Plassais Jocelyn, Lagoutte Laetitia, Correard Solenne, Paradis Manon, Guaguère Eric, Hédan Benoit, Pommier Alix, Botherel Nadine, Cadiergues Marie-Christine, Pilorge Philippe, Silversides David, Bizot Maud, Samuels Mark, Arnan Carme, Johnson Rory, Hitte Christophe, Salbert Gilles, Méreau Agnès, Quignon Pascale, Derrien Thomas, André Catherine
CNRS, UMR 6290, Institut de Génétique et Développement de Rennes, Rennes, France.
Université Rennes 1, UEB, Biosit, Faculté de Médecine, Rennes, France.
PLoS Genet. 2016 Dec 29;12(12):e1006482. doi: 10.1371/journal.pgen.1006482. eCollection 2016 Dec.
Human Hereditary Sensory Autonomic Neuropathies (HSANs) are characterized by insensitivity to pain, sometimes combined with self-mutilation. Strikingly, several sporting dog breeds are particularly affected by such neuropathies. Clinical signs appear in young puppies and consist of acral analgesia, with or without sudden intense licking, biting and severe self-mutilation of the feet, whereas proprioception, motor abilities and spinal reflexes remain intact. Through a Genome Wide Association Study (GWAS) with 24 affected and 30 unaffected sporting dogs using the Canine HD 170K SNP array (Illumina), we identified a 1.8 Mb homozygous locus on canine chromosome 4 (adj. p-val = 2.5x10-6). Targeted high-throughput sequencing of this locus in 4 affected and 4 unaffected dogs identified 478 variants. Only one variant perfectly segregated with the expected recessive inheritance in 300 sporting dogs of known clinical status, while it was never present in 900 unaffected dogs from 130 other breeds. This variant, located 90 kb upstream of the GDNF gene, a highly relevant neurotrophic factor candidate gene, lies in a long intergenic non-coding RNAs (lincRNA), GDNF-AS. Using human comparative genomic analysis, we observed that the canine variant maps onto an enhancer element. Quantitative RT-PCR of dorsal root ganglia RNAs of affected dogs showed a significant decrease of both GDNF mRNA and GDNF-AS expression levels (respectively 60% and 80%), as compared to unaffected dogs. We thus performed gel shift assays (EMSA) that reveal that the canine variant significantly alters the binding of regulatory elements. Altogether, these results allowed the identification in dogs of GDNF as a relevant candidate for human HSAN and insensitivity to pain, but also shed light on the regulation of GDNF transcription. Finally, such results allow proposing these sporting dog breeds as natural models for clinical trials with a double benefit for human and veterinary medicine.
人类遗传性感觉自主神经病(HSANs)的特征是对疼痛不敏感,有时还伴有自残行为。令人惊讶的是,几种运动犬品种尤其易受此类神经病影响。临床症状出现在幼犬身上,表现为肢体末端镇痛,伴有或不伴有突然强烈舔舐、啃咬以及严重的足部自残行为,而本体感觉、运动能力和脊髓反射仍保持正常。通过使用犬类HD 170K SNP芯片(Illumina)对24只患病和30只未患病的运动犬进行全基因组关联研究(GWAS),我们在犬类4号染色体上鉴定出一个1.8 Mb的纯合位点(校正p值 = 2.5×10-6)。对该位点在4只患病犬和4只未患病犬中进行靶向高通量测序,共鉴定出478个变异。在已知临床状态的300只运动犬中,只有一个变异与预期的隐性遗传完全分离,而在来自130个其他品种的900只未患病犬中从未出现过。这个变异位于胶质细胞源性神经营养因子(GDNF)基因上游90 kb处,GDNF是一个高度相关的神经营养因子候选基因,位于一个长链基因间非编码RNA(lincRNA),即GDNF-AS中。通过人类比较基因组分析,我们发现犬类变异定位到一个增强子元件上。与未患病犬相比,患病犬背根神经节RNA的定量RT-PCR显示GDNF mRNA和GDNF-AS表达水平均显著降低(分别降低60%和80%)。因此,我们进行了凝胶迁移实验(EMSA),结果表明犬类变异显著改变了调控元件的结合。总之,这些结果使我们能够在犬类中鉴定出GDNF是人类HSAN和疼痛不敏感的一个相关候选基因,同时也揭示了GDNF转录的调控机制。最后,这些结果使得可以将这些运动犬品种作为临床试验的天然模型,对人类医学和兽医学都有双重益处。