scholarly journals Convergent transcription induces transcriptional gene silencing in fission yeast and mammalian cells

2012 ◽  
Vol 19 (11) ◽  
pp. 1193-1201 ◽  
Author(s):  
Monika Gullerova ◽  
Nick J Proudfoot
Keyword(s):  
Gene Silencing ◽  
Fission Yeast ◽  
Mammalian Cells ◽  
Transcriptional Gene Silencing ◽  
Convergent Transcription

scholarly journals MicroRNA-directed transcriptional gene silencing in mammalian cells

2008 ◽  
Vol 105 (42) ◽  
pp. 16230-16235 ◽  
Author(s):  
D. H. Kim ◽  
P. Saetrom ◽  
O. Snove ◽  
J. J. Rossi
Keyword(s):  
Gene Silencing ◽  
Mammalian Cells ◽  
Transcriptional Gene Silencing

scholarly journals siRNA Induced Transcriptional Gene Silencing in Mammalian Cells

Cell Cycle ◽  
2005 ◽  
Vol 4 (3) ◽  
pp. 442-448 ◽  
Author(s):  
Hiroaki Kawasaki ◽  
Kazumari Taira ◽  
Kevin V. Morris
Keyword(s):  
Gene Silencing ◽  
Mammalian Cells ◽  
Transcriptional Gene Silencing

scholarly journals A Truncated Form of the Human CAF-1 p150 Subunit Impairs the Maintenance of Transcriptional Gene Silencing in Mammalian Cells

2001 ◽  
Vol 21 (6) ◽  
pp. 1953-1961 ◽  
Author(s):  
Thierry Tchénio ◽  
Jean-François Casella ◽  
Thierry Heidmann
Keyword(s):  
Gene Silencing ◽  
Reporter Gene ◽  
Mammalian Cells ◽  
Cell Model ◽  
Methylation Status ◽  
Dominant Negative ◽  
Transcriptional Gene Silencing ◽  
Dominant Negative Mutant ◽  
Control Of Gene Expression ◽  
Gene Copies

ABSTRACT Chromatin assembly factor 1 (CAF-1) is a protein complex formed of three subunits, p150, p60, and p48, conserved from the yeast Saccharomyces cerevisiae to humans, which can promote nucleosome assembly onto newly replicated DNA. In S. cerevisiae, deletion of the genes encoding any of the three CAF-1 subunits (cacΔ mutants), although nonlethal, results in a silencing defect of genes packaged into heterochromatin. Here we report on a mammalian cell model that we devised to monitor gene silencing and its reversal in a quantitative manner. This model relies on the use of a cell line stably transfected with a reporter gene in a silenced state. Reversal of reporter gene silencing was achieved upon treatment of the cells with 5-azacytidine, which resulted in the demethylation of the reporter gene copies. We show that expression of a cDNA for the human p150 CAF-1 subunit harboring 5′ truncations, but not that of a cDNA encoding the full-length p150 CAF-1 subunit, increases by more than 500-fold the frequency at which transcriptional silencing of the reporter gene copies is reversed in these cells. Reversal of gene silencing is dependent upon expression of a truncated protein, possibly acting as a dominant negative mutant of the wild-type CAF-1, is associated with alterations in chromatin structure as measured by an endonuclease sensitivity assay and is not associated with detectable changes in the methylation status of the silenced genes. These results suggest that the role of CAF-1 in the epigenetic control of gene expression has been conserved between yeast and mammals, despite the lack of DNA methylation in yeast chromatin.

scholarly journals The git5 Gβ and git11 Gγ Form an Atypical Gβγ Dimer Acting in the Fission Yeast Glucose/cAMP Pathway

Genetics ◽  
2001 ◽  
Vol 157 (3) ◽  
pp. 1159-1168 ◽  
Author(s):  
Sheila Landry ◽  
Charles S Hoffman
Keyword(s):  
Fission Yeast ◽  
Mammalian Cells ◽  
Glucose Repression ◽  
Coiled Coil ◽  
Carboxy Terminus ◽  
Amino Terminal ◽  
Camp Pathway ◽  
Coiled Coil Domain ◽  
Mutational Activation ◽  
Two Hybrid

AbstractFission yeast adenylate cyclase, like mammalian adenylate cyclases, is regulated by a heterotrimeric G protein. The gpa2 Gα and git5 Gβ are both required for glucose-triggered cAMP signaling. The git5 Gβ is a unique member of the Gβ family in that it lacks an amino-terminal coiled-coil domain shown to be essential for mammalian Gβ folding and interaction with Gγ subunits. Using a git5 bait in a two-hybrid screen, we identified the git11 Gγ gene. Co-immunoprecipitation studies confirm the composition of this Gβγ dimer. Cells deleted for git11 are defective in glucose repression of both fbp1 transcription and sexual development, resembling cells lacking either the gpa2 Gα or the git5 Gβ. Overexpression of the gpa2 Gα partially suppresses loss of either the git5 Gβ or the git11 Gγ, while mutational activation of the Gα fully suppresses loss of either Gβ or Gγ. Deletion of gpa2 (Gα), git5 (Gβ), or git11 (Gγ) confer quantitatively distinct effects on fbp1 repression, indicating that the gpa2 Gα subunit remains partially active in the absence of the Gβγ dimer and that the git5 Gβ subunit remains partially active in the absence of the git11 Gγ subunit. The addition of the CAAX box from the git11 Gγ to the carboxy-terminus of the git5 Gβ partially suppresses the loss of the Gγ. Thus the Gγ in this system is presumably required for localization of the Gβγ dimer but not for folding of the Gβ subunit. In mammalian cells, the essential roles of the Gβ amino-terminal coiled-coil domains and Gγ partners in Gβ folding may therefore reflect a mechanism used by cells that express multiple forms of both Gβ and Gγ subunits to regulate the composition and activity of its G proteins.

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