Suppressor mutations in Rpf2-Rrs1 or Rpl5 bypass the Cgr1 function for pre-ribosomal 5S RNP-rotation.
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Thoms M
Biochemistry Centre, University of Heidelberg, Heidelberg, 69120, Germany. matthias.thoms@bzh.uni-heidelberg.de.
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Mitterer V
Biochemistry Centre, University of Heidelberg, Heidelberg, 69120, Germany.
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Kater L
Gene Center, University of Munich, Munich, 81377, Germany.
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Falquet L
University of Fribourg and Swiss Institute of Bioinformatics, Fribourg, 1700, Switzerland.
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Beckmann R
Gene Center, University of Munich, Munich, 81377, Germany.
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Kressler D
University of Fribourg and Swiss Institute of Bioinformatics, Fribourg, 1700, Switzerland.
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Hurt E
Biochemistry Centre, University of Heidelberg, Heidelberg, 69120, Germany. ed.hurt@bzh.uni-heidelberg.de.
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Published in:
- Nature communications. - 2018
English
During eukaryotic 60S biogenesis, the 5S RNP requires a large rotational movement to achieve its mature position. Cryo-EM of the Rix1-Rea1 pre-60S particle has revealed the post-rotation stage, in which a gently undulating α-helix corresponding to Cgr1 becomes wedged between Rsa4 and the relocated 5S RNP, but the purpose of this insertion was unknown. Here, we show that cgr1 deletion in yeast causes a slow-growth phenotype and reversion of the pre-60S particle to the pre-rotation stage. However, spontaneous extragenic suppressors could be isolated, which restore growth and pre-60S biogenesis in the absence of Cgr1. Whole-genome sequencing reveals that the suppressor mutations map in the Rpf2-Rrs1 module and Rpl5, which together stabilize the unrotated stage of the 5S RNP. Thus, mutations in factors stabilizing the pre-rotation stage facilitate 5S RNP relocation upon deletion of Cgr1, but Cgr1 itself could stabilize the post-rotation stage.
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Language
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Open access status
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gold
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Persistent URL
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https://sonar.ch/global/documents/93864
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