scholarly journals The mutagenicity of amino acid analogues inCoprinus lagopus

1974 ◽  
Vol 23 (1) ◽  
pp. 47-61 ◽  
Author(s):  
Philippa J. Talmud ◽  
D. Lewis
Keyword(s):  
Amino Acid ◽  
Mutation Frequency ◽  
Spontaneous Mutation ◽  
Base Change ◽  
Response Curves ◽  
Amino Acid Analogues ◽  
Single Base Change ◽  
Protein Incorporation ◽  
Dose Dependent ◽  
Spontaneous Mutation Frequency

SummaryThe amino acid analoguesp-fluorophenylalanine (PFP) and ethionine (ETH) are strongly mutagenic inCoprinus lagopus. The most pronounced effect was found with suppressor mutations of themet-1locus. PFP, at a concentration of 2·4 × 10−4M, increased the mutation frequency 500 fold and ETH, at a concentration of 2·4 × 10−3M, 30 fold over the spontaneous mutation frequency. From the spectrum of suppressors of themet-1locus and the dominant revertants of thead-82locus, induced by analogue treatments, it was concluded that both analogues induce single base-change mutations. The dose response curves follow a sigmoid plot, revealing that within a certain range of analogue concentrations, muta-genesis is strongly dose dependent.Using analogue resistant mutants, it has been shown that PFP mutagenesis is a function of its incorporation into protein. However, ETH mutagenesis is independent of protein incorporation but can be correlated with the degree of ethylation of nucleic acids. The synergistic effect PFP and ETH supports the evidence of the different mutagenic actions of the two analogues.

scholarly journals SPONTANEOUS UNSTABLE UNC-22 IV MUTATIONS IN C. ELEGANS VAR. BERGERAC

Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 859-877
Author(s):  
D G Moerman ◽  
R H Waterston
Keyword(s):  
Mutation Frequency ◽  
Spontaneous Mutation ◽  
Phenotypic Effect ◽  
C Elegans ◽  
High Mutation Frequency ◽  
Mutator Activity ◽  
Discrete Site ◽  
Unstable Mutations ◽  
Spontaneous Mutation Frequency ◽  
Forward Mutation

ABSTRACT This paper describes a mutator system in the nematode Caenorhabditis elegans var. Bergerac for the gene unc-22. Of nine C. elegans and two C. briggsae strains tested only the Bergerac BO strain yielded mutant animals at a high frequency and the unc-22 IV gene is a preferred mutational target. The forward spontaneous mutation frequency at the unc-22 locus in Bergerac BO is about 1 × 10-4, and most of these spontaneous unc-22 mutations revert at frequencies between 2 × 10-3 and 2 × 10-4. Both the forward mutation frequency and the reversion frequency are sensitive to genetic background. Spontaneous unc-22 mutations derived in a Bergerac background and placed in a primarily Bristol background revert at frequencies of <10-6. When reintroduced into a Bergerac/Bristol hybrid background the mutations once again become unstable. The mutator activity could not be localized to a discrete site in the Bergerac genome. Nor did mutator activity require the Bergerac unc-22 gene as a target since the Bristol unc-22 homolog placed in a Bergerac background also showed high mutation frequency. Intragenic mapping of two spontaneous unc-22 alleles, st136 and st137, place both mutations in the central region of the known unc-22 map. However, these mutations probably recombine with one another, suggesting that the unstable mutations can occur in more than one site in unc-22. Examination of the phenotypic effect of these mutations on muscle structure indicates that they are less severe in their effect than a known amber allele. We suggest that this mutator system is polygenic and dispersed over the nematode genome and could represent activity of the transposable element Tc1.

