Regulation of transcription elongation by RNA polymerase II (Pol II) is a key regulatory step in gene transcription. Recently, the little elongation complex (LEC)—which contains the transcription elongation factor ELL/EAF—was found to be required for the transcription of Pol II-dependent small nuclear RNA (snRNA) genes. Here, we show that the human Mediator subunit MED26 plays a role in the recruitment of LEC to a subset of snRNA genes through direct interaction of EAF and the N-terminal domain (NTD) of MED26. Loss of MED26 in cells decreases the occupancy of LEC at a subset of snRNA genes and results in a reduction in their transcription. Our results suggest that the MED26 NTD functions as a molecular switch in the exchange of TBP-associated factor 7 (TAF7) for LEC in order to facilitate the transition from initiation to elongation during transcription of a subset of snRNA genes.

Mediator is a coregulatory complex that regulates transcription of Pol II-dependent genes. Previously, we showed that human Mediator subunit MED26 plays a role in the recruitment of Super Elongation Complex (SEC) or Little Elongation Complex (LEC) to regulate the expression of certain genes. MED26 plays a role in recruiting SEC to protein-coding genes including c-myc and LEC to small nuclear RNA (snRNA) genes. However, how MED26 engages SEC or LEC to regulate distinct genes is unclear. Here, we provide evidence that MED26 recruits LEC to modulate transcription termination of non-polyadenylated transcripts including snRNAs and mRNAs encoding replication-dependent histone (RDH) at Cajal bodies. Our findings indicate that LEC recruited by MED26 promotes efficient transcription termination by Pol II through interaction with CBC-ARS2 and NELF/DSIF, and promotes 3′ end processing by enhancing recruitment of Integrator or Heat Labile Factor to snRNA or RDH genes, respectively.

1 These two individuals contributed equally to this work. Key words: TRIM45, NF-B, MAPK, TNF , cell proliferation 2 AbstractThe NF-B signaling pathway plays an important role in cell survival, immunity, inflammation, carcinogenesis, and organogenesis. Activation of NF-B is regulated by several posttranslational modifications including phosphorylation, neddylation and ubiquitination. The NF-B signaling pathway is activated by two distinct signaling mechanisms and is strictly modulated by the ubiquitin-proteasome system. It has been reported that overexpression of TRIM45, one of the TRIM family ubiquitin ligases, suppresses transcriptional activities of Elk-1 and AP-1, which are targets of the MAPK signaling pathway. In this study, we showed that TRIM45 also negatively regulates TNF -induced NF-B-mediated transcription by a luciferase reporter assay and that TRIM45 lacking a RING domain also has an activity to inhibit the NF-B signal.Moreover, we found that TRIM45 overexpression suppresses cell growth. These findings suggest that TRIM45 acts as a repressor for the NF-B signal and regulates cell growth.3

We present ionized gas properties of nine local ultra/luminous infrared galaxies (U/LIRGs) at z < 0.04 through Integral Field Unit (IFU) observations with KOOLS-IFU on the Seimei Telescope. The observed targets are drawn from the Great Observatories All-sky LIRG Survey (GOALS), covering a wide range of merger stages. We successfully detect emission lines such as Hβ, [O iii]λ5007, Hα, [N ii]λλ6549, 6583, and [S ii]λλ6717, 6731 with a spectral resolution of R = 1500–2000, which provides (i) a spatially resolved (∼200–700 pc) moment map of ionized gas and (ii) diagnostics for an active galactic nucleus (AGN) within the central ∼3–11 kpc in diameter for our sample. We find that the [O iii] outflow that is expected to be driven by an AGN tends to be stronger (i) towards the galactic center and (ii) as a sequence of the merger stage. In particular, the outflow strength in the late-stage (stage D) mergers is about 1.5 times stronger than that in the early-state (stage B) mergers, which indicates that galaxy mergers could induce AGN-driven outflow and play an important role in the co-evolution of galaxies and supermassive black holes.