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The transcription and export complex THO/TREX contributes to transcription termination in plants

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journal contribution
posted on 01.02.2021, 01:32 by Ghazanfar Abbas Khan, Jules Deforges, Rodrigo S Reis, Yi-Fang Hsieh, Jonatan Montpetit, Wojciech Antosz, Luca Santuari, Christian S Hardtke, Klaus D Grasser, Yves Poirier
Transcription termination has important regulatory functions, impacting mRNA stability, localization and translation potential. Failure to appropriately terminate transcription can also lead to read-through transcription and the synthesis of antisense RNAs which can have profound impact on gene expression. The Transcription-Export (THO/TREX) protein complex plays an important role in coupling transcription with splicing and export of mRNA. However, little is known about the role of the THO/TREX complex in the control of transcription termination. In this work, we show that two proteins of the THO/TREX complex, namely TREX COMPONENT 1 (TEX1 or THO3) and HYPER RECOMBINATION1 (HPR1 or THO1) contribute to the correct transcription termination at several loci in Arabidopsis thaliana. We first demonstrate this by showing defective termination in tex1 and hpr1 mutants at the nopaline synthase (NOS) terminator present in a T-DNA inserted between exon 1 and 3 of the PHO1 locus in the pho1-7 mutant. Read-through transcription beyond the NOS terminator and splicing-out of the T-DNA resulted in the generation of a near full-length PHO1 mRNA (minus exon 2) in the tex1 pho1-7 and hpr1 pho1-7 double mutants, with enhanced production of a truncated PHO1 protein that retained phosphate export activity. Consequently, the strong reduction of shoot growth associated with the severe phosphate deficiency of the pho1-7 mutant was alleviated in the tex1 pho1-7 and hpr1 pho1-7 double mutants. Additionally, we show that RNA termination defects in tex1 and hpr1 mutants leads to 3'UTR extensions in several endogenous genes. These results demonstrate that THO/TREX complex contributes to the regulation of transcription termination.


This work was supported by the Swiss National Fund (grant no. 31003A-159998 and 31003A-182462 to YP and the German Research Foundation (grant GR1159/14-2, to KDG. The purchase of the Pacific Biosciences RSII instrument at the University of Lausanne was financed in part by the Loterie Romande through the "Fondation pour la Recherche en Medecine Gentique" ( funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.


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23p. (p. 1-23)


Public Library of Science



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