Journal
HEREDITY
Volume 112, Issue 5, Pages 543-551Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/hdy.2013.137
Keywords
genome-wide association study; bovine tuberculosis; novel resistance loci
Categories
Funding
- Biotechnology and Biological Sciences Research Council, through CEDFAS initiative grants [BB/E018335/1, BB/E018335/2]
- Roslin Institute Strategic Programme Grant
- European Union Framework 7 Project Grant [KBBE-211602-MACROSYS]
- Department of Agriculture and Rural Development Veterinary Service
- Biotechnology and Biological Sciences Research Council [BB/E018386/1, BBS/E/D/20310000, BBS/E/D/20231760, BBS/E/D/20211553, BBS/E/D/20211554, BB/E018335/2, BB/E018335/1] Funding Source: researchfish
- BBSRC [BBS/E/D/20310000, BB/E018335/1, BBS/E/D/20211553, BBS/E/D/20211554, BB/E018386/1, BBS/E/D/20231760, BB/E018335/2] Funding Source: UKRI
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Tuberculosis (TB) caused by Mycobacterium bovis is a re-emerging disease of livestock that is of major economic importance worldwide, as well as being a zoonotic risk. There is significant heritability for host resistance to bovine TB (bTB) in dairy cattle. To identify resistance loci for bTB, we undertook a genome-wide association study in female Holstein-Friesian cattle with 592 cases and 559 age-matched controls from case herds. Cases and controls were categorised into distinct phenotypes: skin test and lesion positive vs skin test negative on multiple occasions, respectively. These animals were genotyped with the Illumina BovineHD 700K BeadChip. Genome-wide rapid association using linear and logistic mixed models and regression (GRAMMAR), regional heritability mapping (RHM) and haplotype-sharing analysis identified two novel resistance loci that attained chromosome-wise significance, protein tyrosine phosphatase receptor T (PTPRT; P = 4.8 x 10(-7)) and myosin IIIB (MYO3B; P = 5.4 x 10(-6)). We estimated that 21% of the phenotypic variance in TB resistance could be explained by all of the informative single-nucleotide polymorphisms, of which the region encompassing the PTPRT gene accounted for 6.2% of the variance and a further 3.6% was associated with a putative copy number variant in MYO3B. The results from this study add to our understanding of variation in host control of infection and suggest that genetic marker-based selection for resistance to bTB has the potential to make a significant contribution to bTB control.
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