Increasing studies have revealed that long noncoding RNAs (lncRNAs) are not transcriptional noise but play important roles in the regulation of a wide range of biological processes, and the dysregulation of lncRNA genes is associated with disease development. Alzheimer’s disease (AD) is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. However, little is known about the roles of lncRNA genes in AD and how the lncRNA genes are transcriptionally regulated.
Here, researchers from the Harbin Institute of Technology analyzed RNA-seq data and ChIP-seq histone modification data from CK-p25 AD model and control mice and identified 72 differentially expressed lncRNA genes, 4,917 differential peaks of H3K4me3, and 1,624 differential peaks of H3K27me3 between AD and control samples, respectively. Furthermore, they found 92 differential peaks of histone modification H3K4me3 are located in the promoter of 39 differentially expressed lncRNA genes and 8 differential peaks of histone modification H3K27me3 are located upstream of 7 differentially expressed lncRNA genes, which suggest that the majority of lncRNA genes may be transcriptionally regulated by histone modification in AD.
Positive association between expression level of differential lncRNA genes and H3K4me3 modification level in promoters of the differential lncRNA genes
(a) Scatter diagram and a fitting line show the positive association between fold change of lncRNA gene expression and fold change of H3K4me3 modification level in the promoter. (b) Boxplot of expression level of differential lncRNA genes and H3K4me3 modification level in the promoters of the differential lncRNA genes in AD and control samples, respectively, which shows that lncRNA genes with high H3K4me3 level in the promoters have high expression level. The circle in (b) refers to a singular point in statistics, differential from other points. But the singular point has statistical significance, showing the accuracy and objectivity of this article.