SNAP output for PDB entry 5ola [SNAP web server]

PDB-id

5ola; SNAP-derived features in text and JSON formats; DNAproDB

Class

transcription

Method

X-ray (3.904 Å)

Summary

Structure of mitochondrial transcription elongation complex in complex with elongation factor tefm

Reference

Hillen HS, Parshin AV, Agaronyan K, Morozov YI, Graber JJ, Chernev A, Schwinghammer K, Urlaub H, Anikin M, Cramer P, Temiakov D (2017): "Mechanism of Transcription Anti-termination in Human Mitochondria." Cell, 171, 1082-1093.e13. doi: 10.1016/j.cell.2017.09.035.

Abstract

In human mitochondria, transcription termination events at a G-quadruplex region near the replication origin are thought to drive replication of mtDNA by generation of an RNA primer. This process is suppressed by a key regulator of mtDNA-the transcription factor TEFM. We determined the structure of an anti-termination complex in which TEFM is bound to transcribing mtRNAP. The structure reveals interactions of the dimeric pseudonuclease core of TEFM with mobile structural elements in mtRNAP and the nucleic acid components of the elongation complex (EC). Binding of TEFM to the DNA forms a downstream "sliding clamp," providing high processivity to the EC. TEFM also binds near the RNA exit channel to prevent formation of the RNA G-quadruplex structure required for termination and thus synthesis of the replication primer. Our data provide insights into target specificity of TEFM and mechanisms by which it regulates the switch between transcription and replication of mtDNA.