Dependence Of Mutation Rates Research Articles

PREFERRED SEQUENCES OF GENETIC EVENTS IN CARCINOGENESIS: QUANTITATIVE ASPECTS OF THE PROBLEM

In this paper we discuss some natural limitations in quantitative inference about the frequency, correlation and ordering of genetic events occurring in the course of tumor development. We consider a simple, yet frequently used experimental design, under which independent tumors are examined once for the presence/absence of specific mutations of interest. The most typical factors that affect the inference on the chronological order of genetic events are: a possible dependence of mutation rates, the sampling bias that arises from the observation process and small sample sizes. Our results clearly indicate that just these three factors alone may dramatically distort the outcome of data analysis, thereby leading to estimates of limited utility as an underpinning for mechanistic models of carcinogenesis.

Equilibrium distributions of microsatellite repeat length resulting from a balance between slippage events and point mutations.

We describe and test a Markov chain model of microsatellite evolution that can explain the different distributions of microsatellite lengths across different organisms and repeat motifs. Two key features of this model are the dependence of mutation rates on microsatellite length and a mutation process that includes both strand slippage and point mutation events. We compute the stationary distribution of allele lengths under this model and use it to fit DNA data for di-, tri-, and tetranucleotide repeats in humans, mice, fruit flies, and yeast. The best fit results lead to slippage rate estimates that are highest in mice, followed by humans, then yeast, and then fruit flies. Within each organism, the estimates are highest in di-, then tri-, and then tetranucleotide repeats. Our estimates are consistent with experimentally determined mutation rates from other studies. The results suggest that the different length distributions among organisms and repeat motifs can be explained by a simple difference in slippage rates and that selective constraints on length need not be imposed.

The Dose Dependence of Mutation Rates in the RAD Range, in the Light of Experiments with Higher Plants

The Dose Dependence of Mutation Rates in the RAD Range, in the Light of Experiments with Higher Plants

The Dose Dependence of Mutation Rates in the Rad Range, in the Light of Experiments with Higher Plants

The Dose Dependence of Mutation Rates in the Rad Range, in the Light of Experiments with Higher Plants

The Dose Dependence of Mutation Rates in the Rad Range, in the Light of Experiments with Higher Plants

The Dose Dependence of Mutation Rates in the Rad Range, in the Light of Experiments with Higher Plants