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Edward M. Berger

Researcher at Dartmouth College

Publications -  61
Citations -  2765

Edward M. Berger is an academic researcher from Dartmouth College. The author has contributed to research in topics: Drosophila melanogaster & Ecdysterone. The author has an hindex of 29, co-authored 61 publications receiving 2707 citations. Previous affiliations of Edward M. Berger include University at Albany, SUNY.

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Temporal regulation of microRNA expression in Drosophila melanogaster mediated by hormonal signals and Broad-Complex gene activity

TL;DR: This work characterized the developmental expression profile of 24 miRNAs in Drosophila, and found 7 mi RNAs that are either upregulated or downregulated in conjunction with metamorphosis, indicating the participation of both these hormones in the temporal regulation of mir-34, -100, -125, and let-7 expression in vivo.
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Ecdysterone induces the transcription of four heat-shock genes in Drosophila S3 cells and imaginal discs.

TL;DR: A parallel in vivo situation is now described in imaginal discs isolated from pupariating larvae, where induction by ecdysterone appears to be a primary hormone response.
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The expression of the let-7 small regulatory RNA is controlled by ecdysone during metamorphosis in Drosophila melanogaster.

TL;DR: An interaction between steroid hormone signaling and the heterochronic pathway in insects is demonstrated, indicating that the ecdysone pathway regulates the temporal expression of let-7 in Drosophila.
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Gene-enzyme variation in three sympatric species of littorina

TL;DR: Gene-enzyme variation was examined, electrophoretically, at three non-specific esterase loci in 15 sympatric populations of the prosobranch gastropods Littorina littorea, revealing marked differences between the species.
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Synthesis of low molecular weight heat shock peptides stimulated by ecdysterone in a cultured Drosophila cell line

TL;DR: Berger et al. as discussed by the authors identified p7 as the 23,000-dalton heat shock polypeptide (hsp23), and showed that ecdysterone stimulation was the result of an increase in the hsp23 RNA content of S3 cells.