scholarly journals Integrative Role of 14-3-3ε in Sleep Regulation

2021 ◽  
Vol 22 (18) ◽  
pp. 9748
Author(s):  
Yu Wei ◽  
Juan Du ◽  
Zhangwu Zhao
Keyword(s):  
Transcription Factor ◽  
Circadian Rhythm ◽  
Proteomic Analysis ◽  
Regulatory Mechanism ◽  
Sleep Regulation ◽  
Pigment Dispersing Factor ◽  
Octopamine Receptor ◽  
Related Proteins ◽  
Circadian Transcription

Sleep is a crucial factor for health and survival in all animals. In this study, we found by proteomic analysis that some cancer related proteins were impacted by the circadian clock. The 14-3-3ε protein, expression of which is activated by the circadian transcription factor Clock, regulates adult sleep of Drosophila independent of circadian rhythm. Detailed analysis of the sleep regulatory mechanism shows that 14-3-3ε directly targets the Ultrabithorax (Ubx) gene to activate transcription of the pigment dispersing factor (PDF). The dopamine receptor (Dop1R1) and the octopamine receptor (Oamb), are also involved in the 14-3-3ε pathway, which in 14-3-3ε mutant flies causes increases in the dopR1 and OAMB, while downregulation of the DopR1 and Oamb can restore the sleep phenotype caused by the 14-3-3ε mutation. In conclusion, 14-3-3ε is necessary for sleep regulation in Drosophila.

Regulatory mechanism of TNFα autoregulation in HaCaT cells: The role of the transcription factor EGR-1

2008 ◽  
Vol 374 (4) ◽  
pp. 777-782 ◽  
Author(s):  
Sang Wook Son ◽  
Byong Wook Min ◽  
Yoongho Lim ◽  
Young Han Lee ◽  
Soon Young Shin
Keyword(s):  
Transcription Factor ◽  
Regulatory Mechanism ◽  
Hacat Cells

Circular RNA HECTD1 Mitigates Ulcerative Colitis by Promoting Enterocyte Autophagy Via miR-182-5p/HuR Axis

2021 ◽  
Author(s):  
Yan Xu ◽  
Yuxi Tian ◽  
Fujun Li ◽  
Ying Wang ◽  
Junwen Yang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Regulatory Mechanism ◽  
Therapeutic Potential ◽  
Circular Rna ◽  
Unknown Etiology ◽  
Mucosal Tissues ◽  
Related Proteins

Abstract Objective Ulcerative colitis (UC) is a chronic colitis with unknown etiology. Circular RNA (circRNA) has shown regulatory effect in many diseases, but the role of circRNA in UC is barely known. This study uncovers the function and regulatory mechanism of circRNA HECTD1 (circHECTD1) in UC. Methods Colonic mucosal tissues of 60 patients with active UC and 30 healthy controls were collected for H&E staining. Lipopolysaccharide (LPS) and dextran sulfate sodium (DSS) were used to induce inflammation and UC in Caco-2 cells and C57BL/6 mice where modification of circHECTD1, miR-182–5p and/or human antigen R (HuR) took place. The Caco-2 cells and the colon tissues of DSS-treated mice were collected for analysis of the expression levels of inflammatory cytokines, NLRP3 inflammasome, and autophagy-related proteins. The interactions among circHECTD1, miR-182–5p, and HuR were verified. Results The colonic mucosal tissues of UC patients showed impaired autophagy and decreased expressions of circHECTD1 and HuR. Overexpression of circHECTD1 or HuR or inhibition of miR-182–5p suppressed inflammation and promoted autophagy of LPS-induced Caco-2 cells. The expression of HuR was promoted by circHECTD1 via miR-182–5p in Caco-2 cells. Overexpression of circHECTD1 reduced colonic injuries and inflammation by promoting autophagy in DSS-treated mice. Conclusion Overexpression of circHECTD1 alleviates UC by promoting HuR-dependent autophagy via miR-182–5p. This study highlights the therapeutic potential of circHECTD1 for UC and adds to the knowledge of circRNA in the pathogenesis of UC.

