File:Thyroid branching model cartoon.jpg

Thyroid branching model cartoon

Proposed models of branching morphogenesis in thyroid development. Left: Bifurcation of the thyroid primordium into two lobes connected across the midline by the isthmus portion may be considered as the first generation of branching morphogenesis. Regression of the thyroglossal duct disconnects the embryonic thyroid from the pharyngeal endoderm. In late thyroid development, branching growth stimulated by Fgf10 derived from adjacent mesenchyme promotes the generation and maturation of follicles and acquisition of final organ size. Arrows indicate growth directions. The precise role of differentially expressed Sox9 in these processes, presumably acting in concert with other thyroid transcription factors (e.g. Nkx2-1 and Pax8), remains to be clarified. Right: An ancestral budding-branching mechanism could hypothetically be involved in an evolutionary switch of thyroid homologs from the exocrine endostyle found in protochordates to the follicular thyroid gland present in all vertebrates with the metamorphosing lamprey representing an intermediate species. b, bud; d, duct (thyroglossal); D, distal; e, endostyle; P, proximal; th, thyroid; ub, ultimobranchial body (the remnant after being fused with the midline thyroid primordium).

Development. 2018 Jan 25;145(2). pii: dev146829. doi: 10.1242/dev.146829. A branching morphogenesis program governs embryonic growth of the thyroid gland. Liang S1, Johansson E1, Barila G2, Altschuler DL2, Fagman H1,3, Nilsson M4. Author information 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. KEYWORDS: Differentiation; Fgf10; Growth; Mouse; Progenitor; Sox9; Thyroid PMID: 29361553 DOI: 10.1242/dev.146829

Fig. 10.

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