scholarly journals Floral organ abscission is regulated by a positive feedback loop

2015 ◽  
Vol 112 (9) ◽  
pp. 2906-2911 ◽  
Author(s):  
O. Rahul Patharkar ◽  
John C. Walker
Keyword(s):  
Map Kinase ◽  
Positive Feedback ◽  
Regulatory Networks ◽  
Feedback Loop ◽  
Dynamic Range ◽  
Floral Organ ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Positive Feedback Loop ◽  
Genetic Components

Abscission is the process by which plants shed unwanted organs, either as part of a natural developmental program or in response to environmental stimuli. Studies in Arabidopsis thaliana have elucidated a number of the genetic components that regulate abscission of floral organs, including a pair of related receptor-like protein kinases, HAESA and HAESA-like 2 (HAE/HSL2) that regulate a MAP kinase cascade that is required for abscission. HAE is transcriptionally up-regulated in the floral abscission zone just before cell separation. Here, we identify AGAMOUS-like 15 (AGL15; a MADS-domain transcription factor) as a putative regulator of HAE expression. Overexpression of AGL15 results in decreased expression of HAE as well as a delayed abscission phenotype. Chromatin immunoprecipitation experiments indicate that AGL15 binds the HAE promoter in floral receptacles. AGL15 is then differentially phosphorylated through development in floral receptacles in a MITOGEN-ACTIVATED PROTEIN KINASE KINASE 4/5-dependent manner. MAP kinase phosphorylation of AGL15 is necessary for full HAE expression, thus completing a positive feedback loop controlling HAE expression. Together, the network components in this positive feedback loop constitute an emergent property that regulates the large dynamic range of gene expression (27-fold increase in HAE) observed in flowers when the abscission program is initiated. This study helps define the mechanisms and regulatory networks involved in a receptor-mediated signaling pathway that controls floral organ abscission.

scholarly journals A positive-feedback loop between HBx and ALKBH5 promotes hepatocellular carcinogenesis

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Siming Qu ◽  
Li Jin ◽  
Hanfei Huang ◽  
Jie Lin ◽  
Weiwu Gao ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Hbv Infection ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Dependent Manner ◽  
Liver Carcinogenesis ◽  
Nude Mouse Model ◽  
Positive Feedback Loop

Abstract Background Hepatitis B Virus (HBV) contributes to liver carcinogenesis via various epigenetic mechanisms. The newly defined epigenetics, epitranscriptomics regulation, has been reported to involve in multiple cancers including Hepatocellular Carcinoma (HCC). Our previous study found that HBx, HBV encodes X protein, mediated H3K4me3 modification in WDR5-dependent manner to involve in HBV infection and contribute to oncogene expression. AlkB Homolog 5 (ALKBH5), one of epitranscriptomics enzymes, has been identified to be associated with various cancers. However, whether and how ALKBH5 is dysregulated in HBV-related HCC remains unclear yet. This study aims to investigate ALKBH5 function, clinical significance and mechanism in HBV related HCC (HBV-HCC) patients derived from Chinese people. Methods The expression pattern of ALKBH5 was evaluated by RT-qPCR, Western blot, data mining and immunohistochemistry in total of 373 HBV-HCC tissues and four HCC cell lines. Cell Counting Kit 8 (CCK8) assay, Transwell and nude mouse model were performed to assess ALKBH5 function by both small interference RNAs and lentiviral particles. The regulation mechanism of ALKBH5 was determined in HBx and WDR5 knockdown cells by CHIP-qPCR. The role of ALKBH5 in HBx mRNA N6-methyladenosine (m6A) modification was further evaluated by MeRIP-qPCR and Actinomycin D inhibitor experiment in HBV-driven cells and HBx overexpression cells. Result ALKBH5 increased in tumor tissues and predicts a poor prognosis of HBV-HCC. Mechanically, the highly expressed ALKBH5 is induced by HBx-mediated H3K4me3 modification of ALKBH5 gene promoter in a WDR5-dependent manner after HBV infection. The increased ALKBH5 protein catalyzes the m6A demethylation of HBx mRNA, thus stabilizing and favoring a higher HBx expression level. Furthermore, there are positive correlations between HBx and ALKBH5 in HBV-HCC tissues, and depletion of ALKBH5 significantly inhibits HBV-driven tumor cells’ growth and migration in vitro and in vivo. Conclusions HBx-ALKBH5 may form a positive-feedback loop to involve in the HBV-induced liver carcinogenesis, and targeting the loop at ALKBH5 may provide a potential way for HBV-HCC treatment.

