Cold-inducible RNA binding protein is required for the expression of adhesion molecules and embryonic cell movement in Xenopus laevis

• Published in: Biochemical and biophysical research communications 2006-05, Vol.344 (1), p.416-424
• Main Authors: Peng, Ying, Yang, Pai-Hao, Tanner, Julian A., Huang, Jian-Dong, Li, Ming, Lee, Henry F., Xu, Ren-He, Kung, Hsiang-Fu, Lin, Marie C.M.
• Format: Article
• Language: English
• Subjects: Animals; Cell Adhesion Molecules - genetics; Cell Adhesion Molecules - metabolism; Cell Lineage - genetics; Cell movement; Cell Movement - genetics; Cold-inducible RNA binding protein; Embryo, Nonmammalian - cytology; Gene Expression Regulation, Developmental; Morphogenetic lineage migration; Nerve Tissue Proteins - antagonists & inhibitors; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - physiology; Neural development; RNA, Antisense - genetics; RNA, Antisense - pharmacology; RNA-Binding Proteins - antagonists & inhibitors; RNA-Binding Proteins - genetics; RNA-Binding Proteins - physiology; Xenopus; Xenopus laevis; Xenopus laevis - embryology; Xenopus laevis - genetics; Xenopus laevis - metabolism; Xenopus Proteins - antagonists & inhibitors; Xenopus Proteins - genetics; Xenopus Proteins - physiology
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2006.03.086

We have previously shown that the Xenopus homologue of cold-inducible RNA binding protein, XCIRP-1, is required for the morphogenetic migration of the pronephros during embryonic development. However, the underlying molecular mechanisms remain elusive. Here, we report that XCIRP is essential for embryonic cell movement, as suppression of XCIRP by microinjection of anti-sense mRNA and morpholino antisense oligonucleotides (MOs) significantly reduced protein expression, inhibited the cell migration rate, and inhibited eFGF and activin-induced animal cap elongation. By immunoprecipitation and RT-PCR, we further showed that the mRNA of a panel of adhesion molecules, including αE- and β-catenin, C- and E-cadherin, and paraxial proto-cadherin, are the targets of XCIRP. Consistently, in animal cap explant studies, suppression of XCIRP by MOs inhibited the expression of these adhesion molecules, while over-expression of sense XCIRP-1 mRNA fully rescued this inhibition. Taken together, these results suggest for the first time that XCIRP is required to maintain the expression of adhesion molecules and cell movement during embryonic development.