IP Library Granted Patent US 12,497,659
Granted Patent B2
US 12,497,659 · App. 16/088,247 · Granted Dec 16, 2025

Method of detecting inherited equine myopathy

Inventors: Jeremy Scott Edwards (Albuquerque, NM); Paul Szauter (Albuquerque, NM); Robert B. Sinclair (Ashville, NC)
Assignees: UNM RAINFOREST INNOVATIONS; JEREMY SCOTT EDWARDS
C12Q1/6883C12Q2600/124C12Q2600/156
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Quick Facts
Patent No.
US 12,497,659
App. No.
16/088,247
Granted
Dec 16, 2025
Kind
B2
Abstract

This disclosure describes detecting genetically distinct kinds of inherited myopathies in horses, variously referred to as Polysaccharide Storage Myopathy type 2 (PSSM2), Myofibrillar Myopathy (MFM), or idiopathic myopathy.

Claims (56)

1 . A method of mating a horse comprising:

(a) detecting in a biological sample obtained from said horse, the biological sample comprising nucleic acids that include the coding regions for myotilin (MYOT), filamin-C(FLNC) and myozenin-3 (MYOZ3):

1) a guanine (G) or an adenine (A) at nucleotide 1001 of the forward strand of SEQ ID NO:1, wherein detection of the guanine indicates the presence of variant P2;

2) an adenine (A) or a guanine (G) at nucleotide 1001 of SEQ ID NO:2, wherein detection of the adenine indicates the presence of variant P3a,;

3) an adenine (A) or a guanine (G) at nucleotide 1001 of SEQ ID NO:3, wherein detection of the adenine indicates the presence of variant P3b; and

4) an adenine (A) or a guanine (G) at nucleotide 1001 of the forward strand of SEQ ID NO:4, wherein detection of the adenine indicates the presence of variant P4;

wherein in each case the presence of the specified nucleotide can be inferred from detecting the nucleotide present at the complement thereof;

wherein said horse is not homozygous for the presence of P2, P3a, P3b or P4;

wherein and said horse is heterozygous for at least one of P2, P3a, P3b or P4; and

(b) mating said horse with a mare or sire.

2 . The method according to claim 1 wherein said mare or sire is free from variants P2, P3a, P3b and P4.

3 . The method according to claim 1 wherein said mare or sire is heterozygous for variant P2, P3a, P3b or P4.

4 . The method of claim 1 , further comprising:

contacting the nucleic acids of the sample with at least one oligonucleotide probe to form a hybridized nucleic acid; and

amplifying the hybridized nucleic acid.

5 . The method of claim 4 , wherein:

Exon 6 of the equine myotilin coding region (MYOT) or a portion thereof is amplified; Exon 15 of the equine filamin-C coding region (FLNC) or a portion thereof is amplified; exon 21 of the equine filamin-C coding region (FLNC) or a portion thereof is amplified and exon 3 of the equine myozenin-3 coding region (MYOZ3), or a portion thereof is amplified.

6 . The method according to claim 5 , wherein the nucleic acid is genomic DNA.

7 . The method according to claim 5 , wherein the nucleic acid is RNA.

8 . The method according to claim 7 , wherein the method comprises converting the RNA into DNA by reverse transcriptase.

9 . The method of claim 4 , wherein the hybridized nucleic acid is amplified using polymerase chain reaction, strand displacement amplification, ligase chain reaction, or nucleic acid sequence-based amplification.

10 . The method according to claim 9 , wherein the nucleic acid is genomic DNA.

11 . The method according to claim 9 , wherein the nucleic acid is RNA.

12 . The method according to claim 11 , wherein the method comprises converting the RNA into DNA by reverse transcriptase.

13 . The method of claim 4 , wherein said at least one oligonucleotide probe is immobilized on a solid surface or a semisolid surface.

14 . The method according to claim 13 , wherein the nucleic acid is genomic DNA.

15 . The method according to claim 13 , wherein the nucleic acid is RNA.

16 . The method according to claim 15 wherein the method comprises converting the RNA into DNA by reverse transcriptase.

