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A. E. Tinch

Researcher at University of Stirling

Publications -  23
Citations -  1726

A. E. Tinch is an academic researcher from University of Stirling. The author has contributed to research in topics: Population & Quantitative trait locus. The author has an hindex of 17, co-authored 22 publications receiving 1488 citations.

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Major quantitative trait loci affect resistance to infectious pancreatic necrosis in Atlantic salmon (Salmo salar).

TL;DR: The identified genomewide quantitative trait loci can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality.
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Development and validation of a high density SNP genotyping array for Atlantic salmon (Salmo salar)

TL;DR: This manuscript describes the first high-density SNP genotyping array for Atlantic salmon, likely to be used as a platform for high-resolution genetics research into traits of evolutionary and economic importance in salmonids and in aquaculture breeding programs via genomic selection.
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Genome wide association and genomic prediction for growth traits in juvenile farmed Atlantic salmon using a high density SNP array

TL;DR: The high density SNP array can effectively capture the additive genetic variation in complex traits, however, the traits of weight and length both appear to be very polygenic with only one SNP surpassing the chromosome-wide threshold.
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Genomic prediction of host resistance to sea lice in farmed Atlantic salmon populations

TL;DR: Host resistance to sea lice in farmed Atlantic salmon has a significant genetic component, and Phenotypes relating to host resistance can be predicted with moderate to high accuracy within populations, with a major advantage of genomic over pedigree-based methods, even at relatively sparse SNP densities.
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The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

TL;DR: The results suggest that a single QTL on linkage group 21 explains almost all the genetic variation in IPN mortality under the authors' experimental conditions, and highlight the importance of the major QTL in the genetic regulation of IPN resistance across distinct physiological lifecycle stages, environmental conditions and viral isolates.