Hedgehog mediated degradation of Ihog adhesion proteins modulates cell segregation in Drosophila wing imaginal discs

Elaine Y. C. Hsia, Ya Zhang, Hai Son Tran, Agnes Lim, Ya-Hui Chou, Ganhui Lan, Philip A. Beachy () and Xiaoyan Zheng ()
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Elaine Y. C. Hsia: George Washington University School of Medicine and Health Sciences
Ya Zhang: George Washington University School of Medicine and Health Sciences
Hai Son Tran: George Washington University School of Medicine and Health Sciences
Agnes Lim: Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine
Ya-Hui Chou: Academia Sinica
Ganhui Lan: George Washington University
Philip A. Beachy: Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine
Xiaoyan Zheng: George Washington University School of Medicine and Health Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract The Drosophila Hedgehog receptor functions to regulate the essential downstream pathway component, Smoothened, and to limit the range of signaling by sequestering Hedgehog protein signal within imaginal disc epithelium. Hedgehog receptor function requires both Patched and Ihog activity, the latter interchangeably encoded by interference hedgehog (ihog) or brother of ihog (boi). Here we show that Patched and Ihog activity are mutually required for receptor endocytosis and degradation, triggered by Hedgehog protein binding, and causing reduced levels of Ihog/Boi proteins in a stripe of cells at the anterior/posterior compartment boundary of the wing imaginal disc. This Ihog spatial discontinuity may contribute to classically defined cell segregation and lineage restriction at the anterior/posterior wing disc compartment boundary, as suggested by our observations that Ihog activity mediates aggregation of otherwise non-adherent cultured cells and that loss of Ihog activity disrupts wing disc cell segregation, even with downstream genetic rescue of Hedgehog signal response.

Date: 2017
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DOI: 10.1038/s41467-017-01364-z

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