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Molecular and Cellular Biology, August 2001, p. 4985-4995, Vol. 21, No. 15
Department of Genetics, Cell Biology, and
Development, University of Minnesota, St. Paul, Minnesota 55108
Received 29 March 2001/Accepted 4 May 2001
Mutations in the smu-1 gene of Caenorhabditis
elegans were previously shown to suppress mutations in the
genes mec-8 and unc-52. mec-8 encodes a putative RNA binding protein that
affects the accumulation of specific alternatively spliced mRNA
isoforms produced by unc-52 and other genes.
unc-52 encodes a set of basement membrane proteins,
homologs of mammalian perlecan, that are important for body wall muscle
assembly and attachment to basement membrane, hypodermis, and cuticle.
We show that a presumptive null mutation in smu-1
suppresses nonsense mutations in exon 17 but not exon 18 of
unc-52 and enhances the phenotype conferred by an
unc-52 splice site mutation in intron 16. We have used
reverse transcription-PCR and RNase protection to show
that loss-of-function smu-1 mutations enhance
accumulation in larvae of an alternatively spliced isoform that
skips exon 17 but not exon 18 of unc-52. We have
identified smu-1 molecularly; it encodes a
nuclearly localized protein that contains five WD motifs and is
ubiquitously expressed. The SMU-1 amino acid sequence is more than 60%
identical to a predicted human protein of unknown function. We propose
that smu-1 encodes a trans-acting factor
that regulates the alternative splicing of the pre-mRNA of
unc-52 and other genes.
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.15.4985-4995.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Analysis of smu-1, a Gene That Regulates the
Alternative Splicing of unc-52 Pre-mRNA in
Caenorhabditis elegans
*
Corresponding author. Mailing address: Department of
Genetics, Cell Biology, and Development, University of Minnesota, 250 BioScience Center, 1445 Gortner Ave., St. Paul, MN 55108. Phone: (612)
624-6203. Fax: (612) 625-5754. E-mail: bob-h{at}umn.edu.
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