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Background  Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of  runx2  and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls ventral activity of maternal  runx2  and how  twists  function in zebrafish embryogenesis still remain unclear.    Methodology/Principal Findings  By studying the loss of  twist  induced by injection of morpholino-oligonucleotide in zebrafish, we found that  twist1a  and  twist1b , but not  twist2  or  twist3 , were required for proper skeletal development and dorsoventral patterning in early embryos. Overexpression of  twist1a  or  twist1b  following mRNA injection resulted in deteriorated skeletal development and formation of typical dorsalized embryos, whereas knockdown of  twist1a  and  twist1b  led to the formation of abnormal embryos with enhanced skeletal formation and typical ventralized patterning. Overexpression of  twist1a  or  twist1b  decreased the expression of  runx2b , whereas twist1a and twist1b knockdown increased  runx2b  expression. We have further demonstrated that phenotypes induced by  twist1a  and  twist1b  knockdown were rescued by  runx2b  knockdown.    Conclusions/Significance  Together, these results suggest that twist1a and twist1b control skeletal development and dorsoventral patterning by regulating  runx2b  in zebrafish and provide potential targets for the treatment of diseases or syndromes associated with decreased skeletal development.

Twist Controls Skeletal Development and Dorsoventral Patterning by Regulating Runx2 in Zebrafish