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 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 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 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 Multiple Posttranscriptional Strategies To Regulate the Herpes Simplex Virus 1 vhs Endoribonuclease

2018 ◽  
Vol 92 (17) ◽  
Author(s):  
Gillian Elliott ◽  
Kathleen Pheasant ◽  
Katja Ebert-Keel ◽  
Julianna Stylianou ◽  
Ashley Franklyn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Herpes Simplex Virus 1 ◽  
Nuclear Retention ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTThe herpes simplex virus 1 (HSV-1) virion host shutoff (vhs) protein is an endoribonuclease that binds to the cellular translation initiation machinery and degrades associated mRNAs, resulting in the shutoff of host protein synthesis. Hence, its unrestrained activity is considered lethal, and it has been proposed that vhs is regulated by two other virus proteins, VP22 and VP16. We have found that during infection, translation of vhs requires VP22 but not the VP22-VP16 complex. Moreover, in the absence of VP22, vhs is not overactive against cellular or viral transcripts. In transfected cells, vhs was also poorly translated, correlating with the aberrant localization of its mRNA. Counterintuitively, vhs mRNA was predominantly nuclear in cells where vhs protein was detected. Likewise, transcripts from cotransfected plasmids were also retained in the same nuclei where vhs mRNA was located, while poly(A) binding protein (PABP) was relocalized to the nucleus in a vhs-dependent manner, implying a general block to mRNA export. Coexpression of VP16 and VP22 rescued the cytoplasmic localization of vhs mRNA but failed to rescue vhs translation. We identified a 230-nucleotide sequence in the 5′ region of vhs that blocked its translation and, when transferred to a heterologous green fluorescent protein transcript, reduced translation without altering mRNA levels or localization. We propose that expression of vhs is tightly regulated by a combination of inherent untranslatability and autoinduced nuclear retention of its mRNA that results in a negative feedback loop, with nuclear retention but not translation of vhs mRNA being the target of rescue by the vhs-VP16-VP22 complex.IMPORTANCEA myriad of gene expression strategies has been discovered through studies carried out on viruses. This report concerns the regulation of the HSV-1 vhs endoribonuclease, a virus factor that is important for counteracting host antiviral responses by degrading their mRNAs but that must be regulated during infection to ensure that it does not act against and inhibit the virus itself. We show that regulation of vhs involves multifaceted posttranscriptional cellular and viral processes, including aberrant mRNA localization and a novel, autoregulated negative feedback loop to target its own and coexpressed mRNAs for nuclear retention, an activity that is relieved by coexpression of two other virus proteins, VP22 and VP16. These studies reveal the interplay of strategies by which multiple virus-encoded factors coordinate gene expression at the time that they are needed. These findings are broadly relevant to both virus and cellular gene expression.

Sign in / Sign up

Export Citation Format

Share Document