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For linkage mapping of Mendelian disease in humans using DNA polymorphisms.
QTL analysis was performed using mycobacterial load and percent of IFN-γ-producing cells in the lungs as quantitative traits (QTX MapManager, Software for genetic mapping of mendelian markers and quantitative trait loci, program for Windows).
The development of low density microsatellite based linkage maps [29] have lead to the mapping of Mendelian diseases [30] [32] and subsequent discovery of mutations underlying at least three genetic diseases in sheep [32] [34], however many others remain uncharacterized [35].
Genetic linkage maps are necessary for mapping of mendelian traits and quantitative trait loci (QTLs).
However, successful mapping of Mendelian and quantitative phenotypic traits depends critically on the availability of fast and preferably high-throughput genotyping platforms.
The development of the canine genotyping array of ~27000 SNPs show that genome-wide association mapping of mendelian traits in dog breeds can be achieved with only ~20 dogs [ 44].
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However, successful mapping of both Mendelian and complex traits depends critically on the availability of fast, cost-effective and high-throughput genotyping platform.
Since gene mapping for Mendelian diseases has been very successful, there have been strong expectations for the discovery of genetic variations responsible for complex diseases.
Because barley genome sequencing is still in progress (Schulte et al. 2009), these populations are proposed as a key tool for high-resolution mapping of QTL and Mendelian loci and subsequent identification of the causal genes.
Eighty one of the 145 small CNA were mapped to Mendelian CNV (mCNV) in the Database of Genomic Variants.
The second factor causing uncertainty in map construction is distortion of Mendelian inheritance ratios, owing to strong viability selection, as documented in several previous studies of oysters (Bierne et al. 1998; Launey and Hedgecock 2001; Plough and Hedgecock 2011; Plough 2012).
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