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1.
Sci Rep ; 13(1): 19077, 2023 11 04.
Article in English | MEDLINE | ID: mdl-37925523

ABSTRACT

Dilated cardiomyopathy (DCM) is characterized by decreased systolic function and dilation of one or both ventricles, often leading to heart failure or sudden death. Two 10-month-old sibling Nova Scotia Duck Tolling Retrievers (NSDTR) died acutely with evidence of dilated cardiomyopathy with myocardial fibrosis. Association analysis using two cases and 35 controls identified three candidate regions homozygous in the two cases. Whole genome sequencing identified a frameshift deletion in the LMNA gene (NC_049228.1:g.41688530del, NP_001274080:p.(Asp576ThrfsTer124)). Three retrospectively identified NSDTRs with sudden death before 2 years of age and severe myocardial fibrosis were also homozygous for the deletion. One 5 year old with sudden death and myocardial fibrosis was heterozygous for the deletion. This variant was not identified in 722 dogs of other breeds, nor was it identified to be homozygous in 784 NSDTR. LMNA codes for lamin A/C proteins, which are type V intermediate filaments that provide structural support to the nuclear membrane. In humans, LMNA variants can cause DCM with sudden death as well as diseases of striated muscles, lipodystrophy, neuropathies, and accelerated aging disorders. This frameshift deletion is predicted to affect processing of prelamin A into lamin A. Pedigree analysis in the NSDTR and functional evaluation of heterozygotes is consistent with a predominantly recessive mode of inheritance and possibly low penetrance in heterozygotes in contrast to people, where most pathogenic LMNA variants are dominantly inherited.


Subject(s)
Cardiomyopathy, Dilated , Lamin Type A , Humans , Dogs , Animals , Adolescent , Lamin Type A/genetics , Cardiomyopathy, Dilated/genetics , Cardiomyopathy, Dilated/veterinary , Retrospective Studies , Nova Scotia , Fibrosis , Death, Sudden , Pedigree , Mutation
2.
Plant Dis ; 103(7): 1507-1514, 2019 Jul.
Article in English | MEDLINE | ID: mdl-31025904

ABSTRACT

Spread and in-field spatial patterns of vines infected with grapevine red blotch virus (GRBV) were documented in Oregon vineyards using field sampling, molecular diagnostics, and spatial analysis. Grapevine petiole tissue collected from 2013 to 2016 was tested using quantitative polymerase chain reaction for GRBV. At Jacksonville in southern Oregon, 3.1% of vines were infected with GRBV in 2014, and GRBV incidence reached 58.5% of study vines by 2016. GRBV-infected plants and GRBV-uninfected plants were spatially aggregated at this site in 2015, and infected plants were spatially associated between years 2015 and 2016. In a southern Oregon vineyard near Talent, 10.4% of vines were infected with GRBV in 2014, and infection increased annually to 21.5% in 2016. At Talent, distribution of the infected vines was spatially associated across all years. GRBV infection was highest at Yamhill, in the Willamette Valley, where 31.7% of the tested vines had GRBV infection in 2014. By 2016, 59.2% of the vines tested positive for GRBV. Areas of aggregation increased and were spatially associated across all years. From 2013 to 2015, GRBV was not detected at Milton-Freewater in eastern Oregon. Spatial patterns of GRBV infection support evidence of spread by a mobile insect vector. GRBV is a significant threat to Oregon wine grape production because of its drastic year-over-year spread in affected vineyards.


Subject(s)
Geminiviridae , Vitis , Animals , Farms , Geminiviridae/physiology , Oregon , Plant Diseases/virology , Vitis/virology
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