This principle shows that traditional natural selection indirectly affecting modifier loci is actually often expected to decrease mutation and recombination rates (to shut down evolvability) [ 32, 61- 63, 263- 266].
Because only a single strong modifier locus was found in each backcross, we applied a haplotype analysis to map crossovers and successfully narrowed the critical intervals for each locus.
In a recent genome-wide association study of bone mineral density a significant modifier locus was detected near the SOST gene at 17q21, which encodes sclerostin.
A RET-dependent modifier locus was mapped to 9q31 in families bearing no coding sequence (CDS) RET mutations.
One of the candidate genes which might play the role of a modifier locus is MURR1 (renamed COMMD1).
A strong lung tumor modifier locus was also found on chromosome 6, in the same region of Par4 locus (Manenti et al. 1997).
In this scenario, the expression of the modifier locus is sex-specific (e.g. comparable to sex-specific effects of additive loci as reported e.g. in Vaughn et al. [ 23] and occurs during gametogenesis in offspring.
RET is the primary HSCR gene, accounting for 50% of familial cases; however, many modifier loci have been proposed, including two associated regions mapping to chromosome 9q31 (Tang et al., 2010a).
To determine whether either one of these modifier loci might be responsible for the accession-specific effect of nrpd1a-8 on SI, markers tightly linked to these modifiers were used to analyze F2 progenies of the Col-0 nrpd1a-8[ SRKb] × C24 WT[ SRKb-SCRb] cross.
