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Development. 2016 Aug 1;143(15):2803-17. doi: 10.1242/dev.136010. Epub 2016 Jun 17.

LGN plays distinct roles in oral epithelial stratification, filiform papilla morphogenesis and hair follicle development.

Author information

1
Department of Pathology & Laboratory Medicine and Department of Biology, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525, USA.
2
Department of Pathology & Laboratory Medicine and Department of Biology, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525, USA scott_williams@med.unc.edu.

Abstract

Oral epithelia protect against constant challenges by bacteria, viruses, toxins and injury while also contributing to the formation of ectodermal appendages such as teeth, salivary glands and lingual papillae. Despite increasing evidence that differentiation pathway genes are frequently mutated in oral cancers, comparatively little is known about the mechanisms that regulate normal oral epithelial development. Here, we characterize oral epithelial stratification and describe multiple distinct functions for the mitotic spindle orientation gene LGN (Gpsm2) in promoting differentiation and tissue patterning in the mouse oral cavity. Similar to its function in epidermis, apically localized LGN directs perpendicular divisions that promote stratification of the palatal, buccogingival and ventral tongue epithelia. Surprisingly, however, in dorsal tongue LGN is predominantly localized basally, circumferentially or bilaterally and promotes planar divisions. Loss of LGN disrupts the organization and morphogenesis of filiform papillae but appears to be dispensable for embryonic hair follicle development. Thus, LGN has crucial tissue-specific functions in patterning surface ectoderm and its appendages by controlling division orientation.

KEYWORDS:

Gpsm2; Hair follicle; LGN; Oral epithelia; Oriented cell divisions; Papillae; Placode; Tongue

PMID:
27317810
PMCID:
PMC5004909
DOI:
10.1242/dev.136010
[Indexed for MEDLINE]
Free PMC Article

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