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The SMC Loader Scc2 Promotes ncRNA Biogenesis and Translational Fidelity
by
Gerton, Jennifer L
, Peak, Allison
, Blanchette, Marco
, Seidel, Chris
, Ross, Rhonda Trimble
, Zakari, Musinu
in
Biosynthesis
/ Chromosomes
/ Defects
/ Deoxyribonucleic acid
/ DNA
/ Experiments
/ Funding
/ Gene expression
/ Growth rate
/ Mutation
/ Protein synthesis
/ Proteins
/ Saccharomyces cerevisiae
/ Yeast
2015
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The SMC Loader Scc2 Promotes ncRNA Biogenesis and Translational Fidelity
by
Gerton, Jennifer L
, Peak, Allison
, Blanchette, Marco
, Seidel, Chris
, Ross, Rhonda Trimble
, Zakari, Musinu
in
Biosynthesis
/ Chromosomes
/ Defects
/ Deoxyribonucleic acid
/ DNA
/ Experiments
/ Funding
/ Gene expression
/ Growth rate
/ Mutation
/ Protein synthesis
/ Proteins
/ Saccharomyces cerevisiae
/ Yeast
2015
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
The SMC Loader Scc2 Promotes ncRNA Biogenesis and Translational Fidelity
by
Gerton, Jennifer L
, Peak, Allison
, Blanchette, Marco
, Seidel, Chris
, Ross, Rhonda Trimble
, Zakari, Musinu
in
Biosynthesis
/ Chromosomes
/ Defects
/ Deoxyribonucleic acid
/ DNA
/ Experiments
/ Funding
/ Gene expression
/ Growth rate
/ Mutation
/ Protein synthesis
/ Proteins
/ Saccharomyces cerevisiae
/ Yeast
2015
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The SMC Loader Scc2 Promotes ncRNA Biogenesis and Translational Fidelity
Journal Article
The SMC Loader Scc2 Promotes ncRNA Biogenesis and Translational Fidelity
2015
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Overview
The Scc2-Scc4 complex is essential for loading the cohesin complex onto DNA. Cohesin has important roles in chromosome segregation, DSB repair, and chromosome condensation. Here we report that Scc2 is important for gene expression in budding yeast. Scc2 and the transcriptional regulator Paf1 collaborate to promote the production of Box H/ACA snoRNAs which guide pseudouridylation of RNAs including ribosomal RNA. Mutation of SCC2 was associated with defects in the production of ribosomal RNA, ribosome assembly, and splicing. While the scc2 mutant does not have a general defect in protein synthesis, it shows increased frameshifting and reduced cap-independent translation. These findings suggest Scc2 normally promotes a gene expression program that supports translational fidelity. We hypothesize that translational dysfunction may contribute to the human disorder Cornelia de Lange syndrome, which is caused by mutations in NIPBL, the human ortholog of SCC2.
Publisher
Public Library of Science
Subject
MBRLCatalogueRelatedBooks
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