Frameshift Suppression/Suppressor

1990 ◽  
Vol 18 (17) ◽  
pp. 5031-5036 ◽  
Author(s):  
R.A. Spanjaard ◽  
K. Chen ◽  
J.R. Walker ◽  
J. van Duin

1985 ◽  
Vol 5 (9) ◽  
pp. 2247-2256 ◽  
Author(s):  
L Mathison ◽  
M R Culbertson

Fifteen independent ICR-170-induced his4 mutations in Saccharomyces cerevisiae were examined by DNA sequence analysis. All of the mutations contained a +1 G-C base pair addition in the HIS4 coding region. Eleven different sites of insertion were identified. Combined with previous DNA sequence data, 21 ICR-170-induced his4 mutations distributed at 16 different sites were analyzed. The insertions were always located in a consecutive run of two or more G-C base pairs, with all base pairs in each run having identical orientation. Long consecutive G-C runs were preferred target sites over short runs. Although some consecutive G-C runs appeared to be preferred target sites over others of identical length, such preference was not due to any particular type of nucleotide pair immediately adjacent to a given target site. In addition, DNA sequence analyses of the his4 mutations provided a basis for examining the mechanism of mRNA sequence recognition by extragenic suppressors of ICR-170-induced mutations. The implications of these results for mechanisms of frameshift suppression are discussed.


1984 ◽  
Vol 4 (10) ◽  
pp. 2052-2061 ◽  
Author(s):  
R F Gaber ◽  
M R Culbertson

A genetic approach has been used to establish the molecular basis of 4-base codon recognition by frameshift suppressor tRNA containing an extra nucleotide in the anticodon. We have isolated all possible base substitution mutations at the position 4 (N) in the 3'-CCCN-5' anticodon of a Saccharomyces cerevisiae frameshift suppressor glycine tRNA encoded by the SUF16 gene. Base substitutions at +1 frameshift sites in the his4 gene have also been obtained such that all possible 4-base 5'-GGGN-3' codons have been identified. By testing for suppression in different strains that collectively represent all 16 possible combinations of position 4 nucleotides, we show that frameshift suppression does not require position 4 base pairing. Nonetheless, position 4 interactions influence the efficiency of suppression. Our results suggest a model in which 4-base translocation of mRNA on the ribosome is directed primarily by the number of nucleotides in the anticodon loop, whereas the resulting efficiency of suppression is dependent on the nature of position 4 nucleotides.


Genetics ◽  
1980 ◽  
Vol 95 (4) ◽  
pp. 833-853 ◽  
Author(s):  
Michael R Culbertson ◽  
Karen M Underbrink ◽  
Gerald R Fink

ABSTRACT Suppressors of ICR-induced mutations that exhibit behavior similar to bacterial frameshift suppressors have been identified in the yeast Saccharomyces cerevisiae. The yeast suppressors have been divided into two groups. One of these groups (Group II: SUFI, SUF3, SUF4, SUF5 and SUF6) appears to include a set of informational suppressors in which the vehicle of suppression is glycyl-tRNA. Some of the genetic properties of Group II suppressors are described in this communication.—Corevertants of the Group II frameshift mutations his4-519 and leu2-3 have been characterized to determine the spectrum of reversion events induced by the frameshift mutagen ICR-170. Seventythree ICR-induced corevertants were analyzed. With the exception of one corevertant, which carried an allele of SUF1, all carried alleles of SUF3 or SUF5, SUF1, SUF3, SUF4 and SUF6 were represented among spontaneous and UV-induced corevertants. In the course of these experiments one of the suppressors was mapped. SUF5, the probable structural gene for tRNAGLY1, is located between ade2 and ade9 on chromosome XV.—SUF1, SUF4 and SUF6 have novel properties and comprise a distinct subset of suppressors. Although these suppressors show no genetic linkage to each other, they share several common features including lethality in haploid pairwise combinations, reduced tRNAGLY3 isoacceptor activity and increased efficiency of suppression in strains carrying the cytoplasmically inherited [PSI] element. In addition, strains carrying SUFI, SUF4 or SUF6 are phenotypically unstable and give rise to mitotic Suf+ segregants at high frequency. These segregants invariably contain a linked, second-site mutation that maps in or adjacent to the suppressor gene itself. Strains carrying any of these suppressors also give rise to mitotic segregants that exhibit enhanced efficiency of suppression; mutations responsible for this phenotype map at two loci, upf1 and upf2. These genes show no genetic linkage to any of the Group II suppressors.—Methods that permit positive selection for mutants with decreased or enhanced efficiency of suppression have been devised in order to examine large numbers of variants. The importance of these interacting mutants is underscored by their potential utility in studying suppressor function at the molecular level.


Genetics ◽  
1986 ◽  
Vol 112 (4) ◽  
pp. 727-739
Author(s):  
Robert B Weiss ◽  
Jonathan A Gallant

ABSTRACT Under certain conditions aminoacyl-tRNA limitation can phenotypically suppress frameshift alleles. The observed suppression is due to an increase in abnormal translocation of ribosomes translating codons that have a short supply of aminoacyl-tRNA. The rIIB frameshift alleles of bacteriophage T4 are used here to pinpoint the sites of ribosome frameshifting caused by these hypothetical decoding errors. The data indicate that not all hungry codons are associated with abnormal translocation, only a relatively small subset. Analysis of the hungry codons which are associated with ribosome frameshifting points to the existence of severe context effects determining the shiftiness of these codons.


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