Research Paper Volume 12, Issue 5 pp 4268—4282
GAA compound heterozygous mutations associated with autophagic impairment cause cerebral infarction in Pompe disease
- 1 Joint Laboratory for Translational Medicine Research, Liaocheng People's Hospital, Liaocheng 252000, Shandong, P.R. China
- 2 BGI-Qingdao, BGI-Shenzhen, Qingdao 266555, P.R. China
- 3 Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, Liaocheng 252000, Shandong, P.R. China
- 4 Department of Clinical laboratory, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, Liaocheng 252000, Shandong, P.R. China
- 5 Department of Radiology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, Liaocheng 252000, Shandong, P.R. China
- 6 Shandong First Medical University, Taian 271016, Shandong, P.R. China
- 7 Department of Ophthalmology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, Liaocheng 252000, Shandong, P.R. China
- 8 BGI-Shenzhen, Shenzhen 518083, P.R. China
- 9 China National GeneBank, BGI-Shenzhen, Shenzhen 518120, P.R. China
- 10 BGI-Fuyang, BGI-Shenzhen, Fuyang 236009, P.R. China
- 11 School of Biology and Biological Engineering, South China University of Technology, Guangzhou 510006, P.R. China
- 12 School of Medicine Shandong University, Jinan 250012, Shandong, P.R. China
Received: November 5, 2019 Accepted: February 4, 2020 Published: March 3, 2020
https://doi.org/10.18632/aging.102879How to Cite
Copyright © 2020 Jia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Clinical manifestations of the late-onset adult Pompe disease (glycogen storage disease type II) are heterogeneous. To identify genetic defects of a special patient population with cerebrovascular involvement as the main symptom, we performed whole-genome sequencing (WGS) analysis on a consanguineous Chinese family of total eight members including two Pompe siblings both had cerebral infarction. Two novel compound heterozygous variants were found in GAA gene: c.2238G>C in exon 16 and c.1388_1406del19 in exon 9 in the two patients. We verified the function of the two mutations in leading to defects in GAA protein expression and enzyme activity that are associated with autophagic impairment. We further performed a gut microbiome metagenomics analysis, found that the child’s gut microbiome metagenome is very similar to his mother. Our finding enriches the gene mutation spectrum of Pompe disease, and identified the association of the two new mutations with autophagy impairment. Our data also indicates that gut microbiome could be shared within Pompe patient and cohabiting family members, and the abnormal microbiome may affect the blood biochemical index. Our study also highlights the importance of deep DNA sequencing in potential clinical applications.