Journal
DEVELOPMENTAL CELL
Volume 12, Issue 1, Pages 99-112Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2006.12.006
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R37NS033642, R01NS033642] Funding Source: NIH RePORTER
- MRC [G0200709] Funding Source: UKRI
- Medical Research Council [G0200709] Funding Source: Medline
- NINDS NIH HHS [R37 NS033642, R01 NS033642] Funding Source: Medline
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We show that removing the Shh signal tranducer Smoothened from skin epithelium secondarily results in excess Shin levels in the mesenchyme. Moreover, the phenotypes we observe reflect decreased epithelial Shin signaling, yet increased mesenchymal Shh signaling. For example, the latter contributes to exuberant hair follicle (HF) induction, while the former depletes the resulting follicular stem cell niches. This disruption of the niche apparently also allows the remaining stem cells to initiate hair formation at inappropriate times. Thus, the temporal structure of the hair cycle may depend on the physical structure of the niche. Finally, we find that the ablation of epithelial Shh signaling results in unexpected transformations: the follicular outer root sheath takes on an epidermal character, and certain HFs disappear altogether, having adopted a strikingly mammary gland-like fate. Overall, our study uncovers a multifaceted function for Shin in sculpting and maintaining the integrity and identity of the developing HF.
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