Abstract:
:A long-unresolved question in the developmental biology of Drosophila melanogaster has been whether methyl farnesoid hormones secreted by the ring gland are necessary for larval maturation and metamorphosis. In this study, we have used RNAi techniques to inhibit 3-Hydroxy-3-Methylglutaryl CoA Reductase (HMGCR) expression selectively in the corpora allatal cells that produce the circulating farnesoid hormones. The developing larvae manifest a number of developmental, metabolic and morphogenetic derangements. These defects included the exhibition of an "ultraspiracle" death phenotype at the 1st to 2nd instar larval molt, similar to that exhibited by animals that are null for the farnesoid receptor ultraspiracle. The few larvae surviving past a second lethal period at the 2nd to 3rd instar larval molt, again with "ultraspiracle" phenotype, often became developmentally arrested after either attaining a misformed puparium or after formation of the white pupa. Survival past the "ultraspiracle" lethal phenotype could be rescued by dietary provision of an endogenous dedicated precursor to the three naturally secreted methyl farnesoid hormones. In addition to these developmental and morphogenetic defects, most larvae that survived to the late second instar exhibited a posterior-originating melanization of the tracheal system. These results support the hypothesis that larval methyl farnesoid hormones are necessary for larval survival and morphogenetic transformation through the larval and pupal metamorphic processes.
journal_name
Gen Comp Endocrinoljournal_title
General and comparative endocrinologyauthors
Jones D,Jones G,Teal P,Hammac C,Messmer L,Osborne K,Belgacem YH,Martin JRdoi
10.1016/j.ygcen.2009.07.006subject
Has Abstractpub_date
2010-01-15 00:00:00pages
244-54issue
2eissn
0016-6480issn
1095-6840pii
S0016-6480(09)00310-4journal_volume
165pub_type
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