Charge Propagation in “Ion Channel Sensors” Based on Protein-Modified Electrodes and Redox Marker Ions

Schön, Peter; Degefa, Tesfaye Hailu; Asaftei, Simona; Meyer, Wolfdietrich; Walder, Lorenz

doi:10.1021/ja051574c

Cited by 29 publications

(42 citation statements)

References 42 publications

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“…Gel loading was controlled by hybridization with the 5S rRNA probe. (Schon et al, 2005) can involve an early loss of photosynthesis and ROS accumulation in chloroplasts (Joo et al, 2005). Moreover, photosynthetic electron transport inhibitors block lesion formation in the lesion mimic mutant (LMM), lsd1.…”

Section: Aa Deficiency Stimulates the Innate Immune Response Via Actimentioning

confidence: 99%

Ascorbic Acid Deficiency Activates Cell Death and Disease Resistance Responses in Arabidopsis

et al. 2005

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Programmed cell death, developmental senescence, and responses to pathogens are linked through complex genetic controls that are influenced by redox regulation. Here we show that the Arabidopsis (Arabidopsis thaliana) low vitamin C mutants, vtc1 and vtc2, which have between 10% and 25% of wild-type ascorbic acid, exhibit microlesions, express pathogenesis-related (PR) proteins, and have enhanced basal resistance against infections caused by Pseudomonas syringae. The mutants have a delayed senescence phenotype with smaller leaf cells than the wild type at maturity. The vtc leaves have more glutathione than the wild type, with higher ratios of reduced glutathione to glutathione disulfide. Expression of green fluorescence protein (GFP) fused to the nonexpressor of PR protein 1 (GFP-NPR1) was used to detect the presence of NPR1 in the nuclei of transformed plants. Fluorescence was observed in the nuclei of 6-to 8-week-old GFP-NPR1 vtc1 plants, but not in the nuclei of transformed GFP-NPR1 wild-type plants at any developmental stage. The absence of senescence-associated gene 12 (SAG12) mRNA at the time when constitutive cell death and basal resistance were detected confirms that elaboration of innate immune responses in vtc plants does not result from activation of early senescence. Moreover, H 2 O 2 -sensitive genes are not induced at the time of systemic acquired resistance execution. These results demonstrate that ascorbic acid abundance modifies the threshold for activation of plant innate defense responses via redox mechanisms that are independent of the natural senescence program.The complex relationships between programmed cell death (PCD) and natural senescence observed during leaf development are far from understood. However, one clear distinction is that senescence in leaves is essentially reversible, but PCD is not (Thomas et al., 2003). The genetically programmed cell suicide events that comprise PCD are triggered by enhanced levels of reactive oxygen species (ROS; Chen and Dickman, 2004;Laloi et al., 2004;Wagner et al., 2004). However, senescence-enhanced genes are also expressed in response to ROS (Navabpour et al., 2003).While the chemical nature of ROS dictates that they are potentially harmful to cells, plants use ROS as second messengers in signal transduction cascades regulating diverse processes such as mitosis, tropisms, and cell death. It is now well accepted that ROS accumulation is crucial to plant development as well as defense (Foyer and Noctor, 2005a). ROS signal transduction will ensue only if ROS escape destruction by cellular antioxidants that determine the lifetime and specificity of the signal. Ascorbic acid (AA) and glutathione are the major redox buffers of the plant cells, and they themselves are also signal-transducing molecules that can either signal independently or further transmit ROS signals (Fig. 1). They are thus intrinsic to redox homeostasis and redox-signaling events (Foyer and Noctor, 2005b).ROS production is often genetically programmed, for example, during the hypersen...

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Section: Aa Deficiency Stimulates the Innate Immune Response Via Actimentioning

confidence: 99%

Ascorbic Acid Deficiency Activates Cell Death and Disease Resistance Responses in Arabidopsis

et al. 2005

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“…[25][26][27] Previous studies have well documented that ssDNA is a flexible ''soft'' polymer that is prone to lie at the surface, while dsDNA is a rigid polymer that favors a stand-up configuration. [12,13,28] Since DNA is a heavily negatively charged polyelectrolyte, a surface-attached ssDNA probe that covers the active area of the electrode effectively blocks the interfacial electron transfer of Fe(CN) 6…”

Section: àmentioning

confidence: 99%

Gating of Redox Currents at Gold Nanoelectrodes via DNA Hybridization

Liu¹,

Sun²,

Di³

et al. 2010

Advanced Materials

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DNA immobilized at the surface of cone-shaped gold nanoelectrodes provides a favorable platform for artificial ion channels that can gate the redox reaction of ferricyanide. This effect arises from the nanometer-scale curvature and the enhanced mass transfer at nanoelectrodes. The label-free feature based on this ion-channel effect provides a means to develop label-free electrochemical DNA sensors.National Natural Science Foundation [20725516, 20873175, 20805055, 90913014]; National Basic Research Program of China [2006CB933000, 2007CB936000, 2007CB935603]; Ministry of Health [2009ZX10004-301, 2009ZX10004-302]; Shanghai Municipal Commission for Science and Technology [0952nm04600

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“…The group of Walder presented a detailed study at the mechanism of charge propagation of such sensors, utilizing seven different proteins in combination with seven different redox markers ions. 166 They were able to give a number of general statements that will be useful in understanding these devices and in developing new types of sensors.…”

Section: Other Immunosensorsmentioning

confidence: 99%