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sox21a directs lateral line patterning by modulating FGF signaling

ABSTRACT The development of organs composed by repeated functional units is, in many cases, accomplished by the transition of cells from a progenitor to a differentiation domain, triggering a reiterated developmental program. Yet, how these discrete fields are formed during development is still a la...

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Published in:Developmental neurobiology (Hoboken, N.J.) N.J.), 2015-01, Vol.75 (1), p.80-92
Main Authors: Ariza‐Cosano, Ana, Bensimon‐Brito, Anabela, Gómez‐Skarmeta, José Luis, Bessa, José
Format: Article
Language:English
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Summary:ABSTRACT The development of organs composed by repeated functional units is, in many cases, accomplished by the transition of cells from a progenitor to a differentiation domain, triggering a reiterated developmental program. Yet, how these discrete fields are formed during development is still a largely unresolved question. The posterior lateral line (pLL), a sensory organ present in fish and amphibians, develops from a primordium that migrates along the flanks of the animal periodically depositing neuromasts, the pLL functional units. In zebrafish (Danio rerio), the developmental program of the pLL is triggered by the transit of progenitor cells from a Wnt to a Fgf signaling domain. It has been proposed that these two fields are defined by the antagonistic activity of these two signaling pathways, but how they are formed and maintained is still an open question in the development of the pLL. In this work, we show that sox21a, an HMG ‐box transcription factor, is expressed within the Fgf domain. We demonstrate that, while the Fgf signaling pathway do not control sox21a, knockdown of sox21a causes impairment of Fgf signaling, expansion of the Wnt signaling domain and disruption of neuromast development. These results suggest that sox21a is a key player in the pLL primordium patterning, fine‐tuning the border of the Fgf and Wnt signaling domains. © 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 80–92, 2015
ISSN:1932-8451
1932-846X
DOI:10.1002/dneu.22211