Sostdc1 defines the size and number of skin appendage placodes
Mammary glands and hair follicles develop as ectodermal organs sharing common features during embryonic morphogenesis. The molecular signals controlling the initiation and patterning of skin appendages involve the bone morphogenetic proteins and Wnt family members, which are commonly thought to serv...
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Veröffentlicht in: | Developmental biology 2012-04, Vol.364 (2), p.149-161 |
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Sprache: | eng |
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Zusammenfassung: | Mammary glands and hair follicles develop as ectodermal organs sharing common features during embryonic morphogenesis. The molecular signals controlling the initiation and patterning of skin appendages involve the bone morphogenetic proteins and Wnt family members, which are commonly thought to serve as inhibitory and activating cues, respectively. Here, we have examined the role of the Bmp and Wnt pathway modulator Sostdc1 in mammary gland, and hair and vibrissa follicle development using Sostdc1-null mice. Contrary to previous speculations, loss of Sostdc1 did not affect pelage hair cycling. Instead, we found that Sostdc1 limits the number of developing vibrissae and other muzzle hair follicles, and the size of primary hair placodes. Sostdc1 controls also the size and shape of mammary buds. Furthermore, Sostdc1 is essential for suppression of hair follicle fate in the normally hairless nipple epidermis, but its loss also promotes the appearance of supernumerary nipple-like protrusions. Our data suggest that functions of Sostdc1 can be largely attributed to its ability to attenuate Wnt/β-catenin signaling.
► Sostdc1 (ectodin, Wise, Usag-1) is a secreted Wnt and Bmp pathway modulator. ► Sostdc1 is expressed around developing hair, vibrissae, and mammary placodes. ► Sostdc1 null mice have ectopic vibrissae, but normal hair follicle cycling. ► Loss of Sostdc1 allows more cells to be recruited into mammary buds. ► Loss of Sostdc1 correlates with increased Wnt/β-catenin signaling activity. |
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ISSN: | 0012-1606 1095-564X |
DOI: | 10.1016/j.ydbio.2012.01.026 |