Medical Genetic Institute of Henan Province, Henan Provincial Key Laboratory of Genetic Diseases and Functional Genomics, National Health Commission Key Laboratory of Birth Defects Prevention, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, China.
People's Hospital of Henan University, School of Medicine, Henan University, Zhengzhou, China.
Dev Neurosci. 2022;44(2):113-120. doi: 10.1159/000518923. Epub 2021 Aug 31.
Microcephaly with or without chorioretinopathy, lymphedema, or mental retardation (MCLMR) is an inherited disorder characterized by severe microcephaly and abnormal facial features. Kinesin family member 11 (KIF11) mutations have been reported closely related to microcephaly in different cases, while the pathogenicity was still unclear. Here, we report a de novo heterozygous mutation in exon 20 of the KIF11 (c.2922G>T; p.Pro974=) from a microcephaly patient through whole-exome sequencing. Further studies identified that this variant affected the normal splicing of KIF11 pre-mRNA, thus leading to the c.2815_2922 deletion of exon 20 through PBMC-derived pre-mRNA splicing assay and minigene experiment. Moreover, c.2815_2922 deletion would produce a shortened KIF11 protein, which may competitively bind to the normal KIF11 protein, suggesting a dominant negative effect mechanism in c.2922G>T mutation-induced MCLMR.
小头畸形伴或不伴脉络膜视网膜病变、淋巴水肿或智力障碍(MCLMR)是一种遗传性疾病,其特征为严重的小头畸形和异常的面部特征。已有报道称,驱动蛋白家族成员 11(KIF11)突变与不同病例中的小头畸形密切相关,但致病性仍不清楚。在这里,我们通过全外显子组测序报道了一名小头畸形患者 KIF11 第 20 外显子的从头杂合突变(c.2922G>T;p.Pro974=)。进一步的研究表明,该变体影响了 KIF11 前体 mRNA 的正常剪接,从而通过 PBMC 衍生的前体 mRNA 剪接分析和微基因实验导致第 20 外显子的 c.2815_2922 缺失。此外,c.2815_2922 缺失会产生缩短的 KIF11 蛋白,这可能会与正常的 KIF11 蛋白竞争结合,提示 c.2922G>T 突变诱导的 MCLMR 中存在显性负效应机制。