First report of polymorphisms and genetic characteristics of the prion-like protein gene (PRND) in bats
- 1Korea Zoonosis Research Institute, Jeonbuk National University , ,
- 2Laboratory of Veterinary Infectious Diseases, College of Veterinary Medicine, Jeonbuk National University , ,
Abstract
Background: Prion diseases are fatal brain disorders caused by the misfolding of the normal cellular prion protein (PrPC) into its infectious isoform (PrPSc). Previous studies have reported that many polymorphisms within the prion-like protein gene (PRND), a prion protein family member, are significantly associated with disease susceptibility in various species. There have been no natural cases of prion disease found in bats. The genetic polymorphisms of the PRND gene in bats commonly found in Korea were characterized for the first time in this study.
Methods: A total of 98 bat samples were used to extract genomic DNA to investigate bat PRND polymorphisms. Next, amplicon sequencing focusing on the coding region of the bat PRND gene was conducted. To assess the linkage among the PRND single nucleotide polymorphisms (SNPs), linkage disequilibrium (LD) analysis was performed. The LD analysis was also conducted to investigate genetic associations between PRND and prion protein gene (PRNP) SNPs. In addition, we conducted sequence alignment and evolutionary analysis with ClustalW and MEGA 12.1, and assessed the effects of non-synonymous SNPs on Doppel protein using in silico tools.
Results: We found 7 novel SNPs in the bat PRND gene. No pairwise LD value between the analyzed PRNP and PRND polymorphisms exceeded the threshold for strong LD (r2 > 0.333). Furthermore, according to preliminary computational analyses (SIFT and MutPred2), one non-synonymous SNP, c.392G>C (R131T), was predicted to have a potentially deleterious effect on bat Doppel protein.
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BibTeX
@article{choi2026first,
title = {{First report of polymorphisms and genetic characteristics of the prion-like protein gene (PRND) in bats}},
author = {Da-In Choi and Min-Ju Jeong and Eun-Jee Na and Jae-Ku Oem and Byung-Hoon Jeong},
journal = {Frontiers in veterinary science},
year = {2026},
month = oct,
doi = {10.3389/fvets.2026.1967863},
url = {https://europepmc.org/article/PMC/PMC13725429},
note = {CC BY},
}
RIS
TY - JOUR
TI - First report of polymorphisms and genetic characteristics of the prion-like protein gene (PRND) in bats
AU - Da-In Choi
AU - Min-Ju Jeong
AU - Eun-Jee Na
AU - Jae-Ku Oem
AU - Byung-Hoon Jeong
PY - 2026
DA - 2026/10/19
JO - Frontiers in veterinary science
DO - 10.3389/fvets.2026.1967863
UR - https://europepmc.org/article/PMC/PMC13725429
AB - Background: Prion diseases are fatal brain disorders caused by the misfolding of the normal cellular prion protein (PrPC) into its infectious isoform (PrPSc). Previous studies have reported that many polymorphisms within the prion-like protein gene (PRND), a prion protein family member, are significantly associated with disease susceptibility in various species. There have been no natural cases of prion disease found in bats. The genetic polymorphisms of the PRND gene in bats commonly found in Korea were characterized for the first time in this study. Methods: A total of 98 bat samples were used to extract genomic DNA to investigate bat PRND polymorphisms. Next, amplicon sequencing focusing on the coding region of the bat PRND gene was conducted. To assess the linkage among the PRND single nucleotide polymorphisms (SNPs), linkage disequilibrium (LD) analysis was performed. The LD analysis was also conducted to investigate genetic associations between PRND and prion protein gene (PRNP) SNPs. In addition, we conducted sequence alignment and evolutionary analysis with ClustalW and MEGA 12.1, and assessed the effects of non-synonymous SNPs on Doppel protein using in silico tools. Results: We found 7 novel SNPs in the bat PRND gene. No pairwise LD value between the analyzed PRNP and PRND polymorphisms exceeded the threshold for strong LD (r2 > 0.333). Furthermore, according to preliminary computational analyses (SIFT and MutPred2), one non-synonymous SNP, c.392G>C (R131T), was predicted to have a potentially deleterious effect on bat Doppel protein.
SN - 2297-1769
ER -