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Molecular and Cellular Biology, January 2000, p. 181-186, Vol. 20, No. 1
Department of Molecular Biology and Genetics,
Cornell University, Ithaca, New York 14853
Received 13 May 1999/Returned for modification 17 June
1999/Accepted 27 September 1999
B52, an essential SR protein of Drosophila
melanogaster, stimulates pre-mRNA splicing in splicing-deficient
mammalian S100 extracts. Surprisingly, mutant larvae depleted of B52
were found to be capable of splicing at least several pre-mRNAs tested
(H. Z. Ring and J. T. Lis, Mol. Cell. Biol. 14:7499-7506,
1994). In a homologous in vitro system, we demonstrated that B52
complements a Drosophila S100 extract to allow splicing
of a Drosophila fushi tarazu
(ftz) mini-pre-mRNA. Moreover, Kc cell nuclear extracts that were immunodepleted of B52 lost their ability to splice this ftz pre-mRNA. In contrast, splicing of this same
ftz pre-mRNA occurred in whole larvae homozygous for the
B52 deletion. Other SR protein family members isolated from
these larvae could substitute for B52 splicing activity in vitro. We
also observed that SR proteins are expressed variably in different
larval tissues. B52 is the predominant SR protein in specific tissues,
including the brain. Tissues in which B52 is normally the major SR
protein, such as larval brain tissue, failed to produce ftz
mRNA in the B52 deletion line. These observations support a
model in which the lethality of the B52 deletion strain is
a consequence of splicing defects in tissues in which B52 is normally
the major SR protein.
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Pre-mRNA Splicing by the Essential
Drosophila Protein B52: Tissue and Target
Specificity
*
Corresponding author. Mailing address: 416 Biotechnology Building, Cornell University, Ithaca, NY 14850. Phone:
(607) 255-2442. Fax: (607) 272-6249. E-mail:
jtl10{at}cornell.edu.
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