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Worniu, a Snail family zinc‐finger protein, is required for brain development in Drosophila
Author(s) -
Ashraf Shovon I.,
Ganguly Atish,
Roote John,
Ip Y. Tony
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20130
Subject(s) - biology , neuroblast , imaginal disc , snail , zinc finger , genetics , mesoderm , phenotype , microbiology and biotechnology , rna interference , neurogenesis , morphogenesis , cell fate determination , mutant , embryonic stem cell , gene , transcription factor , ecology , rna
The Snail family of zinc‐finger transcriptional repressors is essential for morphogenetic cell movements, mesoderm formation, and neurogenesis during embryonic development. These proteins also control cell cycle, cell death, and cancer progression. In Drosophila , three members of this protein family, Snail, Escargot, and Worniu, have essential but redundant functions in asymmetric cell division of neuroblasts. In addition, Snail is critical for early mesoderm formation and Escargot is required for maintaining diploidy in wing imaginal disc cells. In this report, we demonstrate that Worniu plays a role in brain development. We show that alleles of the l(2)35Da complementation group are mutants of worniu . The developing larvae of these mutant alleles fail to shorten their brainstems. The brain phenotype, as well as the lethality, of these mutants can be rescued by worniu transgenes. Moreover, RNAi experiments targeting the worniu transcript show the same nonshortening phenotype in larval brains. worniu is expressed in the neuroblasts of brain hemispheres and ventral ganglions. The results suggest that the loss of Worniu function within the neuroblasts ultimately causes the larval brainstem to fail to go through shortening during development. Developmental Dynamics 231:379–386, 2004. © 2004 Wiley‐Liss, Inc.