Table 1
Recent literature focusing on enhancer transcription.
| Paper | Major finding | RNA | Enhancer-promoter interactions | Org. | Cell type | Transcript directionality | Poly(A) | length (kb) |
|---|---|---|---|---|---|---|---|---|
| Kim et al. 2010 | Widespread enhancer transcription (eRNA) in response to stimulation of neurons. | RNA-seq | NR | Mo | primary cortical neurons | bi | (−) | < 2 |
| DeSanta et al. 2010 | Pol II occupies intragenic sites and many are transcriptionally active enhancers. Enhancer activity induced by LPS. | FANTOM, RNA-seq | 3C | Mo | macrophage | uni | (+) | 0.1 to 7 |
| Orom et al. 2010 | Activating RNAs are intergenic transcripts capable of increasing adjacent and non-adjacent gene expression. | GENCODE, custom microarray | NR | Hu | multiple cell lines & primary cells | uni (spliced) | (+) | 0.1 to 9 |
| Wang et al. 2011 | Enhancer responds to AR binding in different ways, suggesting multiple classes of transcriptionally active enhancers. | GRO-seq | 3C | Hu | prostatic adenocarcinoma | bi | NR | ~ 1 |
| Koch et al. 2011 | Enhancer transcripts can be poly(A)+ or poly(A)−, and poly(A)+ enhancers have H3K36me3. Enhancers are primarily bound by the initiating form of Pol II. | RNA-seq | NR | Hu | double-positive thymocytes | both* | 60% (+) 40% (−) | > 4 (+) 2 to 3 (−) |
| Kowalczyk et al. 2012 | Inter and intragenic enhancers produce transcripts that exactly mirror the gene structure with the exception of the first exon. Multi-exonic poly(A)+ RNA (meRNA) | RNA-seq | NR | Mo & Hu | multiple cell lines & primary cells | both** | uni: (+) bi: (−) | uni: length of gene bi: ~ 1 |
| Melo et al. 2013 | Enhancer-promoter interactions exist prior to activation. Tethered eRNA is able to induce transcription of reporter gene. | qRT-PCR | 4C | Hu | breast adenocarcinoma & primary fibroblasts | uni | (−) | ~ 0.6 |
| Lai et al. 2013 | ncRNA-a physically interact with Mediator and are required for full target gene upregulation and enhancer-promoter interactions. Transcripts stimulate H3S10ph. | qRT-PCR | 3C | Hu | breast adenocarcinoma & lung carcinoma | uni (spliced) | (+) | ~ 0.4 |
| Hah et al. 2013 | Inhibiting eRNA elongation does not prevent enhancer-promoter interactions. | GRO-seq | 3C, ChIA-PET (Fullwood et al. 2009) | Hu | breast adenocarcinoma | both | (+) | 5-Mar |
| Lam et al. 2013 | Rev-Erb binding represses enhancer transcription and consequently enhancer activity. Transcripts are required for enhancer activity. | GRO-seq, 5′-GRO-seq | NR | Mo | macrophage | bi | NR | < 2 |
| Li et al. 2013 | Enhancer transcripts are necessary for enhancer-promoter interactions and their contribution is sequence specific. | GRO-seq | 3D-DSL | Hu | breast adenocarcinoma | bi | NR | NR |
| Kaikkonen et al. 2013 | Enhancer transcription is mechanistically linked to H3K4me1/2 deposition | GRO-seq | NR | Mo | primary bone marrow | both, mostly bi | NR | uni: <1.5 bi: ~2 |
*The majority of both poly(A)+ and poly(A)− transcripts were unidirectional, with an increase in bidirectional transcripts in the poly(A) − fraction.
**A single enhancer can transcribed short (~1 kb), bidirectional poly(A)− transcripts in addition to long, unidirectional poly(A)+ transcripts that mirror the structure of the gene.
3D-DSL = three-dimensional DNA selection and ligation; 3C = chromosome conformation capture; 4C = circularized chromosome conformation capture; NR = not reported; LPS = lipopolysaccharide; AR = androgen receptor; Hu = human; Mo = mouse.