Abstract
The early vertebrate embryo extends from anterior to posterior due to the addition of neural and mesodermal cells from a neuromesodermal progenitor (NMp) population located at the most posterior end of the embryo. In order to produce mesoderm throughout this time, the NMps produce their own niche, which is high in Wnt and low in retinoic acid. Using a loss-of-function approach, we demonstrate here that the two most abundant Hox13 genes in zebrafish have a novel role in providing robustness to the NMp niche by working in concert with the niche-establishing factor Brachyury to allow mesoderm formation. Mutants lacking both hoxa13b and hoxd13a in combination with reduced Brachyury activity have synergistic posterior body defects, in the strongest case producing embryos with severe mesodermal defects that phenocopy brachyury null mutants. Our results provide a new way of understanding the essential role of the Hox13 genes in early vertebrate development.This article has an associated 'The people behind the papers' interview.
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