Showing papers by "Laurence D. Hurst published in 1998"
TL;DR: It is concluded that the natural genetic code is extremely efficient at minimizing the effects of errors, but also that its structure reflects biases in these errors, as might be expected were the code the product of selection.
Abstract: Statistical and biochemical studies of the genetic code have found evidence of nonrandom patterns in the distribution of codon assignments. It has, for example, been shown that the code minimizes the effects of point mutation or mistranslation: erroneous codons are either synonymous or code for an amino acid with chemical properties very similar to those of the one that would have been present had the error not occurred. This work has suggested that the second base of codons is less efficient in this respect, by about three orders of magnitude, than the first and third bases. These results are based on the assumption that all forms of error at all bases are equally likely. We extend this work to investigate (1) the effect of weighting transition errors differently from transversion errors and (2) the effect of weighting each base differently, depending on reported mistranslation biases. We find that if the bias affects all codon positions equally, as might be expected were the code adapted to a mutational environment with transition/transversion bias, then any reasonable transition/transversion bias increases the relative efficiency of the second base by an order of magnitude. In addition, if we employ weightings to allow for biases in translation, then only 1 in every million random alternative codes generated is more efficient than the natural code. We thus conclude not only that the natural genetic code is extremely efficient at minimizing the effects of errors, but also that its structure reflects biases in these errors, as might be expected were the code the product of selection.
500 citations
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TL;DR: Estimates of its quantitative importance are still needed, but many features of sexual behavior may have evolved in part as a result of evolutionary conflict.
Abstract: Evolutionary conflict occurs when the deterministic spread of an allele lowers the fitness either of its bearer or of other individuals in the population, leading to selection for suppressors. Sex promotes conflict because associations between alleles are temporary. Differing selection on males and females, sexual selection, and differences in transmission patterns between classes of nuclear and cytoplasmic genes can all give rise to conflict. Inert Y chromosomes, uniparental inheritance of cytoplasmic genes, mating strains and sexes, and many features of sexual behavior may have evolved in part as a result of evolutionary conflict. Estimates of its quantitative importance, however, are still needed.
174 citations
TL;DR: A majority of estimates using the best direct methods in humans indicate a male bias for point mutations, but the variance in estimates is high and a consensus as to the extent of any male bias is not presently possible.
169 citations
TL;DR: The conflict theory is the only hypothesis to have attracted any critical attention for the evolution of genomic imprinting, but although the earliest data appeared supportive, recent systematic analyses have not confirmed the model's predictions.
82 citations
TL;DR: The error–minimizing ability of the natural code is compared with that of alternative codes which are restricted such that amino acids from the same biochemical pathway all share the same first base, and it is found that although on average the restricted set of codes show a slightly higher efficiency than random ones, the real code remains extremely efficient relative to this subset p=0.3.
Abstract: The average effect of errors acting on a genetic code (the change in amino-acid meaning resulting from point mutation and mistranslation) may be quantified as its 'load'. The natural genetic code shows a clear property of minimizing this load when compared against randomly generated variant codes. Two hypotheses may be considered to explain this property. First, it is possible that the natural code is the result of selection to minimize this load. Second, it is possible that the property is an historical artefact. It has previously been reported that amino acids that have been assigned to codons starting with the same base come from the same biosynthetic pathway. This probably reflects the manner in which the code evolved from a simpler code, and says more about the physicochemical mechanisms of code assembly than about selection. The apparent load minimization of the code may therefore follow as a consequence of the fact that the code could not have evolved any other way than to allow biochemically related amino acids to have related codons. Here then, we ask whether this 'historical' force alone can explain the efficiency of the natural code in minimizing the effects of error. We therefore compare the error-minimizing ability of the natural code with that of alternative codes which, rather than being a random selection, are restricted such that amino acids from the same biochemical pathway all share the same first base. We find that although on average the restricted set of codes show a slightly higher efficiency than random ones, the real code remains extremely efficient relative to this subset P = 0.0003. This indicates that for the most part historical features do not explain the load- minimization property of the natural code. The importance of selection is further supported by the finding that the natural code's efficiency improves relative to that of historically related codes after allowance is made for realistic mutational and mistranslational biases. Once mistranslational biases have been considered, fewer than four per 100,000 alternative codes are better than the natural code.
65 citations
TL;DR: It is predicted that genes for which mutations may often be dominant or semi–dominant should undergo concerted evolution more commonly than others, and that selection will favour homogenization of such genes, and possibly others that are significantly dosage dependent, more often than it favours homogenized in other genes.
Abstract: Concerted evolution is a consequence of processes that convert copies of a gene in a multigene family into the same copy. Here we ask whether this homogenization may be adaptive. Analysis of a modi...
39 citations
TL;DR: The results suggest that, in contrast to previous studies of intragenic variation, Ks patterns are not simply caused by the same forces responsible for Ka/Ks correlations.
