Open AccessBmp signaling maintains a mesoderm progenitor cell state in the mouse tailbud
Author(s) -
Richa Sharma,
Maxwell E.R. Shafer,
Eric Bareke,
Mathieu Tremblay,
Jacek Majewski,
Maxime Bouchard
Publication year - 2017
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.149955
Subject(s) - mesoderm , biology , fgf and mesoderm formation , intermediate mesoderm , brachyury , microbiology and biotechnology , paraxial mesoderm , nodal , progenitor cell , noggin , lateral plate mesoderm , progenitor , embryonic stem cell , stem cell , genetics , bone morphogenetic protein , gene
Caudal somites are generated from a pool of progenitor cells located in the tailbud region. These progenitor cells form the presomitic mesoderm that gradually differentiates into somites under the action of the segmentation clock. The signals responsible for tailbud mesoderm progenitor pool maintenance during axial elongation are still elusive. Here, we show that Bmp signaling is sufficient to activate the entire mesoderm progenitor gene signature in primary cultures of caudal mesoderm cells. Bmp signaling acts through the key regulatory genes Brachyury (T) and Nkx1-2 and contributes to the activation of several other regulators of the mesoderm progenitor gene network. In the absence of Bmp signaling, tailbud mesoderm progenitor cells acquire aberrant gene expression signatures of the heart, blood, muscle and skeletal embryonic lineages. Treatment of embryos with the Bmp inhibitor Noggin confirmed the requirement for Bmp signaling for normal Brachyury expression and the prevention of abnormal lineage marker activation. Together, these results identify Bmp signaling as a non-cell autonomous signal necessary for mesoderm progenitor cell homeostasis.