scholarly journals A Glucose Sensor in Candida albicans

2006 ◽  
Vol 5 (10) ◽  
pp. 1726-1737 ◽  
Author(s):  
Victoria Brown ◽  
Jessica A. Sexton ◽  
Mark Johnston
Keyword(s):  
Candida Albicans ◽  
Glucose Sensor ◽  
Glucose Sensing ◽  
Glucose Sensors ◽  
Glucose Levels ◽  
High Affinity ◽  
Expression Of Genes ◽  
Hexose Transporters ◽  
Genes Encoding ◽  
Sensor Glucose

ABSTRACT The Hgt4 protein of Candida albicans (orf19.5962) is orthologous to the Snf3 and Rgt2 glucose sensors of Saccharomyces cerevisiae that govern sugar acquisition by regulating the expression of genes encoding hexose transporters. We found that HGT4 is required for glucose induction of the expression of HGT12, HXT10, and HGT7, which encode apparent hexose transporters in C. albicans. An hgt4Δ mutant is defective for growth on fermentable sugars, which is consistent with the idea that Hgt4 is a sensor of glucose and similar sugars. Hgt4 appears to be sensitive to glucose levels similar to those in human serum (∼5 mM). HGT4 expression is repressed by high levels of glucose, which is consistent with the idea that it encodes a high-affinity sugar sensor. Glucose sensing through Hgt4 affects the yeast-to-hyphal morphological switch of C. albicans cells: hgt4Δ mutants are hypofilamented, and a constitutively signaling form of Hgt4 confers hyperfilamentation of cells. The hgt4Δ mutant is less virulent than wild-type cells in a mouse model of disseminated candidiasis. These results suggest that Hgt4 is a high-affinity glucose sensor that contributes to the virulence of C. albicans.

scholarly journals Hexokinase Regulates Kinetics of Glucose Transport and Expression of Genes Encoding Hexose Transporters inSaccharomyces cerevisiae

2000 ◽  
Vol 182 (23) ◽  
pp. 6815-6818 ◽  
Author(s):  
Thomas Petit ◽  
Jasper A. Diderich ◽  
Arthur L. Kruckeberg ◽  
Carlos Gancedo ◽  
Karel Van Dam
Keyword(s):  
Glucose Transport ◽  
Mrna Levels ◽  
High Affinity ◽  
Expression Of Genes ◽  
Hexose Transporters ◽  
Genes Encoding ◽  
High Concentrations ◽  
Kinetics Of ◽  
Very High ◽  
Null Strain

ABSTRACT Glucose transport kinetics and mRNA levels of different glucose transporters were determined in Saccharomyces cerevisiaestrains expressing different sugar kinases. During exponential growth on glucose, a hxk2 null strain exhibited high-affinity hexose transport associated with an elevated transcription of the genesHXT2 and HXT7, encoding high-affinity transporters, and a diminished expression of the HXT1 andHXT3 genes, encoding low-affinity transporters. Deletion ofHXT7 revealed that the high-affinity component is mostly due to HXT7; however, a previously unidentified very-high-affinity component (Km = 0.19 mM) appeared to be due to other factors. Expression of genes encoding hexokinases from Schizosaccharomyces pombe orYarrowia lipolytica in a hxk1 hxk2 glk1 strain prevented derepression of the high-affinity transport system at high concentrations of glucose.

scholarly journals Two glucose sensing/signaling pathways stimulate glucose-induced inactivation of maltose permease in Saccharomyces.

1997 ◽  
Vol 8 (7) ◽  
pp. 1293-1304 ◽  
Author(s):  
H Jiang ◽  
I Medintz ◽  
C A Michels
Keyword(s):  
Signaling Pathways ◽  
Glucose Transport ◽  
Glucose Sensor ◽  
Constitutive Expression ◽  
Glucose Sensing ◽  
Regulation Of Transcription ◽  
Carbohydrate Utilization ◽  
Maltose Permease ◽  
Glucose Levels ◽  
Dependent Signal

