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The LIM protein, CRP1, is a smooth muscle marker
Author(s) -
Henderson James R.,
Macalma Teresita,
Brown Doris,
Richardson James A.,
Olson Eric N.,
Beckerle Mary C.
Publication year - 1999
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/(sici)1097-0177(199903)214:3<229::aid-aja6>3.0.co;2-s
Subject(s) - biology , in situ hybridization , microbiology and biotechnology , embryonic stem cell , ectopic expression , gene expression , zinc finger , skeletal muscle , gene , genetics , anatomy , transcription factor
LIM domains are double zinc‐finger motifs found in many proteins that play central roles in cell differentiation. Members of the cysteine‐rich protein (CRP) family display two LIM domains and are implicated in muscle development. Here we describe the characterization of one member of this family, CRP1, in the mouse. We have isolated and sequenced murine cDNAs that encode CRP1. We have determined by Northern analysis and in situ hybridization that CRP1 expression is developmentally regulated in the embryonic mouse and displays organ specific regulation in adults. The gene encoding CRP1 is expressed in the smooth muscle cells (SMCs) of the dorsal aorta at E9.5, thus illustrating that CRP1 is an early marker for SMC differentiation at that site. As development proceeds, CRP1 transcripts are observed throughout the SMC lineage, with minimal, transient expression detected in skeletal and cardiac muscle. Interestingly, although several markers of mature smooth muscle are already expressed, CRP1 expression in the bladder is not upregulated until the onset of bladder expansion at embryonic day 16.5, at which time its expression becomes very prominent. CRP1 expression persists into adulthood with prominent expression observed in both vascular and visceral smooth muscle. The results reported here define CRP1 as a general marker of smooth muscle lineages. Dev Dyn 1999;214:229–238. © 1999 Wiley‐Liss, Inc.