The nuclear SUV3-1 mutation affects a variety of post-transcriptional processes in yeast mitochondria
The SUV3-1 mutation was isolated earlier as a suppressor of a deletion of a conserved RNA processing site (dodecamer) near the 3' end of the var1 gene. Previous studies indicate that the suppressor enhances translation of mutant var1 messages; unexpectedly, it also causes over-accumulation of e...
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Published in | Nucleic acids research Vol. 18; no. 6; pp. 1369 - 1376 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
25.03.1990
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Subjects | |
Online Access | Get full text |
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Summary: | The SUV3-1 mutation was isolated earlier as a suppressor of a deletion of a conserved RNA processing site (dodecamer) near the 3' end of the var1 gene. Previous studies indicate that the suppressor enhances translation of mutant var1 messages; unexpectedly, it also causes over-accumulation of excised intron RNA of the large rRNA gene intron and blocks cleavage at the dodecamer site within that intron. In this study most mitochondrial genes in SUV3-1 and suv3 nuclear contexts are surveyed for changes in levels of mRNA, for interference with dodecamer cleavage and splicing and for levels of excised intron RNAs. SUV3-1 has little or no effect on the size or abundance of unspliced RNAs tested. It results, however, in a marked increase in the abundance of seven of eight excised group I intron RNAs tested, most of which are not detectable in wild-type (suv3) strains. The suppressor lowers levels of the cob and coxl mRNAs about 2-5 and 20-fold, respectively. The effect on coxl mRNA results from a decrease in the splicing of its intron 5 beta. Despite the reduction in these mRNA levels, the amounts of coxl and cyt b polypeptides were close to wild-type levels in SUV3-1 cells. These data show that the suv3 gene plays a prominent role in post-transcriptional and translation events in yeast mitochondria. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0305-1048 1362-4962 |
DOI: | 10.1093/nar/18.6.1369 |