title: Lobe and Serrate are required for cell survival during early eye development in Drosophila.
abstract: 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.
authors.affiliation: Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. asingh@bcm.edu
authors.forename: Amit
authors.initials: A
authors.lastname: Singh
authors.forename: Xiao
authors.initials: X
authors.lastname: Shi
authors.forename: Kwang-Wook
authors.initials: KW
authors.lastname: Choi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002135:Calcium-Binding Proteins / Q000235:genetics*; D020169:Caspases / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics; D029721:Drosophila Proteins / Q000235:genetics*; D004331:Drosophila melanogaster / Q000166:cytology / Q000235:genetics* / Q000254:growth & development*; D005123:Eye / Q000166:cytology / Q000254:growth & development*; D005136:Eye Proteins / Q000235:genetics*; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D000072100:Jagged-1 Protein; D008565:Membrane Proteins / Q000235:genetics*; D008954:Models, Biological; D009154:Mutation; D010641:Phenotype; D011518:Proto-Oncogene Proteins / Q000235:genetics; D000072099:Serrate-Jagged Proteins; D015398:Signal Transduction; D051155:Wnt1 Protein
chemical_list: D002135:Calcium-Binding Proteins; D029721:Drosophila Proteins; D005136:Eye Proteins; D036341:Intercellular Signaling Peptides and Proteins; D000072100:Jagged-1 Protein; C465399:L protein, Drosophila; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; C000606278:Ser protein, Drosophila; D000072099:Serrate-Jagged Proteins; D051155:Wnt1 Protein; C074622:wg protein, Drosophila; D048031:JNK Mitogen-Activated Protein Kinases; D020169:Caspases