The Isolation of Two Juvenile Hormone-Inducible Genes in Drosophila melanogaster

Dubrovsky, Edward B.; Dubrovskaya, Veronica A.; Bilderback, Ann L.; Berger, Edward M.

doi:10.1006/dbio.2000.9800

Cited by 92 publications

(62 citation statements)

References 64 publications

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“…Direct evidence, however, for the immediate interaction with JH and involvement in gene regulation is lacking. To test this hypothesis, we chose S2 cells as experimental material because the use of cultured cells would be advantageous for examining ligand-dependent gene regulation and JH responses in this cell line have been reported [38][39][40]. Our principal new contributions are: (a) demonstration of direct, reversible binding of JH III to MET; (b) demonstration of its JH-dependent transactivation potential.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Drosophila Methoprene ‐tolerant gene product

et al. 2005

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Insect development and reproduction are regulated by two classes of lipid-soluble hormones, the ecdysteroids and juvenile hormones (JHs). The ecdysteroids activate target genes through a heterodimeric receptor complex composing the ecdysone receptor and ultraspiracle (USP) proteins, both of which are members of the nuclear steroid ⁄ thyroid ⁄ retinoid receptor superfamily [1]. During insect development, ecdysteroids induce molting while JH determines the nature of each molt by modulating the ecdysteroid-induced gene expression cascade [2][3][4]. In addition, in adult insects, JH has a wide variety of actions related to reproduction, including oogenesis, migratory behaviour and diapause [2,5,6]. The mode of molecular action of JH, however, is still obscure [7]. JHs are a family of esterified sesquiterpenoids, whose lipid-soluble nature has suggested action directly on the genome through nuclear receptors such as ecdysteroids and the vertebrate steroid ⁄ thyroid ⁄ retinoid hormones [5,8] although actions of JH through the cell membrane are also documented [9,10].Many attempts have been made to identify nuclear JH receptors. Jones and Sharp [11] showed that JH III binds to the Drosophila USP protein, which is a homologue of the vertebrate retinoid X receptor, promoting Juvenile hormones (JHs) of insects are sesquiterpenoids that regulate a great diversity of processes in development and reproduction. As yet the molecular modes of action of JH are poorly understood. The Methoprenetolerant (Met) gene of Drosophila melanogaster has been found to be responsible for resistance to a JH analogue (JHA) insecticide, methoprene. Previous studies on Met have implicated its involvement in JH signaling, although direct evidence is lacking. We have now examined the product of Met (MET) in terms of its binding to JH and ligand-dependent gene regulation. In vitro synthesized MET directly bound to JH III with high affinity (K d ¼ 5.3 ± 1.5 nm, mean ± SD), consistent with the physiological JH concentration. In transient transfection assays using Drosophila S2 cells the yeast GAL4-DNA binding domain fused to MET exerted JH-or JHAdependent activation of a reporter gene. Activation of the reporter gene was highly JH-or JHA-specific with the order of effectiveness: JH III JH II > JH I > methoprene; compounds which are only structurally related to JH or JHA did not induce any activation. Localization of MET in the S2 cells was nuclear irrespective of the presence or absence of JH. These results suggest that MET may function as a JH-dependent transcription factor.

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Section: Discussionmentioning

confidence: 99%

Characterization of the Drosophila Methoprene ‐tolerant gene product

et al. 2005

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“…Moreover, to our knowledge, only one study [46] reported the isolation of two genes (named JH1 and JH2), whose transcripts accumulate rapidly in response to methoprene. Although the 5h regulating sequence of JH1 can confer JH inducibility to a reporter gene, there is no clear evidence that these genes are direct JH targets in i o.…”

Section: Discussionmentioning

confidence: 99%

A novel putative insect chitinase with multiple catalytic domains: hormonal regulation during metamorphosis

Royer

Fraichard

Bouhin

2002

Biochemical Journal

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We have used differential display to identify genes that are regulated by juvenile hormone in the epidermis of the beetle Tenebrio molitor. One of the genes encodes T. molitor chitinase 5 (TmChit5), a chitinase possessing an unusual structure. Sequence analysis of TmChit5 identified five ' chitinase units ' of approx. 480 amino acids with similarity to chitinase family 18. These units are separated by less conserved regions containing putative PEST (rich in proline, glutamic acid, serine and threonine) sequences, putative chitin-binding domains and mucin domains. Northern-blot analysis identified a single transcript of approx. 9 kb, whose abundance correlated with that of

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“…In addition, juvenile hormone inducible (JhI)-1 (CG3298) and JhI-26 (CG3767) are up-regulated in SIN3-deficient cells. JhI-1 and JhI-26 are 2 of the 7 genes that are transcriptionally induced in S2 cells in response to treatment with juvenile hormone (JH), a steroid hormone like ecdysone that coordinates Drosophila metamorphosis (43). Finally, as discussed above, SIN3 may interact with the NHR PPAR ortholog and repress the transcription of genes encoding enzymes involved in fatty acid oxidation.…”

Section: Sin3 Functions As a Corepressor For Max And Mad Transcriptiomentioning

confidence: 99%

The SIN3 Deacetylase Complex Represses Genes Encoding Mitochondrial Proteins

Pile

Spellman

Katzenberger

et al. 2003

Journal of Biological Chemistry

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Deacetylation of histones by the SIN3 complex is a major mechanism utilized in eukaryotic organisms to repress transcription. Presumably, developmental and cellular phenotypes resulting from mutations in SIN3 are a consequence of altered transcription of SIN3 target genes. Therefore, to understand the molecular mechanisms underlying SIN3 mutant phenotypes in Drosophila, we used full-genome oligonucleotide microarrays to compare gene expression levels in wild type Drosophila tissue culture cells versus SIN3-deficient cells generated by RNA interference. Of the 13,137 genes tested, 364 were induced and 35 were repressed by loss of SIN3. The ϳ10-fold difference between the number of induced and repressed genes suggests that SIN3 plays a direct role in regulating these genes. The identified genes are distributed throughout euchromatic regions but are preferentially excluded from heterochromatic regions of Drosophila chromosomes suggesting that the SIN3 complex can only access particular chromatin structures. A number of cell cycle regulators were repressed by loss of SIN3, and functional studies indicate that repression of string, encoding the Drosophila homologue of the yeast CDC25 phosphatase, contributes to the G 2 cell cycle delay of SIN3-deficient cells. Unexpectedly, a substantial fraction of genes induced by loss of SIN3 is involved in cytosolic and mitochondrial energy-generating pathways and other genes encode components of the mitochondrial translation machinery. Increased expression of mitochondrial proteins in SIN3-deficient cells is manifested in an increase in mitochondrial mass. Thus, SIN3 may play an important role in regulating mitochondrial respiratory activity.

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The Isolation of Two Juvenile Hormone-Inducible Genes in Drosophila melanogaster

Cited by 92 publications

References 64 publications

Characterization of the Drosophila Methoprene ‐tolerant gene product

Characterization of the Drosophila Methoprene ‐tolerant gene product

A novel putative insect chitinase with multiple catalytic domains: hormonal regulation during metamorphosis

The SIN3 Deacetylase Complex Represses Genes Encoding Mitochondrial Proteins

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