Table 3.
Results obtained by using methylome sequencing methods (multimodal omics sequencing methods) and categories of those findings.
| Categories | Method | Results | Ref |
|---|---|---|---|
| Development | scCOOL-seq | Chromatin conformation and DNA methylation undergo distinct changes that do not happen simultaneously following fertilization | 74 |
| scNOMeRe-seq | Role of DNA methylation remodeling in reconstructing genetic lineages in early embryos | 86 | |
| scTrio-seq2 | Slower genome demethylation in primitive endoderm cells than in epiblast and trophectoderm cells | 71 | |
| sn-m3C-seq | Remodeling of DNA methylation is temporally separated from chromatin state dynamics and mainly occurs during late-gestational to early-infant-development (In human frontal cortex and hippocampus) | 65 | |
| iscCOOL-seq | Integrating and analyzing of chromatin accessibility, DNA methylation and gene expression in growing mouth oocytes | 73 | |
| scM&T-seq | Correlations of methylation patterns of distal regulatory regions with gene expression (pluripotency factors) | 60 | |
| scNMT-seq | De novo methyltransferase is dispensable for major cell type development at E8.5 in mouse development but crucial for silencing prior or alternative cell fates such as pluripotency and extraembryonic programs | 98 | |
| Brain | scMT-seq | Negative correlation between methylation in non-CGI promoters and gene expression in dorsal root ganglion neurons | 61 |
| snmCAT-seq | Reconstruction of regulatory lineages for cortical cell populations Identification of distinct genetic risk enrichment associated with neuropsychiatric traits | 87 | |
| sn-m3C-seq | Constructing single-cell DNA methylome and 3D genome structure atlas of adult mouse brain | 66 | |
| Senescence | scM&T-seq | Relation of aging with a global increase in transcription and methylation heterogeneity | 99 |
| Tumor | scTrio-seq | Identification of subpopulation of human hepatocellular carcinoma cells and cellular heterogeneity within a subpopulation | 69 |
| scTrio-seq2 | Differences in DNA methylation levels between primary and metastatic colorectal tumors are mainly caused by the different sublineage composition | 70 |