Institute for Auditory Neuroscience and InnerEarLab, University Medical Center Göttingen, Göttingen, Germany
Institute for Auditory Neuroscience and InnerEarLab, University Medical Center Göttingen, Göttingen, Germany.
EMBO Rep. 2017 Nov;18(11):2015-2029. doi: 10.15252/embr.201643689. Epub 2017 Sep 11.
Lipopolysaccharide-responsive beige-like anchor protein (LRBA) belongs to the enigmatic class of BEACH domain-containing proteins, which have been attributed various cellular functions, typically involving intracellular protein and membrane transport processes. Here, we show that LRBA deficiency in mice leads to progressive sensorineural hearing loss. In LRBA knockout mice, inner and outer hair cell stereociliary bundles initially develop normally, but then partially degenerate during the second postnatal week. LRBA deficiency is associated with a reduced abundance of radixin and Nherf2, two adaptor proteins, which are important for the mechanical stability of the basal taper region of stereocilia. Our data suggest that due to the loss of structural integrity of the central parts of the hair bundle, the hair cell receptor potential is reduced, resulting in a loss of cochlear sensitivity and functional loss of the fraction of spiral ganglion neurons with low spontaneous firing rates. Clinical data obtained from two human patients with protein-truncating nonsense or frameshift mutations suggest that LRBA deficiency may likewise cause syndromic sensorineural hearing impairment in humans, albeit less severe than in our mouse model.
脂多糖反应性米色样锚蛋白 (LRBA) 属于神秘的 BEACH 结构域蛋白家族,具有多种细胞功能,通常涉及细胞内蛋白质和膜运输过程。在这里,我们证明了 LRBA 缺陷的小鼠会导致进行性感觉神经性听力损失。在 LRBA 敲除小鼠中,内毛细胞和外毛细胞的纤毛束最初发育正常,但在出生后第二周部分退化。LRBA 缺陷与两种衔接蛋白 radixin 和 Nherf2 的丰度降低有关,这两种衔接蛋白对于纤毛基部锥形区的机械稳定性很重要。我们的数据表明,由于毛束中心部分的结构完整性丧失,毛细胞的感受器电位降低,导致耳蜗敏感性降低,以及自发发放率较低的螺旋神经节神经元部分功能丧失。从两名具有蛋白质截断无义或移码突变的人类患者获得的临床数据表明,LRBA 缺陷也可能导致人类综合征性感觉神经性听力障碍,尽管比我们的小鼠模型要轻。