Disruption of Xpg increases spontaneous mutation frequency, particularly A:T to C:G transversion

2001 ◽  
Vol 487 (3-4) ◽  
pp. 127-135 ◽  
Author(s):  
Naoko Shiomi ◽  
Emiko Hayashi ◽  
Shun-ichi Sasanuma ◽  
Kazuei Mita ◽  
Tadahiro Shiomi
Keyword(s):  
Mutation Frequency ◽  
Spontaneous Mutation ◽  
Spontaneous Mutation Frequency

Premature chromosome condensation is induced by a point mutation in the hamster RCC1 gene

1990 ◽  
Vol 10 (2) ◽  
pp. 577-584
Author(s):  
S Uchida ◽  
T Sekiguchi ◽  
H Nishitani ◽  
K Miyauchi ◽  
M Ohtsubo ◽  
...  
Keyword(s):  
Amino Acid ◽  
Mutant Gene ◽  
Polymerase Chain Reaction Method ◽  
Base Change ◽  
Chromosome Condensation ◽  
Premature Chromosome Condensation ◽  
Base Sequences ◽  
Single Base Change ◽  
Polymerase Chain ◽  
Tsbn2 Cells

At the nonpermissive temperature, premature chromosome condensation (PCC) occurs in tsBN2 cells derived from the BHK cell line, which can be converted to the Ts+ phenotype by the human RCC1 gene. To prove that the RCC1 gene is the mutant gene in tsBN2 cells, which have RCC1 mRNA and protein of the same sizes as those of BHK cells, RCC1 cDNAs were isolated from BHK and tsBN2 cells and sequenced to search for mutations. The hamster (BHK) RCC1 cDNA encodes a protein of 421 amino acids homologous to the human RCC1 protein. In a comparison of the base sequences of BHK and BN2 RCC1 cDNAs, a single base change, cytosine to thymine (serine to phenylalanine), was found in the 256th codon of BN2 RCC1 cDNA. The same transition was verified in the RCC1 genomic DNA by the polymerase chain reaction method. BHK RCC1 cDNA, but not tsBN2 RCC1 cDNA, complemented the tsBN2 mutation, although both have the same amino acid sequence except for one amino acid at the 256th codon. This amino acid change, serine to phenylalanine, was estimated to cause a profound structural change in the RCC1 protein.

scholarly journals A unique sequence of the NZW I-E beta chain and its possible contribution to autoimmunity in the (NZB x NZW)F1 mouse.

1989 ◽  
Vol 170 (3) ◽  
pp. 971-984 ◽  
Author(s):  
J Schiffenbauer ◽  
D M McCarthy ◽  
N R Nygard ◽  
S L Woulfe ◽  
D K Didier ◽  
...  
Keyword(s):  
Amino Acid ◽  
Early Death ◽  
Class Ii ◽  
Base Change ◽  
Unique Sequence ◽  
Chain Reaction ◽  
S Haplotype ◽  
Severe Renal Disease ◽  
Single Base Change ◽  
Polymerase Chain

The (NZB x NZW)F1 mouse strain develops a syndrome of accelerated autoimmunity including severe renal disease and early death. Evidence suggests that class II molecules play a central role in this process. Previous studies have suggested that the NZW strain contributes at least one gene to the development of accelerated autoimmunity that is linked to the H-2 complex, and antibodies to murine class II molecules have been used to ameliorate disease in (NZB x NZW)F1 mice. We therefore wished to sequence the class II molecules from NZW mice to identify any unique sequences that may contribute to disease development. We constructed oligonucleotide primers corresponding to the 5' and 3' regions of the second exon of class II genes from a variety of haplotypes, and used these primers in a polymerase chain reaction to sequence the second exon of the NZW I-A alpha, I-A beta, and I-E beta genes. We report that the second exons of NZW I-A alpha, I-A beta, and I-E alpha are identical to their counterparts of the previously sequenced u haplotype, and that the second exon of NZW I-E beta is identical to its counterpart from u except for a single base change that results in a substitution of arginine for threonine at amino acid 72. This base and amino acid are identical to those found at the same positions in the s haplotype.

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