4.4 Article

Complementary expression of optomotor-blind and the Iroquois complex promotes fold formation to separate wing notum and hinge territories

期刊

DEVELOPMENTAL BIOLOGY
卷 416, 期 1, 页码 225-234

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2016.05.020

关键词

optomotor-blind; Iroquois complex; Hinge notum fold; Drosophila; Wing disc

资金

  1. National Natural Science Foundation of China [31372255]
  2. National Basic Research Program of China (973 Program) [2013CB127603]
  3. Chinese Universities Scientific Fund [2013XJ011, 2016QC079]

向作者/读者索取更多资源

Animal morphogenesis requires folds or clefts to separate populations of cells which are often associated with different cell affinities. In the Drosophila wing imaginal disc, the regional expression of the Iroquois complex (Iro-C) in the notum leads to the formation of the hinge/notum (H/N) fold that separates the wing hinge and notum territories. Although Decapentaplegic (Dpp) signaling has been revealed as essential for the hinge/notum subdivision through the restriction of Iro-C toward the notum region, the mechanism by which the H/N border develops into a fold is unknown. Here, we report that a Dpp target gene, optomotor-blind (omb), mediates the role of Dpp signaling in Iro-C inhibition. omb is complementarily expressed on the dorsal hinge side, abutting the Iro-C domain along the H/N border. Ectopic omb expression inhibits Iro-C in the notum territory, independent of known Iro-C regulators Msh and Stat92E. Uniform manipulation of either omb or Iro-C genes spanning the presumptive H/N border significantly suppresses H/N fold formation via inhibition of the apical microtubule enrichment. Ectopically sharp border or discontinuity in level of Iro-C or Omb is enough to generate ectopic fold formation. These results reveal that omb and Iro-C not only are complementarily expressed but also cooperate to promote H/N fold formation. Our data help to understand how Dpp signaling is interpreted region-specifically during tissue subdivision. (C) 2016 The Authors. Published by Elsevier Inc.

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