scholarly journals β-Actin and Nuclear Myosin I are responsible for nucleolar reorganization during DNA Repair

2019 ◽  
Author(s):  
Elena Cerutti ◽  
Laurianne Daniel ◽  
Lise-Marie Donnio ◽  
Damien Neuillet ◽  
Charlene Magnani ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Rna Polymerase I ◽  
Dna And Rna ◽  
Beta Actin ◽  
Myosin I ◽  
Nuclear Myosin I ◽  
Polymerase I

AbstractDuring DNA Repair, ribosomal DNA and RNA polymerase I (rDNA/RNAP1) are reorganized within the nucleolus. Until now, the proteins and the molecular mechanism governing this reorganisation remained unknown.Here we show that Nuclear Myosin I (NMI) and Nuclear Beta Actin (ACTβ) are essential for the proper reorganisation of the nucleolus, after completion of the DNA Repair reaction.In NMI and ACTβ depleted cells, the rDNA/RNAP1 complex can be displaced at the periphery of the nucleolus after DNA damage but cannot re-enter within the nucleolus after completion of the DNA Repair. Both proteins act concertedly in this process. NMI binds the damaged rDNA at the periphery of the nucleolus, while ACTβ brings the rDNA back within the nucleolus after DNA repair completion. Our results reveal a previously unidentified function for NMI and ACTβ and disclose how these two proteins work in coordination to re-establish the proper rDNA position after DNA repair.

scholarly journals RNase H enables efficient repair of R-loop induced DNA damage

2016 ◽  
Author(s):  
Jeremy D. Amon ◽  
Douglas Koshland
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Ribosomal Dna ◽  
Genome Instability ◽  
Rnase H ◽  
Rna Polymerase I ◽  
Chromosomal Dna ◽  
Polymerase I ◽  
Break Induced Replication ◽  
Kinetics Of

AbstractR-loops, three-stranded structures that form when transcripts hybridize to chromosomal DNA, are potent agents of genome instability. This instability has been explained by the ability of R-loops to induce DNA damage. Here, we show that persistent R-loops also compromise DNA repair. Depleting endogenous RNase H activity impairs R-loop removal in budding yeast, causing DNA damage that occurs preferentially in the repetitive ribosomal DNA locus (rDNA). We analyzed the repair kinetics of this damage and identified mutants that modulate repair. Our results indicate that persistent R-loops in the rDNA induce damage that is slowly repaired by break-induced replication (BIR). Furthermore, R-loop induced BIR at the rDNA leads to lethal repair intermediates when RNA polymerase I elongation is compromised. We present a model to explain how removal of R-loops by RNase H is critical in ensuring the efficient repair of R-loop induced DNA damage by pathways other than BIR.

scholarly journals Nuclear myosin I acts in concert with polymeric actin to drive RNA polymerase I transcription

2008 ◽  
Vol 22 (3) ◽  
pp. 322-330 ◽  
Author(s):  
J. Ye ◽  
J. Zhao ◽  
U. Hoffmann-Rohrer ◽  
I. Grummt
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase I ◽  
Myosin I ◽  
Nuclear Myosin I ◽  
Polymerase I ◽  
Polymeric Actin

Abstract A46: Wnt5a signals through DVL1 to repress ribosomal DNA transcription by RNA polymerase I

2017 ◽  
Author(s):  
Randall Dass ◽  
Aishe Sarshad ◽  
Brittany Carson ◽  
Jennifer Feenstra ◽  
Amanpreet Kaur ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Rna Polymerase I ◽  
Dna Transcription ◽  
Polymerase I

scholarly journals Role of TATA Binding Protein (TBP) in Yeast Ribosomal DNA Transcription by RNA Polymerase I: Defects in the Dual Functions of Transcription Factor UAF Cannot Be Suppressed by TBP

2001 ◽  
Vol 21 (7) ◽  
pp. 2292-2297 ◽  
Author(s):  
Imran Siddiqi ◽  
John Keener ◽  
Loan Vu ◽  
Masayasu Nomura
Keyword(s):  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Binding Protein ◽  
Tata Binding Protein ◽  
Rna Polymerase I ◽  
Pol Ii ◽  
Rrna Transcription ◽  
Pol I ◽  
Mutant Strains ◽  
Polymerase I

ABSTRACT Initiation of ribosomal DNA (rDNA) transcription by RNA polymerase I (Pol I) in the yeast Saccharomyces cerevisiae involves upstream activation factor (UAF), core factor, the TATA binding protein (TBP), and Rrn3p in addition to Pol I. We found previously that yeast strains carrying deletions in the UAF component RRN9switch completely to the use of Pol II for rRNA transcription, with no residual Pol I transcription. These polymerase-switched strains initially grow very slowly, but subsequent expansion in the number of rDNA repeats on chromosome XII leads to better growth. Recently, it was reported that TBP overexpression could bypass the requirement of UAF for Pol I transcription in vivo, producing nearly wild-type levels of growth in UAF mutant strains (P. Aprikian, B. Moorefield, and R. H. Reeder, Mol. Cell. Biol. 20:5269–5275, 2000). Here, we demonstrate that deletions in the UAF component RRN5,RRN9, or RRN10 lead to Pol II transcription of rDNA. TBP overexpression does not suppress UAF mutation, and these strains continue to use Pol II for rRNA transcription. We do not find evidence for even low levels of Pol I transcription in UAF mutant strains carrying overexpressed TBP. In diploid strains lacking both copies of the UAF componentRRN9, Pol II transcription of rDNA is more strongly repressed than in haploid strains but TBP overexpression still fails to activate Pol I. These results emphasize that UAF plays an essential role in activation of Pol I transcription and silencing of Pol II transcription of rDNA and that TBP functions to recruit the Pol I machinery in a manner completely dependent on UAF.

scholarly journals Interaction of RNA polymerase I transcription factors with a promoter in the nontranscribed spacer of rat ribosomal DNA

1990 ◽  
Vol 18 (7) ◽  
pp. 1677-1718 ◽  
Author(s):  
S.David Smith ◽  
Emmanuel Oriahi ◽  
Hsin-Fang Yang-Yen ◽  
WenQin Xie ◽  
Catherine Chen ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Rna Polymerase I ◽  
Nontranscribed Spacer ◽  
Polymerase I
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