Elsevier

Developmental Biology

Volume 392, Issue 1, 1 August 2014, Pages 52-61
Developmental Biology

Regulation of broad by the Notch pathway affects timing of follicle cell development

https://doi.org/10.1016/j.ydbio.2014.04.024Get rights and content
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Highlights

  • Broad is directly regulated by Notch signaling during Drosophila midoogenesis.

  • The regulation of Broad by Notch is through the Su(H) binding sites.

  • Broad, together with Hindsight and Cut, plays a role in the mitotic/endocycle switch.

Abstract

During Drosophila oogenesis, activation of Notch signaling in the follicular epithelium (FE) around stage 6 of oogenesis is essential for entry into the endocycle and a series of other changes such as cell differentiation and migration of subsets of the follicle cells. Notch induces the expression of zinc finger protein Hindsight and suppresses homeodomain protein Cut to regulate the mitotic/endocycle (ME) switch. Here we report that broad (br), encoding a small group of zinc-finger transcription factors resulting from alternative splicing, is a transcriptional target of Notch nuclear effector Suppressor of Hairless (Su(H)). The early pattern of Br in the FE, uniformly expressed except in the polar cells, is established by Notch signaling around stage 6, through the binding of Su(H) to the br early enhancer (brE) region. Mutation of the Su(H) binding site leads to a significant reduction of brE reporter expression in follicle cells undergoing the endocycle. Chromatin immunoprecipitation results further confirm Su(H) binding to the br early enhancer. Consistent with its expression in follicle cells during midoogenesis, loss of br function results in a delayed entry into the endocycle. Our findings suggest an important role of br in the timing of follicle cell development, and its transcriptional regulation by the Notch pathway.

Keywords

Endocycle
Mitotic cycle
Notch
broad

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1

Current address: Structural Biology Center, National Institute of Genetics, 1111 Yata, Mishima 411-8540, Japan