17 . A method according to claim 4 , wherein the nucleic acid is genomic DNA.

18 . The method according to claim 4 , wherein the nucleic acid is RNA.

19 . The method according to claim 18 , wherein the method comprises converting the RNA into DNA by reverse transcriptase.

20 . The method according to claim 1 , wherein the nucleic acid is genomic DNA.

21 . The method according to claim 1 , wherein the nucleic acid is RNA.

22 . The method according to claim 21 , wherein the method comprises converting the RNA into DNA by reverse transcriptase.

23 . The method according to claim 21 , wherein the method comprises

detecting in said nucleic acid:

(1) a cytosine (C) or a thymine (T) at nucleotide position 694 of SEQ ID NO: 5, wherein detection of the cytosine indicates the presence of variant P2;

(2) an adenine (A) for a guanine (G) at nucleotide position 2257 of SEQ ID NO: 6, wherein detection of the adenine indicates the presence of variant P3a;

(3) an adenine (A) for a guanine (G) at nucleotide position 3619 of SEQ ID NO: 6, wherein detection of the adenine indicates the presence of variant P3b, and

(4) a thymine (T) for cytosine (C) at nucleotide position 125 of SEQ ID NO: 8, wherein detection of the thymine indicates the presence of variant P4;

wherein in each case the presence of the nucleotide can be inferred from detecting the nucleotide present at the complement thereof;

wherein said horse is not homozygous for the presence of P2, P3a, P3b or P4;

wherein said horse is heterozygous for at least one of P2, P3a, P3b or P4; and

(b) mating said horse with a mare or sire.

24 . The method according to claim 23 wherein said mare or sire is free from variants P2, P3a, P3b and P4.

25 . The method according to claim 23 wherein said mare or sire is heterozygous for variant P2, P3a, P3b or P4.

26 . A method of mating a horse

(a) detecting in a biological sample obtained from said horse, the biological sample comprising nucleic acids that includes the coding regions for myotilin (MYOT), filamin-C(FLNC) and myozenin-3 (MYOZ3):

(1) a proline (P) or a serine(S) at position 232 of SEQ ID NO:10, wherein detection of proline indicates the presence of variant P2;

(2) a lysine (K) or a glutamate (E) residue at position 753 of SEQ ID NO: 13, wherein detection of proline indicates the presence of variant P3a,

(3) a threonine (T) or an alanine (A) at position 1207 of SEQ ID NO:13, wherein detection of threonine indicates the presence of of variant P3b and

(4) a leucine (L) or a serine(S) at position 42 of SEQ ID NO:16, wherein detection of leucine indicates the presence of variant P4, wherein said horse is not homozygous for the presence of P2, P3a, P3b or P4;

wherein said horse is heterozygous for at least one of P2, P3a, P3b or P4; and

(b) mating said horse with a mare or sire.

27 . The method according to claim 26 wherein said mare or sire is free from variants P2, P3a, P3b and P4.

28 . The method according to claim 26 wherein said mare or sire is heterozygous for variant P2, P3a, P3b or P4.