scholarly journals Anisotropy of plasmalemmal sterols and cell mating require StARkin domain proteins Ysp2 and Lam4

2021 ◽  
Author(s):  
Neha Chauhan ◽  
Gregory D. Fairn
Keyword(s):  
Plasma Membrane ◽  
Map Kinase ◽  
Cell Polarity ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Budding Yeast ◽  
Mapk Signaling ◽  
Polarized Growth ◽  
Positive Feedback Loop ◽  
Mating Efficiency

AbstractIn the budding yeast S. cerevisiae Cdc42 is required for polarized growth and the formation of mating projections (shmoos). Negatively charged lipids including phosphatidylserine and phosphatidylinositol 4,5-bisphosphate support a positive feedback loop that recruits Cdc42 effectors and MAP kinase scaffolds, many of which contain polybasic patches that directly interact with the membrane. Here, using genetically encoded sterol sensor ALOD4 we find that ergosterol is accumulated in the cytosolic leaflet of buds and shmoos. The accumulation of ergosterol in the plasma membrane requires both Osh and Lam proteins however cells lacking Ysp2/Lam2 and Lam4 displayed a reversal in the polarity of ergosterol. The redistribution of ergosterol impairs the polarization of phosphatidylserine and phosphatidylinositol 4,5-bisphophate which further impacts shmoo formation, MAPK signaling and mating efficiency. Our observations demonstrate that the ability of Lam proteins to deliver ergosterol from the plasma membrane to the ER helps maintain a gradient of ergosterol which in turn supports robust cell polarity.SummaryThe sterol sensor ALOD4 is enriched at sites of polarized growth. Elimination of the Osh proteins solubilized the ALOD4 whereas elimination of Ysp2 and Lam4 reversed ALOD4 polarization. Cells lacking Ysp2 and Lam4 have defects in mating and MAP kinase signaling.

scholarly journals Diabetes-Induced Oxidative Stress in Endothelial Progenitor Cells May Be Sustained by a Positive Feedback Loop Involving High Mobility Group Box-1

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Han Wu ◽  
Ran Li ◽  
Zhong-Hai Wei ◽  
Xin-Lin Zhang ◽  
Jian-Zhou Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Positive Feedback ◽  
Feedback Loop ◽  
High Mobility ◽  
High Mobility Group ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Positive Feedback Loop ◽  
Culture Supernatants

Oxidative stress is considered to be a critical factor in diabetes-induced endothelial progenitor cell (EPC) dysfunction, although the underlying mechanisms are not fully understood. In this study, we investigated the role of high mobility group box-1 (HMGB-1) in diabetes-induced oxidative stress. HMGB-1 was upregulated in both serum and bone marrow-derived monocytes from diabetic mice compared with control mice. In vitro, advanced glycation end productions (AGEs) induced, expression of HMGB-1 in EPCs and in cell culture supernatants in a dose-dependent manner. However, inhibition of oxidative stress with N-acetylcysteine (NAC) partially inhibited the induction of HMGB-1 induced by AGEs. Furthermore, p66shc expression in EPCs induced by AGEs was abrogated by incubation with glycyrrhizin (Gly), while increased superoxide dismutase (SOD) activity in cell culture supernatants was observed in the Gly treated group. Thus, HMGB-1 may play an important role in diabetes-induced oxidative stress in EPCs via a positive feedback loop involving the AGE/reactive oxygen species/HMGB-1 pathway.

scholarly journals A Novel Positive Feedback Loop Between NTSR1 and Wnt/β-Catenin Contributes to Tumor Growth of Glioblastoma

2017 ◽  
Vol 43 (5) ◽  
pp. 2133-2142 ◽  
Author(s):  
Hualiang Xiao ◽  
Ying Zeng ◽  
Qiushi Wang ◽  
Shirong Wei ◽  
Xiangfeng Zhu
Keyword(s):  
Tumor Growth ◽  
Cancer Progression ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Mitogen Activated Protein Kinase ◽  
Glioblastoma Cells ◽  
Positive Feedback Loop ◽  
Pharmacological Inhibition ◽  
Wnt Proteins

