The N-terminus zinc finger domain of Xenopus SIP1 is important for neural induction, but not for suppression of Xbra expression
Open Access | Short Communication | Published: 1 May 2007
Kazuhiro R. Nitta1, Shuji Takahashi2,3, Yoshikazu Haramoto2, Masakazu Fukuda1, Kousuke Tanegashima2, Yasuko Onuma4 and Makoto Asashima1,2,3,4,5,*
1Department of Biological Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 2Department of Life Sciences (Biology), Graduate School of Arts and Sciences, The University of Tokyo, 3Center for Structuring Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 4Network for Life Science Education, The University of Tokyo, and 5ICORP Organ Regeneration Project, Japan Science and Technology Agency (JST), Tokyo, Japan
Smad-interacting protein-1 (SIP1), also known as deltaEF2, ZEB2 and zfhx1b, is essential for the formation of the neural tube and the somites. Overexpression of Xenopus SIP1 causes ectopic neural induction via inhibition of bone morphogenetic protein (BMP) signaling and inhibition of Xbra expression. Here, we report the functional analyses of 4 domain-deletion mutants of XSIP1. Deletion of the N-terminus zinc finger domain suppressed neural induction and BMP inhibition, but these were not affected by deletion of the other domains (the Smad binding domain, the DNA-binding homeodomain together with the CtBP binding site and the C-terminus zinc finger). Therefore SIP1 does not inhibit BMP signaling by binding to Smad proteins. In contrast, all of the deletion constructs inhibited Xbra expression. These results suggest that the N-terminus zinc finger domain of XSIP1 has an important role in neural induction and that Xbra suppression occurs via a mechanism separate from the neural inducing activity.