Article
Opposing effects on TSC-22 expression by BMP and receptor tyrosine kinase signals in the developing feather tract
Article first published online: 29 NOV 2001
DOI: 10.1002/dvdy.1236
Copyright © 2002 Wiley-Liss, Inc.
Additional Information
How to Cite
Dohrmann, C. E., Noramly, S., Raftery, L. A. and Morgan, B. A. (2002), Opposing effects on TSC-22 expression by BMP and receptor tyrosine kinase signals in the developing feather tract. Dev. Dyn., 223: 85–95. doi: 10.1002/dvdy.1236
Publication History
- Issue published online: 10 JAN 2002
- Article first published online: 29 NOV 2001
- Manuscript Accepted: 10 SEP 2001
- Manuscript Received: 12 MAR 2001
Funded by
- ACS. Grant Number: RPG-00-251-01-DDC
- NIH. Grant Number: R01 HD38465
- Abstract
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- Cited By
Keywords:
- TSC-22;
- chick;
- feather bud;
- appendage development;
- EGF;
- BMP;
- FGF;
- receptor tyrosine kinase;
- TGF-β superfamily;
- pattern formation
Abstract
TSC-22 (transforming growth factor-β–stimulated clone 22) belongs to a family of leucine zipper transcription factors that includes sequences from invertebrates and vertebrates. The single Drosophila family member, encoded by the bunched gene, serves to integrate opposing bone morphogenic protein (BMP) and epidermal growth factor (EGF) signals during oogenesis. Similarly, mammalian TSC-22 expression is regulated by several families of secreted signaling molecules in cultured cells. Here, we show that chick TSC-22 is dynamically expressed in the condensing feather bud, as well as in many tissues of the chick embryo. BMP-2/4, previously shown to inhibit bud development, repress TSC-22 expression during feather bud formation in vivo. Noggin, a BMP antagonist, promotes TSC-22 expression. EGF, TGF-α, and fibroblast growth factor all promote both feather bud development and TSC-22 expression; each can promote ectopic feather buds that are regularly spaced between existing feather buds. Thus, TSC-22 is a candidate to integrate small imbalances in receptor tyrosine kinase and BMP signaling during feather tract development to generate stable and reproducible morphogenetic responses. © 2001 Wiley-Liss, Inc.

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