Sentence examples for mutations of large from inspiring English sources

Most mutational variance appears to be attributable to a few mutations of large effect in, for example, Drosophila (e.g., Bürger 2000 and references therein).

Do changes between species occur through single mutations of large effect, or do they appear incrementally, through the collaboration of many mutations at many different loci?

We discuss how state-of-the-art methods are uncovering a range of genetic mechanisms, from rare mutations of large effect to common polymorphisms that increase risk in a subtle way, while converging on neurogenetic pathways that are shared between distinct disorders.

This theory predicts that with substantial gene flow between populations local adaptation should proceed primarily through mutations of large effect or tightly linked clusters of smaller effect loci.

Indeed, many small populations, both in the experiment and in the simulations, faced handicaps consistent with their diminished access to beneficial mutations of large effect.

It has long been known that deleterious mutations increase VE in certain circumstances, e.g., under inbreeding ([4], p. 289) and in genotypes with known mutations of large effect [5], [6].

Moreover, architectures with many weakly adaptive mutations tended to become replaced by architectures with fewer mutations of larger effect.

This is consistent with our intuition that as the population size grows larger, we increasingly expect the mutations of largest effect to dominate the dynamics.

In contrast, rare mutations of larger effect and a few common variants of small effect in several different genes, which are also involved in different cellular pathways, seem to be causal for many cases of AD.

Part of the debate centres on technical aspects, for example the question whether speciation will still occur for more realistic initial conditions, an increased number of loci, more realistic mutations rates, the inclusion of mutations of larger effect size, or the removal of constraints on the range of possible phenotypes (see Gavrilets 2004; Polechová and Barton 2005; Bürger et al. 2006).

If we think of this as a genetic screen for mutations causing a specific phenotype, with demonstrated saturation mutagenesis of the human population [ 32], then the most effective approach to follow up these discoveries is clear: find the mutations of largest effect and use these as entry points to elucidate the underlying biology.