ALTERNATIVE SPLICE FORM OF TYPE-II PROCOLLAGEN MESSENGER-RNA (IIA) ISPREDOMINANT IN SKELETAL PRECURSORS AND NON-CARTILAGINOUS TISSUES DURING EARLY MOUSE DEVELOPMENT

Citation
Lj. Sandell et al., ALTERNATIVE SPLICE FORM OF TYPE-II PROCOLLAGEN MESSENGER-RNA (IIA) ISPREDOMINANT IN SKELETAL PRECURSORS AND NON-CARTILAGINOUS TISSUES DURING EARLY MOUSE DEVELOPMENT, Developmental dynamics, 199(2), 1994, pp. 129-140
Citations number
34
Categorie Soggetti
Developmental Biology","Anatomy & Morphology
Journal title
ISSN journal
10588388
Volume
199
Issue
2
Year of publication
1994
Pages
129 - 140
Database
ISI
SICI code
1058-8388(1994)199:2<129:ASFOTP>2.0.ZU;2-G
Abstract
Type II collagen, generally considered to be characteristic of cartila ge, has been localized in specific non-cartilaginous structures during embryogenesis and development of the skeleton. Type II procollagen is synthesized in two different forms generated by alternative splicing of exon 2 in the precursor mRNA transcript. One form (type IIA procoll agen) contains a large cysteine-rich domain in the NH2-terminal propep tide, while the second form (type IIB procollagen) does not. These two forms are spatially expressed during development and chondrogenesis w ith the type IIB procollagen mRNA primarily expressed by chondrocytes while the IIA form is expressed in chondroprogenitor cells (Sandell et al. [1991] J. Cell Biol. 114:1307-1319). The present study demonstrat es that the early non-cartilage expression, by somites, mesenchymal an d epithelial cells, is predominately the alternate splice form, type I IA procollagen mRNA. Later in development, the type IIB mRNA splice fo rm is expressed by chondrocytes. During the development of intramembra nous bones, such as the mandible, type IIA procollagen mRNA is also ex pressed. In this tissue, the splice form does not switch to type IIB m RNA and no cartilage is formed. These results show that expression of type IIA mRNA, whether by epithelial or mesenchymal cells, precedes fo rmation of overt skeletal structures. (C) 1994 Wiley-Liss, Inc.