scholarly journals Cloning, expression, and function of TFC5, the gene encoding the B" component of the Saccharomyces cerevisiae RNA polymerase III transcription factor TFIIIB.

1995 ◽  
Vol 92 (21) ◽  
pp. 9786-9790 ◽  
Author(s):  
G. A. Kassavetis ◽  
S. T. Nguyen ◽  
R. Kobayashi ◽  
A. Kumar ◽  
E. P. Geiduschek ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factor ◽  
Rna Polymerase ◽  
Rna Polymerase Iii ◽  
Gene Encoding ◽  
Polymerase Iii ◽  
And Function

scholarly journals Determinants of Replication-Fork Pausing at tRNA Genes in Saccharomyces cerevisiae

Genetics ◽  
2020 ◽  
Vol 214 (4) ◽  
pp. 825-838
Author(s):  
Rani Yeung ◽  
Duncan J. Smith
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Transcription Factor ◽  
Rna Polymerase ◽  
Replication Fork ◽  
Rna Polymerase Iii ◽  
Trna Genes ◽  
Link Type ◽  
Replication Fork Progression ◽  
Polymerase Iii

Transfer RNA (tRNA) genes are widely studied sites of replication-fork pausing and genome instability in the budding yeast Saccharomyces cerevisiae. tRNAs are extremely highly transcribed and serve as constitutive condensin binding sites. tRNA transcription by RNA polymerase III has previously been identified as stimulating replication-fork pausing at tRNA genes, but the nature of the block to replication has not been incontrovertibly demonstrated. Here, we describe a systematic, genome-wide analysis of the contributions of candidates to replication-fork progression at tDNAs in yeast: transcription factor binding, transcription, topoisomerase activity, condensin-mediated clustering, and Rad18-dependent DNA repair. We show that an asymmetric block to replication is maintained even when tRNA transcription is abolished by depletion of one or more subunits of RNA polymerase III. By contrast, analogous depletion of the essential transcription factor TFIIIB removes the obstacle to replication. Therefore, our data suggest that the RNA polymerase III transcription complex itself represents an asymmetric obstacle to replication even in the absence of RNA synthesis. We additionally demonstrate that replication-fork progression past tRNA genes is unaffected by the global depletion of condensin from the nucleus, and can be stimulated by the removal of topoisomerases or Rad18-dependent DNA repair pathways.

The role of the TATA-binding protein in the assembly and function of the multisubunit yeast RNA polymerase III transcription factor, TFIIIB

Cell ◽  
1992 ◽  
Vol 71 (6) ◽  
pp. 1055-1064 ◽  
Author(s):  
George A. Kassavetis ◽  
Claudio A.P. Joazeiro ◽  
Marina Pisano ◽  
E.Peter Geiduschek ◽  
Trenton Colbert ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Binding Protein ◽  
Rna Polymerase Iii ◽  
Tata Binding Protein ◽  
Polymerase Iii ◽  
And Function

scholarly journals Multiple cis-acting elements are required for RNA polymerase III transcription of the gene encoding H1 RNA, the RNA component of human RNase P.

1991 ◽  
Vol 266 (34) ◽  
pp. 22796-22799
Author(s):  
G.J. Hannon ◽  
A. Chubb ◽  
P.A. Maroney ◽  
G. Hannon ◽  
S. Altman ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Iii ◽  
Rnase P ◽  
Gene Encoding ◽  
Cis Acting ◽  
Polymerase Iii ◽  
Human Rnase

scholarly journals Involvement of RNA Polymerase III in Immune Responses

2015 ◽  
Vol 35 (10) ◽  
pp. 1848-1859 ◽  
Author(s):  
Damian Graczyk ◽  
Robert J. White ◽  
Kevin M. Ryan
Keyword(s):  
Transcription Factor ◽  
Immune Responses ◽  
Rna Polymerase ◽  
Rna Polymerase Iii ◽  
Trna Genes ◽  
Malignant Cells ◽  
Polymerase Iii ◽  
Mouse Macrophages ◽  
Tightly Coupled ◽  
Pol Iii

Inflammation in the tumor microenvironment has many tumor-promoting effects. In particular, tumor-associated macrophages (TAMs) produce many cytokines which can support tumor growth by promoting survival of malignant cells, angiogenesis, and metastasis. Enhanced cytokine production by TAMs is tightly coupled with protein synthesis. In turn, translation of proteins depends on tRNAs, short abundant transcripts that are made by RNA polymerase III (Pol III). Here, we connect these facts by showing that stimulation of mouse macrophages with lipopolysaccharides (LPS) from the bacterial cell wall causes transcriptional upregulation of tRNA genes. The transcription factor NF-κB is a key transcription factor mediating inflammatory signals, and we report that LPS treatment causes an increased association of the NF-κB subunit p65 with tRNA genes. In addition, we show that p65 can directly associate with the Pol III transcription factor TFIIIB and that overexpression of p65 induces Pol III-dependent transcription. As a consequence of these effects, we show that inhibition of Pol III activity in macrophages restrains cytokine secretion and suppresses phagocytosis, two key functional characteristics of these cells. These findings therefore identify a radical new function for Pol III in the regulation of macrophage function which may be important for the immune responses associated with both normal and malignant cells.

scholarly journals Role of RNA Polymerase III Transcription Factors in the Selection of Integration Sites by the Dictyostelium Non-Long Terminal Repeat Retrotransposon TRE5-A

2006 ◽  
Vol 26 (22) ◽  
pp. 8242-8251 ◽  
Author(s):  
Oliver Siol ◽  
Moustapha Boutliliss ◽  
Thanh Chung ◽  
Gernot Glöckner ◽  
Theodor Dingermann ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Long Terminal Repeat ◽  
Integration Site ◽  
Rna Polymerase Iii ◽  
Terminal Repeat ◽  
Trna Genes ◽  
Ltr Retrotransposons ◽  
Polymerase Iii

ABSTRACT In the compact Dictyostelium discoideum genome, non-long terminal repeat (non-LTR) retrotransposons known as TREs avoid accidental integration-mediated gene disruption by targeting the vicinity of tRNA genes. In this study we provide the first evidence that proteins of a non-LTR retrotransposon interact with a target-specific transcription factor to direct its integration. We applied an in vivo selection system that allows for the isolation of natural TRE5-A integrations into a known genomic location upstream of tRNA genes. TRE5-A frequently modified the integration site in a way characteristic of other non-LTR retrotransposons by adding nontemplated extra nucleotides and generating small and extended target site deletions. Mutations within the B-box promoter of the targeted tRNA genes interfered with both the in vitro binding of RNA polymerase III transcription factor TFIIIC and the ability of TRE5-A to target these genes. An isolated B box was sufficient to enhance TRE5-A integration in the absence of a surrounding tRNA gene. The RNA polymerase III-transcribed ribosomal 5S gene recruits TFIIIC in a B-box-independent manner, yet it was readily targeted by TRE5-A in our assay. These results suggest a direct role of an RNA polymerase III transcription factor in the targeting process.

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