Hegde Rajat, Hegde Smita, Kulkarni Suyamindra S, Pandurangi Aditya, Gai Pramod B, Das Kusal K
Laboratory of Vascular Physiology and Medicine, Department of Physiology, Shri B.M Patil Medical College, Hospital and Research Centre, BLDE (Deemed to be University), Vijayapura, Karnataka 586101, India.
Karnataka Institute for DNA Research (KIDNAR), Dharwad, Karnataka 580003, India.
Genomics Inform. 2021 Dec;19(4):e44. doi: 10.5808/gi.21029. Epub 2021 Dec 31.
Autism is a complex neurodevelopmental disorder, the prevalence of which has increased drastically in India in recent years. Neuroligin is a type I transmembrane protein that plays a crucial role in synaptogenesis. Alterations in synaptic genes are most commonly implicated in autism and other cognitive disorders. The present study investigated the neuroligin 3 gene in the Indian autistic population by sequencing and in silico pathogenicity prediction of molecular changes. In total, 108 clinically described individuals with autism were included from the North Karnataka region of India, along with 150 age-, sex-, and ethnicity-matched healthy controls. Genomic DNA was extracted from peripheral blood, and exonic regions were sequenced. The functional and structural effects of variants of the neuroligin 3 protein were predicted. One coding sequence variant (a missense variant) and four non-coding variants (two 5'-untranslated region [UTR] variants and two 3'-UTR variants) were recorded. The novel missense variant was found in 25% of the autistic population. The C/C genotype of c.551T>C was significantly more common in autistic children than in controls (p = 0.001), and a significantly increased risk of autism (24.7-fold) was associated with this genotype (p = 0.001). The missense variant showed pathogenic effects and high evolutionary conservation over the functions of the neuroligin 3 protein. In the present study, we reported a novel missense variant, V184A, which causes abnormal neuroligin 3 and was found with high frequency in the Indian autistic population. Therefore, neuroligin is a candidate gene for future molecular investigations and functional analysis in the Indian autistic population.
自闭症是一种复杂的神经发育障碍,近年来在印度其患病率急剧上升。神经连接蛋白是一种I型跨膜蛋白,在突触形成中起关键作用。突触基因的改变最常与自闭症和其他认知障碍有关。本研究通过对印度自闭症患者群体进行测序以及对分子变化进行计算机致病性预测,来研究神经连接蛋白3基因。总共纳入了来自印度北卡纳塔克邦地区的108名临床诊断为自闭症的个体,以及150名年龄、性别和种族匹配的健康对照。从外周血中提取基因组DNA,并对外显子区域进行测序。预测了神经连接蛋白3蛋白变体的功能和结构效应。记录到一个编码序列变体(一个错义变体)和四个非编码变体(两个5'非翻译区[UTR]变体和两个3'UTR变体)。在25%的自闭症患者群体中发现了这种新的错义变体。c.551T>C的C/C基因型在自闭症儿童中比在对照组中显著更常见(p = 0.001),并且这种基因型与自闭症风险显著增加(24.7倍)相关(p = 0.001)。该错义变体对神经连接蛋白3蛋白的功能显示出致病作用和高度的进化保守性。在本研究中,我们报告了一种新的错义变体V184A,它导致神经连接蛋白3异常,并且在印度自闭症患者群体中高频出现。因此,神经连接蛋白是印度自闭症患者群体未来分子研究和功能分析的候选基因。