Sentence examples for mutation to one from inspiring English sources

In each replicate, we assigned a mutation to one founder and simulated the genotypes of other individuals generation by generation.

Specifically, in each replicate, we assigned a mutation to one founder and then simulated the genotypes of all other individuals according to Mendelian inheritance rules.

Approximately 30%% of all human cancers contain a mutation to one of the ras oncogenes (Ki- ras, Ha- ras, N- ras) that causes the resulting protein to be constitutively active [ 13].

Activation of an oncogene requires only a single mutation to one of the two homologous alleles of a proto-oncogene; the remaining intact allele cannot compensate for the resulting dominant oncogenic defect.

As pointed out long ago (Miyata and Yasunaga 1978), this approach is problematic, because a synonymous mutation to one of the overlapping genes may be nonsynonymous to the other gene and thus may be non-neutral.

A previous study showed that a single point mutation to one of the fragments of a complemented protein, which was predicted to lower the affinity between the fragments, reduced background activity [37].

These controls consist of a mixture of oligonucleotides (100 to 120 bases long) each designed for the detection of one or more disease-causing mutation(s), depending on the proximity of the mutations to one another.

Here we show that by using targeted sequencing of multiple samples, we can reduce the number of candidate causative mutations to one or two per line.

This is because some synonymous mutations to one ORF are nonsynonymous to the other ORF and hence have been removed by purifying selection, causing overestimation of ω1 and ω2.

For mutants represented by single alleles, we used high-throughput SNP markers and genetic recombination to map the mutation to a 2- to 3-Mb region (~10% of a chromosome arm), which is usually sufficient to restrict the number of candidate causative coding mutations to one or two.

The formalism we propose here sets a general framework for the study of the impact of mutational mechanisms on genome length with two important features: (i) genomes can undergo both small indels and large chromosomal rearrangements and (ii) genomes undergo a size-dependent number of mutations rather than limiting the mutations to one per replication.