Yasin Heba, Stowe Robert, Wong Chi Kin, Jithesh Puthen Veettil, Zahir Farah R
Life Science, Hamad Bin Khalifa University, Doha, QAT.
Psychiatry and Neurology, University of British Columbia, Vancouver, CAN.
Cureus. 2020 Nov 19;12(11):e11571. doi: 10.7759/cureus.11571.
In 2019, we confirmed that the haploinsufficiency of CHD8 does indeed cause the novel syndromic neurodevelopmental disease we first discovered a dozen years before. Here, we report the first whole transcriptome RNAseq gene expression profiling for a patient with this new syndrome, as a preliminary exploration of potential pathophysiological mechanisms. We compared our patient transcriptome profile with that of all publicly available RNAseq datasets from human cellular models including neuronal progenitor cells, neurons and organoids. We compared differential gene expression profiles overall and conducted phenotype-informed data filtration based on the characteristic syndrome presentation. We found that concordance among differential gene expression profiles was poor across all datasets. Nevertheless, remarkably, we show that the patient blood differential gene expression profile most resembled that of the neuronal cell model, a finding that encourages further transcriptome profiling using patient blood samples. In addition, our custom phenotype-informed analyses yielded important, differentially expressed syndrome pathophysiology target genes. Finally, we note that genes dysregulated due to CHD8 heterozygous deletion are linked to known neurological as well as oncological pathways.
2019年,我们证实CHD8单倍剂量不足确实会引发我们早在十几年前首次发现的新型综合征性神经发育疾病。在此,我们报告了首例针对该新综合征患者的全转录组RNA测序基因表达谱分析,作为对潜在病理生理机制的初步探索。我们将患者的转录组谱与来自人类细胞模型(包括神经祖细胞、神经元和类器官)的所有公开可用RNA测序数据集进行了比较。我们整体比较了差异基因表达谱,并根据特征性综合征表现进行了表型信息数据过滤。我们发现所有数据集中差异基因表达谱之间的一致性较差。然而,值得注意的是,我们发现患者血液中的差异基因表达谱与神经元细胞模型的最为相似,这一发现鼓励使用患者血液样本进行进一步的转录组谱分析。此外,我们基于定制的表型信息分析得出了重要的、差异表达的综合征病理生理靶基因。最后,我们注意到由于CHD8杂合缺失而失调的基因与已知的神经学以及肿瘤学途径相关。