Artigo Acesso aberto Revisado por pares

A branching morphogenesis program governs embryonic growth of the thyroid gland

2017; The Company of Biologists; Volume: 145; Issue: 2 Linguagem: Inglês

10.1242/dev.146829

ISSN

1477-9129

Autores

Shawn Liang, Ellen Johansson, Guillermo Barila, Daniel L. Altschuler, Henrik Fagman, Mikael Nilsson,

Tópico(s)

Animal Genetics and Reproduction

Resumo

ABSTRACT The developmental program that regulates thyroid progenitor cell proliferation is largely unknown. Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. Sox9, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired. These findings demonstrate a novel mechanism of thyroid development reminiscent of the Fgf10-Sox9 program that characterizes organogenesis in classical branching organs, and provide clues to aid understanding of how the endocrine thyroid gland once evolved from an exocrine ancestor present in the invertebrate endostyle.

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