QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online November 7, 2006
doi: 10.1242/10.1242/dev.02686

This Article Figures Only Full Text Full Text (PDF) Supplementary Material Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Singh, A. Articles by Choi, K.-W. Search for Related Content PubMed PubMed Citation Articles by Singh, A. Articles by Choi, K.-W.

Lobe and Serrate are required for cell survival during early eye development in Drosophila

¹ Department of Molecular and Cellular Biology, One Baylor Plaza, Houston, TX 77030, USA.
² Program in Developmental Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
³ Department of Ophthalmology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

^* Authors for correspondence (e-mail: asingh{at}bcm.edu; kchoi{at}bcm.tmc.edu)

Accepted 2 October 2006

Organogenesis involves an initial surge of cell proliferation, leading to differentiation. This is followed by cell death in order to remove extra cells. During early development, there is little or no cell death. However, there is a lack of information concerning the genes required for survival during the early cell-proliferation phase. Here, we show that Lobe (L) and the Notch (N) ligand Serrate (Ser), which are both involved in ventral eye growth, are required for cell survival in the early eye disc. We observed that the loss-of-ventral-eye phenotype in L or Ser mutants is due to the induction of cell death and the upregulation of secreted Wingless (Wg). This loss-of-ventral-eye phenotype can be rescued by (i) increasing the levels of cell death inhibitors, (ii) reducing the levels of Hid-Reaper-Grim complex, or (iii) reducing canonical Wg signaling components. Blocking Jun-N-terminal kinase (JNK) signaling, which can induce caspase-independent cell death, significantly rescued ventral eye loss in L or Ser mutants. However, blocking both caspase-dependent cell death and JNK signaling together showed stronger rescues of the L- or Ser-mutant eye at a 1.5-fold higher frequency. This suggests that L or Ser loss-of-function triggers both caspase-dependent and -independent cell death. Our studies thus identify a mechanism responsible for cell survival in the early eye.

Key words: Drosophila eye, Cell survival, Cell death, JNK Signaling, Wg Signaling, Lobe, Serrate

This article has been cited by other articles:

				N. Oshiro, R. Takahashi, K.-i. Yoshino, K. Tanimura, A. Nakashima, S. Eguchi, T. Miyamoto, K. Hara, K. Takehana, J. Avruch, et al. The Proline-rich Akt Substrate of 40 kDa (PRAS40) Is a Physiological Substrate of Mammalian Target of Rapamycin Complex 1 J. Biol. Chem., July 13, 2007; 282(28): 20329 - 20339. [Abstract] [Full Text] [PDF]