rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
4
|
pubmed:dateCreated |
1998-7-28
|
pubmed:abstractText |
According to the prevailing model, frameshift-suppressing tRNAs with an extra nucleotide in the anticodon loop suppress +1 frameshift mutations by recognizing a four-base codon and promoting quadruplet translocation. We present three sets of experiments that suggest a general alternative to this model. First, base modification should actually block such a four-base interaction by two classical frameshift suppressors. Second, for one Salmonella suppressor tRNA, it is not mutant tRNA but a structurally normal near cognate that causes the +1 shift in-frame. Finally, frameshifting occurs in competition with normal decoding of the next in-frame codon, consistent with an event that occurs in the ribosomal P site after the translocation step. These results suggest an alternative model involving peptidyl-tRNA slippage at the classical CCC-N and GGG-N frameshift suppression sites.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
1097-2765
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
1
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
471-82
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:9660932-Anticodon,
pubmed-meshheading:9660932-DNA Primers,
pubmed-meshheading:9660932-Frameshift Mutation,
pubmed-meshheading:9660932-Gene Expression Regulation, Bacterial,
pubmed-meshheading:9660932-Gene Expression Regulation, Fungal,
pubmed-meshheading:9660932-Guanosine,
pubmed-meshheading:9660932-Nucleic Acid Conformation,
pubmed-meshheading:9660932-Phenotype,
pubmed-meshheading:9660932-Protein Biosynthesis,
pubmed-meshheading:9660932-RNA, Messenger,
pubmed-meshheading:9660932-RNA, Transfer,
pubmed-meshheading:9660932-Saccharomyces cerevisiae,
pubmed-meshheading:9660932-Salmonella typhimurium
|
pubmed:year |
1998
|
pubmed:articleTitle |
A new model for phenotypic suppression of frameshift mutations by mutant tRNAs.
|
pubmed:affiliation |
Department of Microbiology, Umeå University, Sweden.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|