scholarly journals The role of activating transcription factor 6 in hydroxycamptothecin-induced fibroblast autophagy and apoptosis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jin Tao ◽  
Hui Chen ◽  
Xiaolei Li ◽  
Jingcheng Wang
Keyword(s):  
Transcription Factor ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Cell Counting ◽  
Immunofluorescent Staining ◽  
Fibroblast Proliferation ◽  
Activating Transcription Factor ◽  
Related Proteins

Abstract Background The over-proliferation of fibroblasts is considered to be the main cause of scar adhesion after joint surgery. Hydroxycamptothecin (HCPT), though as a potent antineoplastic drug, shows preventive effects on scar adhesion. This study aimed to investigate the role of activating transcription factor 6 (ATF-6) in the HCPT-induced inhibition of fibroblast viability. Methods The cell counting kit-8 (CCK-8) assay, western blot analysis, lentivirus-mediated gene silencing, transmission electron microscopy (TEM) analysis, immunofluorescent staining for autophagy-related protein light chain 3 (LC3) were used to explore the effect of HCPT on triggering fibroblast apoptosis and inhibiting fibroblast proliferation, and the involvement of possible signaling pathways. Results It was found that HCPT exacerbated fibroblast apoptosis and repressed its proliferation. Subsequently, endoplasmic reticulum stress (ERS)-related proteins were determined by western blot prior to ATF6 p50 was screened out and reexamined after it was silenced. As a result, ATF6-mediated ERS played a role in HCPT-induced fibroblast apoptosis. Autophagy-related proteins and autophagosomes were detected after the HCPT administration using western blot and TEM analyses, respectively. Autophagy was activated after the HCPT treatment. With the co-treatment of autophagy inhibitor 3-methyladenine (3-MA), both the western blot analysis and the CCK-8 assay showed inhibited autophagy, which indicated that the effect of HCPT on fibroblast proliferation was partially reversed. Besides, the LC3 immunofluorescence staining revealed suppressed autophagy after silencing ATF6 p50. Conclusion Our results demonstrate that HCPT acts as a facilitator of fibroblast apoptosis and inhibitor of fibroblast proliferation for curbing the postoperative scar adhesion, in which the ATF6-mediated ERS pathway and autophagy are involved.

A novel role of circadian transcription factor DBP in hippocampal plasticity

2006 ◽  
Vol 31 (2) ◽  
pp. 303-314 ◽  
Author(s):  
Matthias Klugmann ◽  
Claudia B. Leichtlein ◽  
C. Wymond Symes ◽  
Bettina C. Klaussner ◽  
Andrew I. Brooks ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Hippocampal Plasticity ◽  
Circadian Transcription

scholarly journals Transcription factor abundance controlled by an auto-regulatory mechanism involving a transcription start site switch

2013 ◽  
Vol 42 (4) ◽  
pp. 2171-2184 ◽  
Author(s):  
Richard Patryk Ngondo ◽  
Philippe Carbon
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcription Start Site ◽  
Regulatory Mechanism ◽  
Start Site ◽  
Transcription Start ◽  
Aberrant Expression ◽  
Alternative Transcription ◽  
Activating Transcription Factor

Abstract A transcriptional feedback loop is the simplest and most direct means for a transcription factor to provide an increased stability of gene expression. In this work performed in human cells, we reveal a new negative auto-regulatory mechanism involving an alternative transcription start site (TSS) usage. Using the activating transcription factor ZNF143 as a model, we show that the ZNF143 low-affinity binding sites, located downstream of its canonical TSS, play the role of protein sensors to induce the up- or down-regulation of ZNF143 gene expression. We uncovered that the TSS switch that mediates this regulation implies the differential expression of two transcripts with an opposite protein production ability due to their different 5′ untranslated regions. Moreover, our analysis of the ENCODE data suggests that this mechanism could be used by other transcription factors to rapidly respond to their own aberrant expression level.

