gce experienced divergent evolutionary pressures following the duplication of an ancestral gce-like gene found in less derived holometabolous insects.

}, keywords = {Amino Acid Sequence, Animals, Drosophila, Drosophila Proteins, Evolution, Gene Duplication, Methoprene, Molecular, Molecular Sequence Data, Phylogeny, Protein Structure, Sequence Alignment, Tertiary}, issn = {1879-1611}, doi = {10.1016/j.jinsphys.2010.05.001}, author = {Baumann, Aaron and Fujiwara, Yoshihiro and Wilson, Thomas G} } @article {6394, title = {Juvenile hormone action requires paralogous genes in Drosophila melanogaster.}, journal = {Genetics}, volume = {185}, year = {2010}, month = {2010}, pages = {1327-36}, author = {Baumann, Aaron and Barry, J and Wang, S and WIlson, TG} } @article {6392, title = {Drosophila melanogaster Methoprene-tolerant (Met) gene homologs from three mosquito species: members of PAS transcriptional factor family.}, journal = {Journal of Insect Physiology}, volume = {53}, year = {2007}, month = {2007 Mar}, pages = {246-53}, abstract = {

The Methoprene-tolerant (Met) gene in Drosophila melanogaster has been shown to function in juvenile hormone (JH) action. Met homologs were isolated from three mosquito species, Culex pipiens, Aedes aegypti and Anopheles gambiae. Sequence similarity was found to be high in bHLH and PAS conserved domains, and the majority of the 7-9 introns in AaMet and AgMet are located in either identical or similar positions, indicating evolutionary relatedness. Sequence comparison with Met and the similar germ-cell expressed (gce) gene in D. melanogaster showed that the mosquito genes are more similar to gce than to Met. Moreover, the multiple introns in AgMet and AaMet are more similar in number with the 7 introns in Dmgce than to the single intron in DmMet; in fact, six intron positions in AaMet and AgMet are similar to those in Dmgce. Efforts to identify a second homologous gene in mosquitoes were unsuccessful, suggesting a single gene in lower Diptera, consistent with the single gene uncovered in genomic sequencing of Ae. aegypti and An. gambiae. These results suggest that a gene duplication occurred during the evolution of higher Diptera, resulting in Met and gce.

}, keywords = {Amino Acid Sequence, Animals, Base Sequence, Basic Helix-Loop-Helix Transcription Factors, Culicidae, DNA, DNA Primers, Drosophila melanogaster, Drosophila Proteins, Evolution, Gene Components, Molecular, Molecular Sequence Data, Phylogeny, Reverse Transcriptase Polymerase Chain Reaction, Sequence Alignment, Sequence Analysis, Sequence Homology, Species Specificity}, issn = {0022-1910}, doi = {10.1016/j.jinsphys.2006.07.011}, author = {Wang, Shaoli and Baumann, Aaron and Wilson, Thomas G} }