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The purpose of this study was to fine map the locus Xq25.1-27-2 in order to identify genetic contributors involved in low caries experience.
A promising avenue for future research might thus be to map the locus responsible for obligate parthenogenesis.
HAM and EMMA analysis were used to map the locus underlying survival after P. berghei infection in 32 different inbred mouse strains.
When we picked recombinants to map the locus on V we found it did not map to a single interval, but could be reconstituted in the transheterozygous F1 progeny of recombinants that had LSJ1 DNA on opposite arms of chromosome V, and N2 DNA at other genomic locations (Figure S3c).
To map the locus or loci responsible for the phenotypes described above we began by analysing all of the available deficiencies, which uncover genomic stretches mapping to this region to which we will refer as the "classical deficiencies" (Figure 2 and see Table S1 for a full list).
To map the locus, 133 microsatellite markers were studied.
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As a next step, it is necessary to map the loci involved in affecting these traits, and quantitative trait locus (QTL) analysis have been used for this.
These recombinant populations could then be used to map the loci that suppress the effects of ppw-1 in QX222.
We used SilkMap tool in silkworm genome database to map the loci of each ABC genes on the 28 chromosomes.
The identification of a substantial genetic effect among accessions in the training set gave us confidence to map the loci responsible for the variation of rosette growth.
Moreover, subsequent analysis showed that the PSG phenotypes also map to the same locations, validating the ability to map the loci of interest.
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