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One appealing explanation is that a set of major effect genes is responsible for effect sizes.
Major effect genes such as ZmCCT, VGT1, and PRR37 did not colocalize with Setaria QTL.
For CQ-hiR, two (or three) major effect genes (PCHAS_031370 (transporter) and ubp1, on chr03 and chr02, respectively) are strongly supported.
An additional 40 fungal pathogen disease resistance QTL and/or major effect genes from 4 additional studies [ 35, 36, 55, 56] were also projected onto the sorghum consensus map following the same strategy.
The former aims to isolate the genes or quantitative trait loci (QTL) responsible for a given phenotype, and has been successful in identifying a number of major effect genes in rice [ 4- 9], maize [ 10, 11] and wheat [ 12, 13].
The near-normal curve distribution of PH, FCH, CAL, GN and TGW suggested a polygene mode of the genetic control; but CL and CN showed a bimodal distribution, suggesting the involvement of major effect genes.
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A major effect gene conferring artemisinin resistance was mapped to chr02 by LGS analysis, as described in the previous section.
Actually, for CQ-R, the present data strongly support the contribution of aat1 (chr11) as a single major effect gene, confirming previous classical genetic linkage analysis [ 19, 20].
The hypothesis that susceptibility alleles for ESRD have higher frequencies in West African than European gene pools led to the identification of the Apolipoprotein L1 gene (APOL1) as a major effect gene [ 2].
However, the discrete nature of these color morphs in combination with previous studies on animal coloration makes it highly likely that there is some genetic influence on coloration, perhaps through some major effect gene.
Here we were able to compare several mapping approaches empirically by using the testa presence/absence phenotype in sorghum and a GBS SNP map that includes a validated SNP in the Tannin1 major effect gene.
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