scholarly journals A negative feedback loop at the nuclear periphery regulates GAL gene expression

2012 ◽  
Vol 23 (7) ◽  
pp. 1367-1375 ◽  
Author(s):  
Erin M. Green ◽  
Ying Jiang ◽  
Ryan Joyner ◽  
Karsten Weis
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Transcriptional Activation ◽  
Feedback Loop ◽  
Nuclear Periphery ◽  
Gene Interaction ◽  
Nuclear Pore ◽  
Negative Feedback Loop ◽  
Gating Model ◽  
Gene Positioning

The genome is nonrandomly organized within the nucleus, but it remains unclear how gene position affects gene expression. Silenced genes have frequently been found associated with the nuclear periphery, and the environment at the periphery is believed to be refractory to transcriptional activation. However, in budding yeast, several highly regulated classes of genes, including the GAL7-10-1 gene cluster, are known to translocate to the nuclear periphery concurrent with their activation. To investigate the role of gene positioning on GAL gene expression, we monitored the effects of mutations that disrupt the interaction between the GAL locus and the periphery or synthetically tethered the locus to the periphery. Localization to the nuclear periphery was found to dampen initial GAL gene induction and was required for rapid repression after gene inactivation, revealing a function for the nuclear periphery in repressing endogenous GAL gene expression. Our results do not support a gene-gating model in which GAL gene interaction with the nuclear pore ensures rapid gene expression, but instead they suggest that a repressive environment at the nuclear periphery establishes a negative feedback loop that enables the GAL locus to respond rapidly to changes in environmental conditions.

scholarly journals Twist Regulates Cytokine Gene Expression through a Negative Feedback Loop that Represses NF-κB Activity

Cell ◽  
2003 ◽  
Vol 112 (2) ◽  
pp. 169-180 ◽  
Author(s):  
Dražen Šošić ◽  
James A. Richardson ◽  
Kai Yu ◽  
David M. Ornitz ◽  
Eric N. Olson
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Cytokine Gene Expression ◽  
Negative Feedback Loop ◽  
Cytokine Gene

scholarly journals Cotranscriptional Recruitment to the mRNA Export Receptor Mex67p Contributes to Nuclear Pore Anchoring of Activated Genes

2006 ◽  
Vol 26 (21) ◽  
pp. 7858-7870 ◽  
Author(s):  
Guennaelle Dieppois ◽  
Nahid Iglesias ◽  
Françoise Stutz
Keyword(s):  
Transcriptional Activation ◽  
Mrna Export ◽  
Nuclear Periphery ◽  
Nuclear Pore ◽  
Coding Region ◽  
Messenger Ribonucleoprotein ◽  
Gene Positioning ◽  
Independent Process ◽  
Stable Association ◽  
Early Recruitment

ABSTRACT Transcription activation of some Saccharomyces cerevisiae genes is paralleled by their repositioning to the nuclear periphery, but the mechanism underlying gene anchoring is poorly defined. We show that the nuclear pore complex-associated Mlp1p and the shuttling mRNA export receptor Mex67p contribute to the stable association of the activated GAL10 and HSP104 genes with the nuclear periphery. However, we find no obligatory link between gene positioning and gene expression. Furthermore, gene anchoring correlates with the cotranscriptional recruitment of Mex67p to transcribing genes. Notably, the association of Mex67p with chromatin is not mediated by RNA. Interestingly, a mutant GAL2 gene lacking the coding region is still able to recruit Mex67p upon transcriptional activation and to relocate to the nuclear periphery. Together these data suggest that, at least for GAL2, nascent messenger ribonucleoprotein does not play a major role in gene anchoring and that the early recruitment of Mex67p contributes to gene repositioning by virtue of an RNA-independent process.

scholarly journals PIL1 Participates in a Negative Feedback Loop that Regulates Its Own Gene Expression in Response to Shade

2014 ◽  
Vol 7 (10) ◽  
pp. 1582-1585 ◽  
Author(s):  
Lin Li ◽  
Qian Zhang ◽  
Ullas V. Pedmale ◽  
Kazumasa Nito ◽  
Wei Fu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop

scholarly journals Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression

2020 ◽  
Vol 94 (10) ◽  
Author(s):  
Nicolás Romero ◽  
Cliff Van Waesberghe ◽  
Herman W. Favoreel
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Pseudorabies Virus ◽  
Negative Feedback Loop ◽  
Tnf Α ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