Glucose is a global metabolic regulator in Saccharomyces. It controls the expression of many genes involved in carbohydrate utilization at the level of transcription, and it induces the inactivation of several enzymes by a posttranslational mechanism. SNF3, RGT2, GRR1 and RGT1 are known to be involved in glucose regulation of transcription. We tested the roles of these genes in glucose-induced inactivation of maltose permease. Our results suggest that at least two signaling pathways are used to monitor glucose levels. One pathway requires glucose sensor transcript and the second pathway is independent of glucose transport. Rgt2p, which along with Snf3p monitors extracellular glucose levels, appears to be the glucose sensor for the glucose-transport-independent pathway. Transmission of the Rgt2p-dependent signal requires Grr1p. RGT2 and GRR1 also play a role in regulating the expression of the HXT genes, which appear to be the upstream components of the glucose-transport-dependent pathway regulating maltose permease inactivation. RGT2-1, which was identified as a dominant mutation causing constitutive expression of several HXT genes, causes constitutive proteolysis of maltose permease, that is, in the absence of glucose. A model of these glucose sensing/signaling pathways is presented.

Cuprous Oxide Films with Hollow Cubic Cage Structure for Nonenzymatic Glucose Detection

NANO ◽  
2019 ◽  
Vol 14 (04) ◽  
pp. 1950045
Author(s):  
Fang Sun ◽  
Lehong Xing ◽  
Xihui Yang ◽  
Hailiang Huang ◽  
Lina Ning
Keyword(s):  
Electrode Materials ◽  
Glucose Sensor ◽  
High Sensitivity ◽  
Fast Response ◽  
Glucose Sensing ◽  
Glucose Sensors ◽  
Cage Structure ◽  
Active Materials ◽  
Nonenzymatic Glucose Sensor ◽  
Step Procedure

In this study, CuO films with hollow cubic cages were prepared by a facile two-step procedure consisting of electrodeposition synthesis and subsequent direct calcination. First, Cu2O nanocubes were fabricated on ITO substrate through a simple electrodeposition procedure. Then, Cu2O nanocubes were converted to CuO hollow cubic cages without obvious morphological change through direct calcination. The obtained CuO cubic cages serving as active materials illustrated a favorable performance for nonenzymatic glucose sensing with high sensitivity of [Formula: see text]A[Formula: see text]mM[Formula: see text][Formula: see text]cm[Formula: see text] at a low applied potential of 0.50[Formula: see text]V, fast-response time (less than 3[Formula: see text]s), low detection limit of 1.0[Formula: see text][Formula: see text]M and wide linear range up from 2.0[Formula: see text][Formula: see text]M to 1.0[Formula: see text]mM ([Formula: see text]). Moreover, the good selectivity of the CuO cubic cages-based nonenzymatic glucose sensor against electroactive compounds such as ascorbic acid, uric acid and dopamine were also demonstrated. These good features indicate that the as-prepared CuO cubic cages can be used as promising electrode materials, which have a great potential in the development of sensitive and selective nonenzymatic glucose sensors.

scholarly journals Mds3 Regulates Morphogenesis in Candida albicans through the TOR Pathway

2010 ◽  
Vol 30 (14) ◽  
pp. 3695-3710 ◽  
Author(s):  
Lucia F. Zacchi ◽  
Jonatan Gomez-Raja ◽  
Dana A. Davis
Keyword(s):  
Candida Albicans ◽  
Ribosomal Proteins ◽  
Ph Sensing ◽  
Tor Pathway ◽  
Preferential Expression ◽  
Human Fungal Pathogen ◽  
Expression Of Genes ◽  
Mucosal Surfaces ◽  
Genes Encoding ◽  
Morphological Defects

ABSTRACT The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3Δ/Δ cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3Δ/Δ mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1Δ/Δ deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4Δ/Δ and mds3Δ/Δ mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.

scholarly journals ERK1/2 mediates glucose-regulated POMC gene expression in hypothalamic neurons

2015 ◽  
Vol 54 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Juan Zhang ◽  
Yunting Zhou ◽  
Cheng Chen ◽  
Feiyuan Yu ◽  
Yun Wang ◽  
...  
Keyword(s):  
Specific Inhibitor ◽  
Neuronal Cell ◽  
Glucose Sensing ◽  
Hypothalamic Neurons ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Low Glucose ◽  
Amp Activated Protein Kinase

