Churchill regulates cell movement and mesoderm specification by repressing Nodal signaling-1

<p><b>Copyright information:</b></p><p>Taken from "Churchill regulates cell movement and mesoderm specification by repressing Nodal signaling"</p><p>http://www.biomedcentral.com/1471-213X/7/120</p><p>BMC Developmental Biology 2007;7():120-120.</p><p>Published online 2 Nov 2007</p><p>PMCID:PMC2180179.</p><p></p>ected with -EnR mRNA. Inhibition of does not alter expression of dorsal mesodermal genes (A, B) or (C, D). Expression of mesodermal markers at shield stage, including (E-F) and (G-H) are expanded slightly in -inhibited embryos. Overexpression of mRNA does not alter expression at shield stage (I-J). inhibition results in a decrease in Sip1 gene expression at bud stage (M-N), while activation results in Sip1 induction at shield stage (K-L). Real-time PCR analysis of mesodermal markers in -inhibited embryos (O). The fold change in transcript levels (y-axis) is graphed relative to control embryos following overexpression of -EnR mRNA, -ATGMO and mRNA. This analysis reveals that the domains of mesodermal genes are expanded at shield stage while dorsal mesodermal genes are unaffected. Conversely, overexpression of mRNA does not result in alteration of early mesodermal gene expression. The induction of expression following inhibition with the ATGMO can be rescued by co-expression of mRNA (P). Real-time PCR analysis of Sip1 mRNA in -EnR and -ATGMO treated embryos (Q). Induction of results in a 50% increase in Sip1 expression, conversely, inhibition of results in a 70% reduction of Sip1 expression. The fold change in Sip1 transcript levels (y-axis) is graphed relative to control embryos. Views: A-B, K-L are animal pole; C-D, M-N are dorsal; E-J are lateral