ABSTRACT The nuclear factor kappa B (NF-κB) is a potent transcription factor, activation of which typically results in robust proinflammatory signaling and triggering of fast negative feedback modulators to avoid excessive inflammatory responses. Here, we report that infection of epithelial cells, including primary porcine respiratory epithelial cells, with the porcine alphaherpesvirus pseudorabies virus (PRV) results in the gradual and persistent activation of NF-κB, illustrated by proteasome-dependent degradation of the inhibitory NF-κB regulator IκB and nuclear translocation and phosphorylation of the NF-κB subunit p65. PRV-induced persistent activation of NF-κB does not result in expression of negative feedback loop genes, like the gene for IκBα or A20, and does not trigger expression of prototypical proinflammatory genes, like the gene for tumor necrosis factor alpha (TNF-α) or interleukin-6 (IL-6). In addition, PRV infection inhibits TNF-α-induced canonical NF-κB activation. Hence, PRV infection triggers persistent NF-κB activation in an unorthodox way and dramatically modulates the NF-κB signaling axis, preventing typical proinflammatory gene expression and the responsiveness of cells to canonical NF-κB signaling, which may aid the virus in modulating early proinflammatory responses in the infected host. IMPORTANCE The NF-κB transcription factor is activated via different key inflammatory pathways and typically results in the fast expression of several proinflammatory genes as well as negative feedback loop genes to prevent excessive inflammation. In the current report, we describe that infection of cells with the porcine alphaherpesvirus pseudorabies virus (PRV) triggers a gradual and persistent aberrant activation of NF-κB, which does not result in expression of hallmark proinflammatory or negative feedback loop genes. In addition, although PRV-induced NF-κB activation shares some mechanistic features with canonical NF-κB activation, it also shows remarkable differences; e.g., it is largely independent of the canonical IκB kinase (IKK) and even renders infected cells resistant to canonical NF-κB activation by the inflammatory cytokine TNF-α. Aberrant PRV-induced NF-κB activation may therefore paradoxically serve as a viral immune evasion strategy and may represent an important tool to unravel currently unknown mechanisms and consequences of NF-κB activation.

scholarly journals The Exosome Regulates Circadian Gene Expression in a Posttranscriptional Negative Feedback Loop

Cell ◽  
2009 ◽  
Vol 138 (6) ◽  
pp. 1236-1246 ◽  
Author(s):  
Jinhu Guo ◽  
Ping Cheng ◽  
Haiyan Yuan ◽  
Yi Liu
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Circadian Gene

scholarly journals Regulation of HDAC9 Gene Expression by MEF2 Establishes a Negative-Feedback Loop in the Transcriptional Circuitry of Muscle Differentiation

2006 ◽  
Vol 27 (2) ◽  
pp. 518-525 ◽  
Author(s):  
Michael Haberland ◽  
Michael A. Arnold ◽  
John McAnally ◽  
Dillon Phan ◽  
Yuri Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Muscle Development ◽  
Transcriptional Repressor ◽  
Muscle Differentiation ◽  
Negative Feedback Loop ◽  
Bhlh Genes

ABSTRACT Skeletal muscle development is controlled by the myocyte enhancer factor (MEF2) and myogenic basic helix-loop-helix (bHLH) families of transcription factors, which associate and synergistically activate muscle gene expression. Muscle differentiation is further reinforced by positive-feedback loops in which myogenic bHLH proteins activate their own expression and the expression of MEF2, while MEF2 stimulates expression of myogenic bHLH genes and the Mef2c gene. Here we describe a myogenic negative-feedback loop that consists of MEF2 proteins and the transcriptional repressor histone deacetylase 9 (HDAC9). We show that the HDAC9 gene is a direct transcriptional target of MEF2 in vitro and in vivo. HDAC9 can associate with MEF2 proteins and suppress their transcriptional activity. The transcriptional repressor HDAC9 thus forms a negative-feedback loop in the transcriptional circuitry of muscle differentiation.

scholarly journals Transcription of the Geminin gene is regulated by a negative-feedback loop

2014 ◽  
Vol 25 (8) ◽  
pp. 1374-1383 ◽  
Author(s):  
Yoshinori Ohno ◽  
Keita Saeki ◽  
Shin'ichiro Yasunaga ◽  
Toshiaki Kurogi ◽  
Kyoko Suzuki-Takedachi ◽  
...  
Keyword(s):  
Negative Feedback ◽  
Transcriptional Activation ◽  
Feedback Loop ◽  
Cellular Proliferation ◽  
Histone H3 ◽  
Dominant Negative ◽  
Dominant Negative Effect ◽  
Negative Feedback Loop ◽  
Histone H2a ◽  
Central Function

Geminin performs a central function in regulating cellular proliferation and differentiation in development and also in stem cells. Of interest, down-regulation of Geminin induces gene transcription regulated by E2F, indicating that Geminin is involved in regulation of E2F-mediated transcriptional activity. Because transcription of the Geminin gene is reportedly regulated via an E2F-responsive region (E2F-R) located in the first intron, we first used a reporter vector to examine the effect of Geminin on E2F-mediated transcriptional regulation. We found that Geminin transfection suppressed E2F1- and E2F2-mediated transcriptional activation and also mildly suppressed such activity in synergy with E2F5, 6, and 7, suggesting that Geminin constitutes a negative-feedback loop for the Geminin promoter. Of interest, Geminin also suppressed nuclease accessibility, acetylation of histone H3, and trimethylation of histone H3 at lysine 4, which were induced by E2F1 overexpression, and enhanced tri­methylation of histone H3 at lysine 27 and monoubiquitination of histone H2A at lysine 119 in E2F-R. However, Geminin5EQ, which does not interact with Brahma or Brg1, did not suppress accessibility to nuclease digestion or transcription but had an overall dominant-negative effect. These findings suggest that E2F-mediated activation of Geminin transcription is negatively regulated by Geminin through the inhibition of chromatin remodeling.

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