Hypothalamic glucose-sensing neurons regulate the expression of genes encoding feeding-related neuropetides POMC, AgRP, and NPY – the key components governing metabolic homeostasis. AMP-activated protein kinase (AMPK) is postulated to be the molecular mediator relaying glucose signals to regulate the expression of these neuropeptides. Whether other signaling mediator(s) plays a role is not clear. In this study, we investigated the role of ERK1/2 using primary hypothalamic neurons as the model system. The primary neurons were differentiated from hypothalamic progenitor cells. The differentiated neurons possessed the characteristic neuronal cell morphology and expressed neuronal post-mitotic markers as well as leptin-regulated orexigenic POMC and anorexigenic AgRP/NPY genes. Treatment of cells with glucose dose-dependently increased POMC and decreased AgRP/NPY expression with a concurrent suppression of AMPK phosphorylation. In addition, glucose treatment dose-dependently increased the ERK1/2 phosphorylation. Blockade of ERK1/2 activity with its specific inhibitor PD98059 partially (approximately 50%) abolished glucose-induced POMC expression, but had little effect on AgRP/NPY expression. Conversely, blockade of AMPK activity with its specific inhibitor produced a partial (approximately 50%) reversion of low-glucose-suppressed POMC expression, but almost completely blunted the low-glucose-induced AgRP/NPY expression. The results indicate that ERK1/2 mediated POMC but not AgRP/NPY expression. Confirming the in vitro findings, i.c.v. administration of PD98059 in rats similarly attenuated glucose-induced POMC expression in the hypothalamus, but again had little effect on AgRP/NPY expression. The results are indicative of a novel role of ERK1/2 in glucose-regulated POMC expression and offer new mechanistic insights into hypothalamic glucose sensing.

scholarly journals Release from Quorum-Sensing Molecules Triggers Hyphal Formation during Candida albicans Resumption of Growth

2005 ◽  
Vol 4 (7) ◽  
pp. 1203-1210 ◽  
Author(s):  
Brice Enjalbert ◽  
Malcolm Whiteway
Keyword(s):  
Candida Albicans ◽  
Quorum Sensing ◽  
Culture Medium ◽  
Pathogenic Fungus ◽  
Hyphal Growth ◽  
Growth Environment ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Hyphal Formation ◽  
Cyclin Genes

ABSTRACT Candida albicans is a pathogenic fungus able to change morphology in response to variations in its growth environment. Simple inoculation of stationary cells into fresh medium at 37°C, without any other manipulations, appears to be a powerful but transient inducer of hyphal formation; this process also plays a significant role in classical serum induction of hyphal formation. The mechanism appears to involve the release of hyphal repression caused by quorum-sensing molecules in the growth medium of stationary-phase cells, and farnesol has a strong but incomplete role in this process. We used DNA microarray technology to study both the resumption of growth of Candida albicans cells and molecular regulation involving farnesol. Maintaining farnesol in the culture medium during the resumption of growth both delays and reduces the induction of hypha-related genes yet triggers expression of genes encoding drug efflux components. The persistence of farnesol also prevents the repression of histone genes during hyphal growth and affects the expression of putative or demonstrated morphogenesis-regulating cyclin genes, such as HGC1, CLN3, and PCL2. The results suggest a model explaining the triggering of hyphae in the host based on quorum-sensing molecules.

scholarly journals Differential Regulation of High-Affinity Phosphate Transport Systems of Mycobacterium smegmatis: Identification of PhnF, a Repressor of the phnDCE Operon

2007 ◽  
Vol 190 (4) ◽  
pp. 1335-1343 ◽  
Author(s):  
Susanne Gebhard ◽  
Gregory M. Cook
Keyword(s):  
Mycobacterium Smegmatis ◽  
Constitutive Expression ◽  
Phosphate Transport ◽  
Phosphate Limitation ◽  
Transport Systems ◽  
New Members ◽  
High Affinity ◽  
Expression Of Genes ◽  
Two Component ◽  
Genes Encoding

