| Autor: |
Hendrick JL; Laboratories of Genetics and Molecular Biology, University of Wisconsin, Madison, Wisconsin 53706, USA., Wilson PG, Edelman II, Sandbaken MG, Ursic D, Culbertson MR |
| Jazyk: |
angličtina |
| Zdroj: |
Genetics [Genetics] 2001 Mar; Vol. 157 (3), pp. 1141-58. |
| DOI: |
10.1093/genetics/157.3.1141 |
| Abstrakt: |
The SUF13 and SUF14 genes were identified among extragenic suppressors of +1 frameshift mutations. SUF13 is synonymous with MBF1, a single-copy nonessential gene coding for a POLII transcription factor. The suf13-1 mutation is a two-nucleotide deletion in the SUF13/MBF1 coding region. A suf13::TRP1 null mutant suppresses +1 frameshift mutations, indicating that suppression is caused by loss of SUF13 function. The suf13-1 suppressor alters sensitivity to aminoglycoside antibiotics and reduces the accumulation of his4-713 mRNA, suggesting that suppression is mediated at the translational level. The SUF14 gene is synonymous with RPS3, a single-copy essential gene that codes for the ribosomal protein S3. The suf14-1 mutation is a missense substitution in the coding region. Increased expression of S3 limits the accumulation of SUF14 mRNA, suggesting that expression is autoregulated. A frameshift mutation in SUF14 that prevents full-length translation eliminated regulation, indicating that S3 is required for regulation. Using CUP1-SUF14 and SUF14-lacZ fusions, run-on transcription assays, and estimates of mRNA half-life, our results show that transcription plays a minor role if any in regulation and that the 5'-UTR is necessary but not sufficient for regulation. A change in mRNA decay rate may be the primary mechanism for regulation. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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