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Publication : Lacrimal gland budding requires PI3K-dependent suppression of EGF signaling.

First Author  Wang Q Year  2021
Journal  Sci Adv Volume  7
Issue  27 PubMed ID  34193412
Mgi Jnum  J:314221 Mgi Id  MGI:6815325
Doi  10.1126/sciadv.abf1068 Citation  Wang Q, et al. (2021) Lacrimal gland budding requires PI3K-dependent suppression of EGF signaling. Sci Adv 7(27)
abstractText  The patterning of epithelial buds is determined by the underlying signaling network. Here, we study the cross-talk between phosphoinositide 3-kinase (PI3K) and Ras signaling during lacrimal gland budding morphogenesis. Our results show that PI3K is activated by both the p85-mediated insulin-like growth factor (IGF) and Ras-mediated fibroblast growth factor (FGF) signaling. On the other hand, PI3K also promotes extracellular signal-regulated kinase (ERK) signaling via a direct interaction with Ras. Both PI3K and ERK are upstream regulators of mammalian target of rapamycin (mTOR), and, together, they prevent expansion of epidermal growth factor (EGF) receptor expression from the lacrimal gland stalk to the bud region. We further show that this suppression of EGF signaling is necessary for induction of lacrimal gland buds. These results reveal that the interplay between PI3K, mitogen-activated protein kinase, and mTOR mediates the cross-talk among FGF, IGF, and EGF signaling in support of lacrimal gland development.
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