Xu Shunbin, Coku Ardian, Muraleedharan Chithra K, Harajli Ali, Mishulin Eric, Dahabra Chafic, Choi Joanne, Garcia William J, Webb Kaylie, Birch David, Goetz Kerry, Li Weifeng
Department of Ophthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, Detroit, MI, United States.
Department of Biological Sciences, Wayne State University, Detroit, MI, United States.
Front Cell Dev Biol. 2020 Dec 23;8:619641. doi: 10.3389/fcell.2020.619641. eCollection 2020.
Inherited retinal dystrophy (IRD) is a heterogenous blinding eye disease and affects more than 200,000 Americans and millions worldwide. By far, 270 protein-coding genes have been identified to cause IRD when defective. However, only one microRNA (miRNA), miR-204, has been reported to be responsible for IRD when a point-mutation occurs in its seed sequence. Previously, we identified that a conserved, polycistronic, paralogous miRNA cluster, the miR-183/96/182 cluster, is highly specifically expressed in all photoreceptors and other sensory organs; inactivation of this cluster in mice resulted in syndromic IRD with multi-sensory defects. We hypothesized that mutations in the miR-183/96/182 cluster in human cause IRD. To test this hypothesis, we perform mutation screening in the pre-miR-183, -96, -182 in >1000 peripheral blood DNA samples of patients with various forms of IRD. We identified six sequence variants, three in pre-miR-182 and three in pre-miR-96. These variants are in the pre-miRNA-182 or -96, but not in the mature miRNAs, and are unlikely to be the cause of the IRD in these patients. In spite of this, the nature and location of these sequence variants in the pre-miRNAs suggest that some may have impact on the biogenesis and maturation of miR-182 or miR-96 and potential roles in the susceptibility to diseases. Although reporting on negative results so far, our study established a system for mutation screening in the miR-183/96/182 cluster in human for a continued effort to unravel and provides deeper insight into the potential roles of miR-183/96/182 cluster in human diseases.
遗传性视网膜营养不良(IRD)是一种异质性致盲眼病,影响超过20万美国人以及全球数百万人。到目前为止,已确定有270个蛋白质编码基因在发生缺陷时会导致IRD。然而,据报道,只有一种微小RNA(miRNA),即miR-204,当其种子序列发生点突变时会导致IRD。此前,我们发现一个保守的、多顺反子的、旁系同源miRNA簇,即miR-183/96/182簇,在所有光感受器和其他感觉器官中高度特异性表达;该簇在小鼠中的失活导致了伴有多感觉缺陷的综合征性IRD。我们推测人类miR-183/96/182簇中的突变会导致IRD。为了验证这一假设,我们对1000多个患有各种形式IRD患者的外周血DNA样本中的前体miR-183、-96、-182进行了突变筛查。我们鉴定出六个序列变体,三个在前体miR-182中,三个在前体miR-96中。这些变体存在于前体miRNA-182或-96中,而不是成熟的miRNA中,不太可能是这些患者IRD的病因。尽管如此,这些前体miRNA中序列变体的性质和位置表明,其中一些可能会影响miR-182或miR-96的生物合成和成熟,并在疾病易感性中发挥潜在作用。尽管目前报道的是阴性结果,但我们的研究建立了一个用于人类miR-183/96/182簇突变筛查的系统,以便继续努力揭示并更深入地了解miR-183/96/182簇在人类疾病中的潜在作用。