scholarly journals The pH-Responsive Transcription Factors YlRim101 and Mhy1 Regulate Alkaline pH-Induced Filamentation in the Dimorphic Yeast Yarrowia lipolytica

mSphere ◽  
2021 ◽  
Vol 6 (3) ◽  
Author(s):  
Tao Shu ◽  
Xin-Yu He ◽  
Jia-Wen Chen ◽  
Yi-Sheng Mao ◽  
Xiang-Dong Gao
Keyword(s):  
Cell Wall ◽  
Transcription Factor ◽  
Yarrowia Lipolytica ◽  
Regulatory Mechanism ◽  
Cell Wall Protein ◽  
Alkaline Ph ◽  
Dimorphic Fungi ◽  
Content Type ◽  
Dimorphic Yeast

ABSTRACT Environmental pH influences cell growth and differentiation. In the dimorphic yeast Yarrowia lipolytica, neutral-alkaline pH strongly induces the yeast-to-filament transition. However, the regulatory mechanism that governs alkaline pH-induced filamentation has been unclear. Here, we show that the pH-responsive transcription factor Y. lipolytica Rim101 (YlRim101) is a major regulator of alkaline-induced filamentation, since the deletion of YlRIM101 severely impaired filamentation at alkaline pH, whereas the constitutively active YlRIM1011-330 mutant mildly induced filamentation at acidic pH. YlRim101 controls the expression of the majority of alkaline-regulated cell wall protein genes. One of these, the cell surface glycosidase gene YlPHR1, plays a critical role in growth, cell wall function, and filamentation at alkaline pH. This finding suggests that YlRim101 promotes filamentation at alkaline pH via controlling the expression of these genes. We also show that, in addition to YlRim101, the Msn2/Msn4-like transcription factor Mhy1 is highly upregulated at alkaline pH and is essential for filamentation. However, unlike YlRim101, which specifically regulates alkaline-induced filamentation, Mhy1 regulates both alkaline- and glucose-induced filamentation, since the deletion of MHY1 abolished them both, whereas the overexpression of MHY1 induced strong filamentation irrespective of the pH or the presence of glucose. Finally, we show that YlRim101 and Mhy1 positively coregulate seven cell wall protein genes at alkaline pH, including YlPHR1 and five cell surface adhesin-like genes, three of which appear to promote filamentation. Together, these results reveal a conserved role of YlRim101 and a novel role of Mhy1 in the regulation of alkaline-induced filamentation in Y. lipolytica. IMPORTANCE The regulatory mechanism that governs pH-regulated filamentation is not clear in dimorphic fungi except in Candida albicans. Here, we investigated the regulation of alkaline pH-induced filamentation in Yarrowia lipolytica, a dimorphic yeast distantly related to C. albicans. Our results show that the transcription factor YlRim101 and the Msn2/Msn4-like transcription factor Mhy1 are the major regulators that promote filamentation at alkaline pH. They control the expression of a number of cell wall protein genes important for cell wall organization and filamentation. Our results suggest that the Rim101/PacC homologs play a conserved role in pH-regulated filamentation in dimorphic fungi.

scholarly journals The role of PDF neurons in setting the preferred temperature before dawn in Drosophila

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xin Tang ◽  
Sanne Roessingh ◽  
Sean E Hayley ◽  
Michelle L Chu ◽  
Nobuaki K Tanaka ◽  
...  
Keyword(s):  
Body Temperature ◽  
Neural Circuit ◽  
Sleep Regulation ◽  
Temperature Preference ◽  
Preferred Temperature ◽  
Pigment Dispersing Factor ◽  
Temperature Rhythm ◽  
Body Temperature Rhythm ◽  
Serotonin Signaling

Animals have sophisticated homeostatic controls. While mammalian body temperature fluctuates throughout the day, small ectotherms, such as Drosophila achieve a body temperature rhythm (BTR) through their preference of environmental temperature. Here, we demonstrate that pigment dispersing factor (PDF) neurons play an important role in setting preferred temperature before dawn. We show that small lateral ventral neurons (sLNvs), a subset of PDF neurons, activate the dorsal neurons 2 (DN2s), the main circadian clock cells that regulate temperature preference rhythm (TPR). The number of temporal contacts between sLNvs and DN2s peak before dawn. Our data suggest that the thermosensory anterior cells (ACs) likely contact sLNvs via serotonin signaling. Together, the ACs-sLNs-DN2s neural circuit regulates the proper setting of temperature preference before dawn. Given that sLNvs are important for sleep and that BTR and sleep have a close temporal relationship, our data highlight a possible neuronal interaction between body temperature and sleep regulation.

