Splicing of Yeast aI5β Group I Intron Requires SUV3 to Recycle MRS1 via Mitochondrial Degradosome-promoted Decay of Excised Intron Ribonucleoprotein (RNP)
Autor: | Mark G. Caprara, Edward M. Turk |
---|---|
Rok vydání: | 2010 |
Předmět: |
Saccharomyces cerevisiae Proteins
Molecular Sequence Data Exonic splicing enhancer Saccharomyces cerevisiae Biology Biochemistry DEAD-box RNA Helicases Mitochondrial Proteins Splicing factor Protein Isoforms Mitochondrial degradosome Molecular Biology Alleles Genetics Base Sequence Group I intron splicing Intron RNA-Binding Proteins RNA Fungal Cell Biology Group II intron Introns Mitochondria Protein Structure Tertiary Cell biology Alternative Splicing Ribonucleoproteins RNA splicing RNA Nucleic Acid Conformation Degradosome RNA Helicases |
Zdroj: | Journal of Biological Chemistry. 285:8585-8594 |
ISSN: | 0021-9258 |
DOI: | 10.1074/jbc.m109.090761 |
Popis: | Yeast Suv3p is a member of the DEXH/D box family of RNA helicases and is a critical component of the mitochondrial degradosome, which also includes a 3' --5' exonuclease, Dss1p. Defects in the degradosome result in accumulation of aberrant transcripts, unprocessed transcripts, and excised group I introns. In addition, defects in SUV3 result in decreased splicing of the aI5beta and bI3 group I introns. Whereas a role for Suv3p in RNA degradation is well established, the function of Suv3p in splicing of group I introns has remained elusive. It has been particularly challenging to determine if Suv3p effects group I intron splicing through RNA degradation as part of the degradosome, or has a direct role in splicing as a chaperone, because nearly all perturbations of SUV3 or DSS1 result in loss of the mitochondrial genome. Here we utilized the suv3-1 allele, which is defective in RNA metabolism and yet maintains a stable mitochondrial genome, to investigate the role of Suv3p in splicing of the aI5beta group I intron. We provide genetic evidence that Mrs1p is a limiting cofactor for aI5beta splicing, and this evidence also suggests that Suv3p activity is required to recycle the excised aI5beta ribonucleoprotein. We also show that Suv3p acts indirectly as a component of the degradosome to promote aI5beta splicing. We present a model whereby defects in Suv3p result in accumulation of stable, excised group I intron ribonucleoproteins, which result in sequestration of Mrs1p, and a concomitant reduction in splicing of aI5beta. |
Databáze: | OpenAIRE |
Externí odkaz: |