Abstract
Juvenile hormone (JH), a sesquiterpenoid produced by the corpora allata, coordinates insect growth, metamorphosis, and reproduction. While JH action for the repression of larval metamorphosis has been well studied, the molecular basis of JH in promoting adult reproduction has not been fully elucidated. Methoprene-tolerant (Met), the JH receptor, has been recently shown to mediate JH action during metamorphosis as well as in vitellogenesis, but again, the precise mechanism underlying the latter has been lacking. We have now demonstrated using Met RNAi to phenocopy a JH-deprived condition in migratory locusts, that JH stimulates DNA replication and increases ploidy in preparation for vitellogenesis. Mcm4 and Mcm7, two genes in the DNA replication pathway were expressed in the presence of JH and Met. Depletion of Mcm4 or Mcm7 inhibited de novo DNA synthesis and polyploidization, and resulted in the substantial reduction of vitellogenin mRNA levels as well as severely impaired oocyte maturation and ovarian growth. By using luciferase reporter and electrophoretic mobility shift assays, we have shown that Met directly regulates the transcription of Mcm4 and Mcm7 by binding to upstream consensus sequences with E-box or E-box-like motifs. Our work suggests that the JH-receptor complex acts on Mcm4 and Mcm7 to regulate DNA replication and polyploidy for vitellogenesis and oocyte maturation.
Highlights
Juvenile hormone (JH) is a key endocrine regulator controlling insect development, metamorphosis and reproduction
Upon JH binding, Met forms a heterodimer with another basic helix–loop–helix (bHLH)-PAS transcription factor, the steroid receptor coactivator (SRC; called Taiman in Drosophila or FISC in the mosquito, Aedes aegypti; we use SRC since the amino acid sequence of the locust orthologue shares a higher similarity to the SRC of the beetle, Tribolium castaneum)
Locusta migratoria, vitellogenesis is dependent on JH, and JH stimulates DNA replication and increases ploidy in the fat body
Summary
Juvenile hormone (JH) is a key endocrine regulator controlling insect development, metamorphosis and reproduction. Methoprene-tolerant (Met), a member of the basic helix–loop–helix (bHLH)-Per-Arnt-Sim (PAS) transcription factor family, has been recently identified as the JH receptor [3,4,5]. Upon JH binding, Met forms a heterodimer with another bHLH-PAS transcription factor, the steroid receptor coactivator (SRC; called Taiman in Drosophila or FISC in the mosquito, Aedes aegypti; we use SRC since the amino acid sequence of the locust orthologue shares a higher similarity to the SRC of the beetle, Tribolium castaneum). The Met-SRC heterodimer forms a ligand-dependent complex which can direct transcription of target genes in several insects [5,7,8,9]. Met exerts its anti-metamorphic role by acting on Kruppel homolog 1 (Kr-h1), which in turn represses the expression of broad, an early 20E response gene in metamorphosis [3,7,10]
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