scholarly journals Unbiased proteomic analysis of proteins interacting with the HIV-1 5′LTR sequence: role of the transcription factor Meis

2012 ◽  
Vol 40 (21) ◽  
pp. e168-e168 ◽  
Author(s):  
A. Tacheny ◽  
S. Michel ◽  
M. Dieu ◽  
L. Payen ◽  
T. Arnould ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Proteomic Analysis ◽  
Hiv 1

Spontaneous, homeostatic, and inflammation-induced sleep in NF-κB p50 knockout mice

2006 ◽  
Vol 291 (5) ◽  
pp. R1516-R1526 ◽  
Author(s):  
K. A. Jhaveri ◽  
V. Ramkumar ◽  
R. A. Trammell ◽  
L. A. Toth
Keyword(s):  
Transcription Factor ◽  
Influenza Virus ◽  
Slow Wave Sleep ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Immune Challenge ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Transcription Factor Nuclear Factor

The dimeric transcription factor nuclear factor-κB (NF-κB) regulates several endogenous sleep-modulatory substances and thereby serves as a pivotal mediator of sleep-wake homeostasis. To further define the role of NF-κB in sleep regulation, we monitored sleep and temperature in mice that lack the p50 subunit of NF-κB [p50 knockout (KO) mice]. Compared with the control B6129PF2/J strain, p50 KO mice spend more time in slow-wave sleep (SWS) and rapid eye movement sleep (REMS) under normal conditions and show enhanced homeostatic recovery of sleep after sleep loss. p50 KO mice also show increased SWS and reduced REMS and temperature after the administration of lipopolysaccharide, yet they are behaviorally less responsive to challenge with influenza virus. These data support a role for NF-κB, and, in particular, for the p50 subunit, in the regulation of sleep in healthy mice and in mice experiencing immune challenge.

scholarly journals The PfAP2-G2 transcription factor is a critical regulator of gametocyte maturation

2020 ◽  
Author(s):  
Suprita Singh ◽  
Joana M. Santos ◽  
Lindsey M. Orchard ◽  
Naomi Yamada ◽  
Riëtte van Biljon ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Regulatory Mechanism ◽  
Critical Role ◽  
Multiplication Rate ◽  
Heterochromatin Protein 1 ◽  
Parasite Life Cycle ◽  
Heterochromatin Protein ◽  
Parasite Multiplication ◽  
Related Proteins

AbstractDifferentiation from asexual blood stages to sexual gametocytes is required for transmission of malaria parasites from the human to the mosquito host. Preventing gametocyte commitment and development would block parasite transmission, but the underlying molecular mechanisms behind these processes remain poorly understood. Here, we report that the ApiAP2 transcription factor, PfAP2-G2 (PF3D7_1408200) plays a critical role in the maturation of Plasmodium falciparum gametocytes. PfAP2-G2 binds to the promoters of a wide array of genes that are expressed at many stages of the parasite life cycle. Interestingly, we also find binding of PfAP2-G2 within the gene body of almost 3000 genes, which strongly correlates with the location of H3K36me3 and several other histone modifications as well as Heterochromatin Protein 1 (HP1), suggesting that occupancy of PfAP2-G2 in gene bodies may serve as an alternative regulatory mechanism. Disruption of pfap2-g2 does not impact asexual development, parasite multiplication rate, or commitment to sexual development but the majority of sexual parasites are unable to mature beyond stage III gametocytes. The absence of pfap2-g2 leads to overexpression of 28% of the genes bound by PfAP2-G2 and none of the PfAP2-g2 bound are downregulated, suggesting that it is a repressor. We also find that PfAP2-G2 interacts with chromatin remodeling proteins, a microrchidia (MORC) protein, and another ApiAP2 protein (PF3D7_1139300). Overall our data demonstrate that PfAP2-G2 is an important transcription factor that establishes an essential gametocyte maturation program in association with other chromatin-related proteins.

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