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Expression of mouse igf2 mRNA‐binding protein 3 and its implications for the developing central nervous system
Author(s) -
Mori Hiroshi,
Sakakibara Shinichi,
Imai Takao,
Nakamura Yuki,
Iijima Takatoshi,
Suzuki Akira,
Yuasa Yoshihiro,
Takeda Masatoshi,
Okano Hideyuki
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1060
Subject(s) - messenger rna , biology , rna binding protein , translation (biology) , microbiology and biotechnology , rna splicing , embryonic stem cell , neuroepithelial cell , gene expression , p bodies , alternative splicing , rna , gene , genetics
Functional analyses of neural RNA‐binding proteins have focused mainly on their roles as modulators of posttranscriptional gene regulation, e.g., alternative splicing, dendritic mRNA localization, and local translation. Here we identified a mouse homologue of human IMP3, which is known to bind to and repress the translation of igf2 leader 3 mRNA. The mouse igf2 mRNA‐binding protein 3 (mIMP3) is a member of the zipcode binding protein‐1 (ZBP‐1) family previously reported in chick fibroblast cells. mIMP3 was expressed in undifferentiated neuroepithelial cells and some postmitotic neurons at early embryonic stages (E10.5–E12.5), and its expression level decreased after the midembryonic stage (E12.5) until birth. The expression profile of mIMP3 is very similar to that of mouse igf2 leader 3 mRNA. In vitro UV cross‐linking experiments showed that mIMP3 preferentially bound to igf2 leader 3 mRNA rather than igf2 leader 4 mRNA and did not bind the zipcode region of β‐actin or c‐myc mRNA. Furthermore, persistent expression of mIMP3 protein in an undifferentiated P19 cell line revealed that mIMP3 inhibited neuronal differentiation morphologically and immunohistochemically. Taken together, these observations raise the possibility that mIMP3 represses neuronal differentiation through the regulation of igf2 mRNA expression. J. Neurosci. Res. 64:132–143, 2001. © 2001 Wiley‐Liss, Inc.