Pre-mRNA Splicing by the Essential Drosophila Protein B52: Tissue and Target Specificity

• Published in: Molecular and cellular biology 2000-01, Vol.20 (1), p.181-186
• Main Authors: Hoffman, Bryan E., Lis, John T.
• Format: Article
• Language: English
• Subjects: Animals; B52 protein; Drosophila; Drosophila melanogaster - genetics; Drosophila Proteins; fushi tarazu (ftz) gene; Gene Expression; Gene Expression Regulation; Mutation; Nuclear Proteins - genetics; Organ Specificity; Phosphoproteins - genetics; RNA Precursors - genetics; RNA Splicing; RNA Splicing Factors; RNA-Binding Proteins - genetics; SR proteins
• ISSN: 0270-7306; 1098-5549; 1098-5549
• DOI: 10.1128/MCB.20.1.181-186.2000

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 thisftz pre-mRNA. In contrast, splicing of this sameftz 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 ftzmRNA 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.