Background/Aims: Neurotensin (NTS), an intestinal hormone, is profoundly implicated in cancer progression through binding its primary receptor NTSR1. The conserved Wnt/β-Catenin pathway regulates cell proliferation and differentiation via activation of the β-catenin/T-cell factor (TCF) complex and subsequent modulation of a set of target genes. In this study, we aimed to uncover the potential connection between NTS/NTSR1 signaling and Wnt/β-Catenin pathway. Methods: Genetic silencing, pharmacological inhibition and gain-of-function studies as well as bioinformatic analysis were performed to uncover the link between NTS/ NTSR1 signaling and Wnt/β-Catenin pathway. Two inhibitors were used in vivo to evaluate the efficiency of targeting NTS/NTSR1 signaling or Wnt/β-Catenin pathway. Results: We found that NTS/NTSR1 induced the activation of mitogen-activated protein kinase (MAPK) and the NF-κB pathway, which further promoted the expression of Wnt proteins, including Wnt1, Wnt3a and Wnt5a. Meanwhile, the mRNA and protein expression levels of NTSR1 were increased by the Wnt pathway activator Wnt3a and decreased by the Wnt inhibitor iCRT3 in glioblastoma cells. Furthermore, pharmacological inhibition of NTS/NTSR1 or Wnt/β-Catenin signaling suppressed tumor growth in vitro and in vivo. Conclusion: These results reveal a positive feedback loop between NTS/NTSR1 and Wnt/β-Catenin signaling in glioblastoma cells that might be important for tumor development and provide potential therapeutic targets for glioblastoma.

scholarly journals Arabidopsis vascular complexity and connectivity controls PIN-FORMED1 dynamics and lateral vein patterning during embryogenesis

Development ◽  
2021 ◽  
Author(s):  
Makoto Yanagisawa ◽  
Arthur Poitout ◽  
Marisa S. Otegui
Keyword(s):  
Plasma Membrane ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Transmembrane Protein ◽  
Vascular Development ◽  
Lateral Vein ◽  
Dependent Manner ◽  
Positive Feedback Loop ◽  
Vein Patterning ◽  
Auxin Efflux Carrier

Arabidopsis VASCULATURE COMPLEXITY AND CONNECTIVITY (VCC) is a plant-specific transmembrane protein that controls the development of veins in cotyledons. Here we show that the expression and localization of the auxin efflux carrier PIN-FORMED1 (PIN1) is altered in vcc developing cotyledons and that overexpression of PIN1-GFP partially rescues vascular defects of vcc in a dosage-dependent manner. Genetic analyses suggest that VCC and PINOID (PID), a kinase that regulates PIN1 polarity, are both required for PIN1-mediated control of vasculature development. VCC expression is upregulated by auxin, likely as part of a positive feedback loop for the progression of vascular development. VCC and PIN1 localized to the plasma membrane in pre-procambial cells but are actively redirected to vacuoles in procambial cells for degradation. In the vcc mutant, PIN1 failed to properly polarize in pre-procambial cells during the formation of basal strands and instead, it is prematurely degraded in vacuoles. VCC plays a role in localization and stability of PIN1, which is critical for the transition of pre-procambial into procambial cells involved in the formation of basal lateral strands in embryonic cotyledons.

scholarly journals Overexpression of Annexin A2 Promotes Proliferation by Forming a Glypican 1 / c-Myc Positive Feedback Loop: Prognostic Significance in Human Glioma

2020 ◽  
Author(s):  
Xin Li ◽  
Shengdan Nie ◽  
Ziyang Lv ◽  
Lingran Ma ◽  
Yuxi Song ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Cellular Proliferation ◽  
Prognostic Significance ◽  
Glioma Cells ◽  
Tumor Grade ◽  
Prognostic Indicator ◽  
Annexin A2 ◽  
Dependent Manner ◽  
Positive Feedback Loop

