Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Nat Neurosci. 2018 Dec;21(12):1670-1679. doi: 10.1038/s41593-018-0270-6. Epub 2018 Nov 19.
In females with X-linked genetic disorders, wild-type and mutant cells coexist within brain tissue because of X-chromosome inactivation, posing challenges for interpreting the effects of X-linked mutant alleles on gene expression. We present a single-nucleus RNA sequencing approach that resolves mosaicism by using single-nucleotide polymorphisms in genes expressed in cis with the X-linked mutation to determine which nuclei express the mutant allele even when the mutant gene is not detected. This approach enables gene expression comparisons between mutant and wild-type cells within the same individual, eliminating variability introduced by comparisons to controls with different genetic backgrounds. We apply this approach to mosaic female mouse models and humans with Rett syndrome, an X-linked neurodevelopmental disorder caused by mutations in the gene encoding the methyl-DNA-binding protein MECP2, and observe that cell-type-specific DNA methylation predicts the degree of gene upregulation in MECP2-mutant neurons. This approach can be broadly applied to study gene expression in mosaic X-linked disorders.
在 X 连锁遗传疾病的女性中,由于 X 染色体失活,野生型和突变型细胞共存于脑组织中,这给解释 X 连锁突变等位基因对基因表达的影响带来了挑战。我们提出了一种单细胞核 RNA 测序方法,该方法利用与 X 连锁突变顺式表达的基因中的单核苷酸多态性来解析镶嵌性,从而确定即使突变基因未被检测到,哪些细胞核表达突变等位基因。这种方法可以在同一个体的突变型和野生型细胞之间进行基因表达比较,消除了与具有不同遗传背景的对照进行比较所引入的变异性。我们将这种方法应用于镶嵌型雌性小鼠模型和患有 Rett 综合征的人类,Rett 综合征是一种由编码甲基化 DNA 结合蛋白 MECP2 的基因突变引起的 X 连锁神经发育障碍,我们观察到细胞类型特异性 DNA 甲基化可预测 MECP2 突变神经元中基因上调的程度。这种方法可以广泛应用于研究 X 连锁镶嵌性疾病中的基因表达。