Assignments (3)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Oct 29, 2025
From: EDWARDS, JEREMY SCOTT
To: THE REGENTS OF THE UNIVERSITY OF NEW MEXICO
Reel/Frame 072716/0499 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Oct 29, 2025
From: THE REGENTS OF THE UNIVERSITY OF NEW MEXICO
To: UNM RAINFOREST INNOVATIONS
Reel/Frame 072716/0642 →
CHANGE OF NAME Recorded Jul 22, 2025
From: STC.UNM
To: UNM RAINFOREST INNOVATIONS
Reel/Frame 071788/0782 →
Continuity (3)
Provisional Application 62421625 · Nov 14, 2016
Provisional Application 62313272 · Mar 25, 2016
Related Publication 20200224270A1 · Jul 16, 2020
References Cited (23)
Williams et al 2020, Candidate gene expression, coding sequence variants and muscle fiber contractile force in Warmblood horses with myofibrillar myopathy, Equine Vet J, (Year: 2020). [cited by examiner]
Valberg et al , Equine Vet J. 2020 Commercial genetic testing for type 2 polysaccharide storage myopathy and myofibrillar myopathy does not correspond to a histopathological diagnosis. (Year: 2020). [cited by examiner]
GenBank XM_014739030, Nov. 20, 2015. (Year: 2015). [cited by examiner]
Williams, BMC Genomics, vol. 22, No. 438, 2021). (Year: 2021). [cited by examiner]
Herrick, J. of Equine Veterinary Science, vol. 100, No. 103607, 2021 (Year: 2021). [cited by examiner]
Valberg, et al (Equine Vet J. vol. 55, pp. 230-238, 2023). [cited by examiner]
Valberg et al Commercial genetic testing for type 2 polysaccharide storage myopathy and myofibrillar myopathy does not correspond to a histopathologic diagnosis. Equine Vet J Jul. 2021; 53(4): 690-700. [cited by examiner]
Broad Institute Horse Genome Project (https://www.broadinstitute.org/horse/horse-genome-project, 2007). [cited by examiner]
Aurino S, et al. Candidate-gene testing for orphan limb-girdle muscular dystrophies. Acta Myologica, 2008;27:90-97. [cited by applicant]
Ferlini A, et al. The medical genetics of dystrophinopathies: Molecular genetic diagnosis and its impact on clinical practice. Neuromuscular Disorders, 2013;23:4-14. [cited by applicant]
Foroud T, et al. A mutation in myotilin causes spheroid bosy myopathy. Neurology, 2005;65(12):abstract. [cited by applicant]
Kley RA, et al. Impairment of protein degradation in myofibrillar myopathy caused by FLNC/filamin C mutations. Autophagy, 2013;9:422-423. [cited by applicant]
Mykkanen AK, et al. MCT1, MCT3 and CD147 gene polymorphisms in healthy horses and horses with myopathy. Veterinary Science, 2011;91:473-477. [cited by applicant]
Nandelstadh, P; et al. A Class III PDZ Binding Motif in the Myotilin and FATZ Families Binds Enigma Family Proteins: a Common Link for Z-Disc Myopathies. Molecular and Cellular Biology, 2009;822-834. [cited by applicant]
Selcen D, Engel AG. Mutations in myotilin cause myofibrillar myopathy. Neurology, 2004;62(8):abstract. [cited by applicant]
Thunes C. Feeding Horses with Neuromuscular Disorders. May 2015 (online) https://thehorse.com/112050/feeding-horses-with-neuromuscular-disorders/. [cited by applicant]
Wackermann K. PSSM2 beim Pferd—die Trainings-Intoleranz. Mar. 2022 (online) https://www.st-georg.de/wissen/ossm2-beim-pferd-die-trainings-intoleranz/. [cited by applicant]
Wackermann K. PSSM2 in horses (english translation). Mar. 2022 (online) https://www.st-georg.de/wissen/ossm2-beim-pferd-die-trainings-intoleranz/. [cited by applicant]
Moro LN, et al. Generation of myostatin edited horse embryos using CRISPR/Cas9 technology and somatic cell nuclear transfer. Scientific Reports, 2020;10:15587 https://doi.org/10.1038/s41598-020-72040-4. [cited by applicant]
Ablondi M, et al. Performance of Swedish Warmblood fragile foal syndrome carriers and breeding prospects. Genetics Selection Evolution, 2022;54:4. [cited by applicant]
Hames M. EquiSeq Review. EquiSeq Facebook Page, May 1, 2022. https://www.facebook.com/EquiSeq1/ posts/2697622740380203. [cited by applicant]
Szauter P. Genetic Basis of Exercise Intolerance in Arabian. Al Khamsa Annual Meeting and Convention, Oct. 13, 2019. [cited by applicant]
Equiseq. Warmblood Fragile Foal Syndrome (WFFS). Aug. 2, 2016 (online) http://equiseq.com/learning_center/health/warmblood-fragile-foal-syndrome-wffs. [cited by applicant]