Abstract Background: Glioma, with varying malignancy grades, is the most common primary brain tumor. It is urgent to set up a reliable prediction system for the tumor grade and prognosis in glioma patients. We aimed to clarify the complicated crosstalk of Annexin A2 (ANXA2) with Glypican 1 (GPC1) and demonstrate whether combined indexes of ANXA2 and GPC1 could improve the prognostic evaluation for glioma patients.Methods: The role of ANXA2 and GPC1 in proliferation and their relationship were validated in glioma cells. 164 glioma samples were analyzed for association between co-expression of ANXA2 and GPC1 and patient clinicopathological features and prognosis. Results: We found that ANXA2 induced glioma cellular proliferation in a c-Myc-dependent manner. ANXA2 increased the expression of GPC1 via c-Myc and the upregulated GPC1 further promoted the c-Myc level forming a positive feedback loop, which eventually led to enhanced proliferation of glioma cells. Both quantitative reverse transcription-polymerase chain reaction (qRT-RCR) and immunohistochemistry revealed that ANXA2 was upregulated in glioma tissues and coincided with the overexpression of GPC1. Glioma patients with high both ANXA2 and GPC1 tended to have higher rate of tumor recurrence and shorter overall survival (OS). Multivariate analyses revealed that the combination of ANXA2 and GPC1 was an independent prognostic indicator for time to recurrence and OS. Conclusions: The overexpression of ANXA2 promotes proliferation by forming a GPC1/c-Myc positive feedback loop, and ANXA2 and its downstream target GPC1 could be a potential “combination biomarker” for predicting prognosis of glioma.

scholarly journals SET/TAF1 forms a distance-dependent feedback loop with Aurora B and Bub1 as a tension sensor at centromeres

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yuichiro Asai ◽  
Rieko Matsumura ◽  
Yurina Hasumi ◽  
Hiroaki Susumu ◽  
Kyosuke Nagata ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Kinase Activity ◽  
Molecular Entity ◽  
Aurora B ◽  
Dependent Manner ◽  
Aurora B Kinase ◽  
Positive Feedback Loop ◽  
Spatiotemporal Regulation ◽  
Tension Sensor

Abstract During mitosis, spatiotemporal regulation of phosphorylation at the kinetochore is essential for accurate chromosome alignment and proper chromosome segregation. Aurora B kinase phosphorylates kinetochore substrates to correct improper kinetochore-microtubule (KT-MT) attachments, whereas tension across the centromeres inactivates Aurora B kinase, and PP2A phosphatase dephosphorylates the kinetochore proteins to stabilize the attachments. However, the molecular entity of the tension sensing mechanism remains elusive. In a previous report, we showed that centromeric SET/TAF1 on Sgo2 up-regulates Aurora B kinase activity via PP2A inhibition in prometaphase. Here we show that Aurora B and Bub1 at the centromere/kinetochore regulate both kinase activities one another in an inter-kinetochore distance-dependent manner, indicating a positive feedback loop. We further show that the centromeric pool of SET on Sgo2 depends on Bub1 kinase activity, and the centromeric localization of SET decreases in a distance-dependent manner, thereby inactivating Aurora B in metaphase. Consistently, ectopic targeting of SET to the kinetochores during metaphase hyperactivates Aurora B via PP2A inhibition, and thereby rescues the feedback loop. Thus, we propose that SET, Aurora B and Bub1 form a distance-dependent positive feedback loop, which spatiotemporally may act as a tension sensor at centromeres.

scholarly journals Overexpression of Annexin A2 promotes proliferation by forming a Glypican 1/c-Myc positive feedback loop: prognostic significance in human glioma

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Xin Li ◽  
Shengdan Nie ◽  
Ziyang Lv ◽  
Lingran Ma ◽  
Yuxi Song ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Prognostic Significance ◽  
Glioma Cells ◽  
Tumor Grade ◽  
Tissue Microarrays ◽  
Annexin A2 ◽  
Dependent Manner ◽  
Positive Feedback Loop ◽  
Downstream Target

AbstractIn order to set up a reliable prediction system for the tumor grade and prognosis in glioma patients, we clarify the complicated crosstalk of Annexin A2 (ANXA2) with Glypican 1 (GPC1) and demonstrate whether combined indexes of ANXA2 and GPC1 could improve the prognostic evaluation for glioma patients. We found that ANXA2-induced glioma cell proliferation in a c-Myc-dependent manner. ANXA2 increased the expression of GPC1 via c-Myc and the upregulated GPC1 further promoted the c-Myc level, forming a positive feedback loop, which eventually led to enhanced proliferation of glioma cells. Both mRNA and protein levels of ANXA2 were upregulated in glioma tissues and coincided with the overexpression of GPC1. Besides, we utilized tissue microarrays (TMAs) and immunohistochemistry to demonstrate that glioma patients with both high expression of ANXA2 and GPC1 tended to have higher rate of tumor recurrence and shorter overall survival (OS). In conclusion, the overexpression of ANXA2 promotes proliferation of glioma cells by forming a GPC1/c-Myc positive feedback loop, and ANXA2 together with its downstream target GPC1 could be a potential “combination biomarker” for predicting prognosis of glioma patients.

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