Abstract
Paratuberculosis is one of the chronic granulomatous enteritis that predominantly affects ruminants worldwide, caused by Mycobacterium avium ssp. paratuberculosis (MAP). In ruminants, microsatellite polymorphisms of the \(3^\prime \) untranslated region (\(3^\prime \)UTR) of the solute carrier family 11 member A1 (SLC11A1) gene were associated with resistance to intracellular pathogen infections. This research was carried out to detect the polymorphisms in A and B regions of the \(3^{\prime }\)UTR of SLC11A1 gene and to evaluate the potential association between these polymorphisms and MAP infection in goats. MAP-specific antibodies were detected by ELISA and MAP infection was confirmed by IS900 PCR in 150 adult goats from different regions of Kerala, India. The polymorphism of microsatellite regions A and B at \(3^{\prime }\)UTR of the SLC11A1 gene was analysed in goats by an automated technique, fragment analysis, using fluorescent-tagged forward primers. Eight alleles with sizes ranging from 221 to 239 bp were found in region A. Region B revealed two alleles, 117 bp (\(\hbox {B}_{7}\)) and 119 bp (\(\hbox {B}_{8}\)). Animals with \(\hbox {B}_{8}\) alleles were found to have higher incidence of paratuberculosis than animals with \(\hbox {B}_{7}\) alleles (\(P< 0.01\)). There was no statistically significant association found between region A genotypes and paratuberculosis incidence. These results suggest that caprine SLC11A1 gene has significant role in paratuberculosis resistance in goats and further studies might help in development of a PCR-based genotyping test for paratuberculosis resistance and selection of superior animals for future goat breeding programmes.
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The authors acknowledge Kerala Veterinary and Animal Sciences University, Kerala, India, for providing the financial support and laboratory facilities for the successful completion of this work.
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Abraham, A., Naicy, T., Raghavan, K.C. et al. Evaluation of the association of SLC11A1 gene polymorphism with incidence of paratuberculosis in goats. J Genet 96, 641–646 (2017). https://doi.org/10.1007/s12041-017-0820-9
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DOI: https://doi.org/10.1007/s12041-017-0820-9