Corpus allatum (CA) ablation results in juvenile hormone (JH) deficiency and pupal lethality in Drosophila. The fly CA produces and releases three sesquiterpenoid hormones: JH III bisepoxide (JHB3), JH III, and methyl farnesoate (MF). In the whole body extracts, MF is the most abundant sesquiterpenoid, followed by JHB3 and JH III. Knockout of JH acid methyl transferase (jhamt) did not result in lethality; it decreased biosynthesis of JHB3, but MF biosynthesis was not affected. RNAi-mediated reduction of 3-hydroxy-3-methylglutaryl CoA reductase (hmgcr) expression in the CA decreased biosynthesis and titers of the three sesquiterpenoids, resulting in partial lethality. Reducing hmgcr expression in the CA of the jhamt mutant further decreased MF titer to a very low level, and caused complete lethality. JH III, JHB3, and MF function through Met and Gce, the two JH receptors, and induce expression of Kr-h1, a JH primary-response gene. As well, a portion of MF is converted to JHB3 in the hemolymph or peripheral tissues. Topical application of JHB3, JH III, or MF precluded lethality in JH-deficient animals, but not in the Met gce double mutant. Taken together, these experiments show that MF is produced by the larval CA and released into the hemolymph, from where it exerts its anti-metamorphic effects indirectly after conversion to JHB3, as well as acting as a hormone itself through the two JH receptors, Met and Gce.

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Published in PLOS Genetics, v. 11, no. 3, article e1005038, p. 1-19.

© 2015 Wen et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

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This study was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB13030700), the 973 program (2012CB114605), and the National Science Foundation of China (31330072, 31125025) to SL. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

journal.pgen.1005038.s001.TIF (662 kB)
S1 Fig. The scheme of JH III biosynthetic pathway in insects.

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S2 Fig. Phenotypic changes of the <em>jhamt</em> mutant.

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S3 Fig. Generation of <em>jhamt<sup>2</sup> CG10527<sup>187</sup></em>.

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S4 Fig. Mutation of <em>CG10527</em> does not enhance JH-associated effects of the <em>jhamt mutant</em>.

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S5 Fig. Lethality of <em>Aug21-GAL4>UAS-hmgcr dsRNA</em> and <em>jhamt<sup>2</sup>/jhamt<em>2</em>; Aug21-GAL4>UAS-hmgcr dsRNA</em>.

journal.pgen.1005038.s006.TIF (421 kB)
S6 Fig. Reduction of <em>USP</em> expression does not affect JH-induced <em>Kr-h1</em> expression.

journal.pgen.1005038.s007.PDF (137 kB)
S1 Table. Primers used in this paper.

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