Abstract: The repeatability of patterns of variation in Ka/Ks and Ks is expected if such patterns are the result of deterministic forces. We have contrasted the molecular evolution of the mammalian insulin-like growth factor type II receptor (Igf2r) in the mouse-rat comparison with that in the human-cow comparison. In so doing, we investigate explanations for both the evolution of genomic imprinting and for Ks variation (and hence putatively for mutation rate evolution). Previous analysis of Igf2r, in the mouse-rat comparison, found Ka/Ks patterns that were suggested to be contrary to those expected under the conflict theory of imprinting. We find that Ka/Ks variation is repeatable and hence confirm these patterns. However, we also find that the molecular evolution of Igf2r signal sequences suggests that positive selection, and hence conflict, may be affecting this region. The variation in Ks across Igf2r is also repeatable. To the best of our knowledge this is the first demonstration of such repeatability. We consider three explanations for the variation in Ks across the gene: (1) that it is the result of mutational biases, (2) that it is the result of selection on the mutation rate, and (3) that it is the product of selection on codon usage. Explanations 2 and 3 predict a Ka-Ks correlation, which is not found. Explanation 3 also predicts a negative correlation between codon bias and Ks, which is also not found. However, in support of explanation 1 we do find that in rodents the rate of silent C --> T mutations at CpG sites does covary with Ks, suggesting that methylation-induced mutational patterns can explain some of the variation in Ks. We find evidence to suggest that this CpG effect is due to both variation in CpG density, and to variation in the frequency with which CpGs mutate. Interestingly, however, a GC4 analysis shows no covariance with Ks, suggesting that to eliminate methyl-associated effects CpG rates themselves must be analyzed. These results suggest that, in contrast to previous studies of intragenic variation, Ks patterns are not simply caused by the same forces responsible for Ka/Ks correlations.
34 citations
TL;DR: Using a methodology that may be considered preferable to that of Hughes and Yeager, it is found that all four of their results are contradicted, which reinforces the need for caution in assembling and analyzing data sets.
Abstract: Employing a set of 43 othologous mouse and rat genes, Hughes and Yeager (J. Mol. Evol. 45:125–130, 1997) reported (1) no correlation between synonymous and nonsynonymous rates of nucleotide substitution, (2) a positive correlation between intronic GC contents (GCi) and intronic substitution rates (Ki), (3) that the average Ki value was very similar to the average Ks value, and (4) that the compositional correlation between the rat and the mouse genes is stronger at the third codon position (GC3) than at the first and second codon positions (GC12). We have examined the robustness of these results to alterations in substitution rate estimation protocol, alignment protocol, and statistical procedure. We find that a significant correlation between Ka and Ks is observed either if a rank correlation statistic is used instead of regression analysis, if one outlier is excluded from the analysis, or if a regression weighted by gene size is employed. The correlation between Ki and GCi we find to be sensitive to changes in alignment protocol and disappears on the use of weighted means. The finding that Ks and Ki are approximately the same is dependent on the method for estimating Ks values. Finally, the variance around the regression line of rat GC3 versus mouse GC3 we find to be significantly higher than that in GC12. The source of the discrepancy between this and Hughes and Yeager's result is unclear. The variance around the line for GC4 is higher still, as might be expected. Using a methodology that may be considered preferable to that of Hughes and Yeager, we find that all four of their results are contradicted. More importantly this analysis reinforces the need for caution in assembling and analyzing data sets, as the degree of sensitivity to what many might consider minor methodological alterations is unexpected.
25 citations
TL;DR: In a study presented on page 362 (ref. 1), Paul Vrana and colleagues attempt to test an appealing and popular hypothesis, one that supposes that imprinting is a consequence of evolutionary conflict between maternally and paternally derived genes2.
Abstract: nature genetics volume 20 december 1998 315 I don’t like flying—especially in planes with only one engine. What if it fails? If you share my fear, you will understand why evolutionists are fascinated by genomic imprinting. In a diploid organism, selection will typically favour two functional alleles, in case one ‘fails’ as a consequence of mutation. Just what sort of selection gives rise to imprinting, where one copy of a gene is inactivated, leaving the organism vulnerable to mutation? In a study presented on page 362 (ref. 1), Paul Vrana and colleagues attempt to test an appealing and popular hypothesis, one that supposes that imprinting is a consequence of evolutionary conflict between maternally and paternally derived genes2. In genomic imprinting, the choice of which allele to inactivate is dependent upon the sex of the parent from which the allele was derived. For example, a fetus inherits a copy of the insulin-like growth factor 2 gene (Igf2) from both its parents, but only the father’s gene is expressed. The conflict model2 proposes that selection acting on paternally and maternally derived genes in the same fetus is different. Each maternally derived allele in a fetus has a 50% likelihood of also being present in any other given fetus from the same mother. Consequently, any detrimental effect of this allele on other progeny, or on the mother, could reduce the probability of that allele spreading. In contrast, a rare paternally derived allele in a fetus sired by a father who has no other offspring with the same mother will not be present in any other progeny of that mother— any detriment to these infants, or to the mother’s future reproductive prospects, might therefore increase the probability of the allele’s spread. Generally, when there is multiple paternity, selection will favour paternally derived alleles that obtain more resources from the mother than is optimal for maternally derived alleles. The maternal genome will therefore tend to silence growth promoters, while the paternal genome will tend to silence growth suppressors2.
14 citations
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TL;DR: Females of many species prefer mates with extravagant traits, but studies of stalk-eyed flies show that, in this case at least, such preference is linked to suppression of a selfish gene that influences the sex ratio of offspring.
Abstract: Females of many species prefer mates with extravagant traits. Studies of stalk-eyed flies show that, in this case at least, such preference is linked to suppression of a selfish gene that influences the sex ratio of offspring.
11 citations