neuralized functions cell-autonomously to regulate a subset of notch-dependent processes during adult Drosophila development

Authors
Citation
Ec. Lai et Gm. Rubin, neuralized functions cell-autonomously to regulate a subset of notch-dependent processes during adult Drosophila development, DEVELOP BIO, 231(1), 2001, pp. 217-233
Citations number
65
Categorie Soggetti
Cell & Developmental Biology
Journal title
DEVELOPMENTAL BIOLOGY
ISSN journal
00121606 → ACNP
Volume
231
Issue
1
Year of publication
2001
Pages
217 - 233
Database
ISI
SICI code
0012-1606(20010301)231:1<217:NFCTRA>2.0.ZU;2-O
Abstract
neuralized (neu) represents one of the strong neurogenic mutants in Drosoph ila. Mutants of this class display, among other phenotypes, a strong overco mmitment to neural fates at the expense of epidermal fates. We analyzed the role of neu during adult development by using mutant clonal analysis, mise xpression of wild-type and truncated forms of Neu, and examination of genet ic interactions with N-pathway mutations. We find that neu is required cell -autonomously for lateral inhibition during peripheral neurogenesis and for multiple asymmetric cell divisions in the sensory lineage. In contrast, ne u is apparently dispensable for other N-mediated processes, including later al inhibition during wing vein development and wing margin induction. Misex pression of wild-type Neu causes defects in both peripheral neurogenesis an d wing vein development, while a truncated form lacking the RING finger is further capable of inhibiting formation of the wing margin. In addition, th e phenotypes produced by misexpression of wild-type and truncated Neu prote ins are sensitive to the dosage of several N-pathway components. Finally, u sing epitope-tagged Neu proteins, we localize Neu to the plasma membrane an d reveal a novel morphology to the sensory organ precursor cells of wing im aginal discs. Collectively, these data indicate a key role for neu in the r eception of the lateral inhibitory signal during peripheral neurogenesis. ( C) 2001 Academic Press.