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Molecular and Cellular Biology, January 2000, p. 181-186, Vol. 20, No. 1
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

Bryan E. Hoffman and John T. Lis*

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.


* 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.


Molecular and Cellular Biology, January 2000, p. 181-186, Vol. 20, No. 1
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



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