Format

Send to

Choose Destination
See comment in PubMed Commons below
Dev Biol. 2013 Nov 1;383(1):75-89. doi: 10.1016/j.ydbio.2013.08.018. Epub 2013 Sep 2.

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity.

Author information

1
Department of Biological Sciences, Western Michigan University, Kalamazoo, MI 49008, USA; Department of Organismal Biology and Anatomy, University of Chicago, 1027 East, 57th Street, Chicago, IL 60637, USA. Electronic address: rachel.warga@wmich.edu.

Abstract

Progenitors of the zebrafish pronephros, red blood and trunk endothelium all originate from the ventral mesoderm and often share lineage with one another, suggesting that their initial patterning is linked. Previous studies have shown that spadetail (spt) mutant embryos, defective in tbx16 gene function, fail to produce red blood cells, but retain the normal number of endothelial and pronephric cells. We report here that spt mutants are deficient in all the types of early blood, have fewer endothelial cells as well as far more pronephric cells compared to wildtype. In vivo cell tracing experiments reveal that blood and endothelium originate in spt mutants almost exclusive from the dorsal mesoderm whereas, pronephros and tail originate from both dorsal and ventral mesoderm. Together these findings suggest possible defects in posterior patterning. In accord with this, gene expression analysis shows that mesodermal derivatives within the trunk and tail of spt mutants have acquired more posterior identity. Secreted signaling molecules belonging to the Fgf, Wnt and Bmp families have been implicated as patterning factors of the posterior mesoderm. Further investigation demonstrates that Fgf and Wnt signaling are elevated throughout the nonaxial region of the spt gastrula. By manipulating Fgf signaling we show that Fgfs both promote pronephric fate and repress blood and endothelial fate. We conclude that Tbx16 plays an important role in regulating the balance of intermediate mesoderm fates by attenuating Fgf activity.

KEYWORDS:

Blood; Endothelium; Fgf8; Intermediate mesoderm; Pronephros; Tbx16

PMID:
24008197
PMCID:
PMC3919442
DOI:
10.1016/j.ydbio.2013.08.018
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center