ABSTRACT The uptake of phosphate into the cell via high-affinity, phosphate-specific transport systems has been studied with several species of mycobacteria. All of these species have been shown to contain several copies of such transport systems, which are synthesized in response to phosphate limitation. However, the mechanisms leading to the expression of the genes encoding these transporters have not been studied. This study reports on the investigation of the regulation of the pstSCAB and the phnDCE operons of Mycobacterium smegmatis. The phn locus contains an additional gene, phnF, encoding a GntR-like transcriptional regulator. Expression analyses of a phnF deletion mutant demonstrated that PhnF acts as a repressor of the phnDCE operon but does not affect the expression of pstSCAB. The deletion of pstS, which is thought to cause the constitutive expression of genes regulated by the two-component system SenX3-RegX3, led to the constitutive expression of the transcriptional fusions pstS-lacZ, phnD-lacZ, and phnF-lacZ, suggesting that phnDCE and phnF are conceivably new members of the SenX3-RegX3 regulon of M. smegmatis. Two presumptive binding sites for PhnF in the intergenic region between phnD and phnF were identified and shown to be required for the repression of phnD and phnF, respectively. We propose a model in which the transcription of pstSCAB is controlled by the two-component SenX3-RegX3 system, while phnDCE and phnF are subject to dual control by SenX3-RegX3 and PhnF.

scholarly journals Human islet preparations distributed for research exhibit a variety of insulin-secretory profiles

2015 ◽  
Vol 308 (7) ◽  
pp. E592-E602 ◽  
Author(s):  
Nora S. Kayton ◽  
Gregory Poffenberger ◽  
Joseph Henske ◽  
Chunhua Dai ◽  
Courtney Thompson ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Human Islets ◽  
Glucose Sensing ◽  
Human Islet ◽  
Altered Expression ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Basal Insulin Secretion ◽  
The Many

Human islet research is providing new insights into human islet biology and diabetes, using islets isolated at multiple US centers from donors with varying characteristics. This creates challenges for understanding, interpreting, and integrating research findings from the many laboratories that use these islets. In what is, to our knowledge, the first standardized assessment of human islet preparations from multiple isolation centers, we measured insulin secretion from 202 preparations isolated at 15 centers over 11 years and noted five distinct patterns of insulin secretion. Approximately three quarters were appropriately responsive to stimuli, but one quarter were dysfunctional, with unstable basal insulin secretion and/or an impairment in stimulated insulin secretion. Importantly, the patterns of insulin secretion by responsive human islet preparations (stable Baseline and Fold stimulation of insulin secretion) isolated at different centers were similar and improved slightly over the years studied. When all preparations studied were considered, basal and stimulated insulin secretion did not correlate with isolation center, biological differences of the islet donor, or differences in isolation, such as Cold Ischemia Time. Dysfunctional islet preparations could not be predicted from the information provided by the isolation center and had altered expression of genes encoding components of the glucose-sensing pathway, but not of insulin production or cell death. These results indicate that insulin secretion by most preparations from multiple centers is similar but that in vitro responsiveness of human islets cannot be predicted, necessitating preexperimental human islet assessment. These results should be considered when one is designing, interpreting, and integrating experiments using human islets.

scholarly journals Expression of genes of putative hexose transporters in the yeast Hansenula polymorpha are differentially regulated by glucose sensors Hxs1 and Gcr1

2012 ◽  
Vol 6 (3) ◽  
pp. 39-54 ◽  
Author(s):  
О. G. Stasyk ◽  
◽  
I. O. Denega ◽  
N. O. Sybirna ◽  
О. V. Stasyk ◽  
...  
Keyword(s):  
Hansenula Polymorpha ◽  
Glucose Sensors ◽  
Expression Of Genes ◽  
Hexose Transporters

scholarly journals Glucose Sensor Using Redox Active Oligonucleotide-Templated Silver Nanoclusters

Nanomaterials ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 1065 ◽  
Author(s):  
Kathryn L. Schroeder ◽  
Renee V. Goreham ◽  
Thomas Nann
Keyword(s):  
Glucose Oxidase ◽  
Glucose Sensor ◽  
Glucose Sensing ◽  
Emission Peak ◽  
Silver Nanoclusters ◽  
Glucose Levels ◽  
Redox Active ◽  
Emission Change

Redox active, photoluminescent silver nanoclusters templated with oligonucleotides were developed for glucose sensing. The silver nanoclusters had a photoluminescent emission at 610 nm that reversibly changed to 530 nm upon oxidation. The reversible emission change was measured with photoluminescent spectroscopy and used to detect H2O2, which is a by-product of the reaction of glucose with glucose oxidase. The ratio of the un-oxidised emission peak (610 nm) and the oxidised analogue (530 nm) was used to measure glucose concentrations up to 20 mM, well within glucose levels found in blood. Also, the reversibility of this system enables the silver nanoclusters to be reused.

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