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A branching morphogenesis program governs embryonic growth of the thyroid gland

Journal article
Authors Shawn Liang
Ellen Johansson
G. Barila
D. L. Altschuler
Henrik Fagman
Mikael Nilsson
Published in Development
Volume 145
Issue 2
ISSN 0950-1991
Publication year 2018
Published at Institute of Biomedicine
Language en
Links dx.doi.org/10.1242/dev.146829
Keywords Thyroid, Progenitor, Fgf10, Sox9, Mouse, Growth, Differentiation, epithelial-mesenchymal interactions, neural crest, lung morphogenesis, chick-embryo, cell differentiation, progenitor cells, gene-expression, essential roles, stem-cells, mouse lung, Developmental Biology, ates of america, v110, pe4456, ates of america, v104, p1865
Subject categories Cell and Molecular Biology

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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