Key result
Long-read sequencing identifies ~18,000 unique genetic variants distinguishing spontaneous hypertensive rat substrains.
Why the study?
Despite a common origin, Spontaneously Hypertensive Rat substrains from different vendors exhibit distinct behavioral phenotypes, particularly in substance use disorder models, but their underlying genomic divergence was uncharacterized.
High-fidelity long-read sequencing of two SHR substrains identified shared variants related to hypertension and unique variants related to synaptic plasticity, providing a genomic resource for studying substance use disorder.
Substrain genomic variants may drive SHR behavioral differences; leaves open standardized models for hypertension and SUD research.
The Spontaneously Hypertensive Rat (SHR) is a widely used model for hypertension and, more recently, for neuropsychiatric disorders such as ADHD and Substance Use Disorder (SUD). Despite a common origin, SHR substrains from different vendors exhibit distinct behavioral phenotypes, particularly in models of SUD. This study characterizes the genomic landscape of two such substrains, SHR/NCrl and SHR/NHsd, using high-fidelity long-read sequencing to identify genetic variants associated with their phenotypic divergence. We identified over 5.8 million variants shared by both substrains compared to the reference genome. These include high-impact variants in genes involved in blood pressure regulation, such as Ramp2 and Npy1r, providing a potential genetic basis for their hypertensive phenotype. We also discovered 17,618 high-confidence variants unique to each substrain. From these, we selected 500 high-quality SNP markers suitable for genetic mapping studies, such as Reduced Complexity Crosses (RCCs). Computational predictions indicated moderate-impact variants in genes involved in neuroplasticity and synaptic function. Notably, the SHR/NHsd substrain carries unique missense variants in Ptpro and Tenm2, genes linked to glutamatergic synapses and SUD-related pathways. In contrast, the SHR/NCrl substrain has unique variants in genes such as Wwc1 and Pcdh10, which are involved in synaptic plasticity and neurotransmission. These findings provide a critical genomic resource for dissecting the heritable components of SUD-related behaviors.
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Abdurahaman et al. (2025) studied Hypertension and Substance Use Disorder (animal model) (n=2). Long-read whole-genome sequencing vs. Reference genome (BN/NHsdMcwi) was evaluated on Identification of shared and unique genetic variants (SNPs, indels, SVs). Long-read whole-genome sequencing identified over 5.8 million shared variants and 17,618 unique variants between SHR/NCrl and SHR/NHsd rat substrains, highlighting genes involved in neuroplasticity and substance use disorders.
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