scholarly journals A lectin receptor kinase as a potential sensor for extracellular nicotinamide adenine dinucleotide in Arabidopsis thaliana

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Chenggang Wang ◽  
Mingqi Zhou ◽  
Xudong Zhang ◽  
Jin Yao ◽  
Yanping Zhang ◽  
...  
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Plant Immunity ◽  
Nicotinamide Adenine ◽  
Receptor Kinase ◽  
Basal Resistance ◽  
Lectin Receptors ◽  
Lectin Domain ◽  
Surface Receptors ◽  
Lectin Receptor

Nicotinamide adenine dinucleotide (NAD+) participates in intracellular and extracellular signaling events unrelated to metabolism. In animals, purinergic receptors are required for extracellular NAD+ (eNAD+) to evoke biological responses, indicating that eNAD+ may be sensed by cell-surface receptors. However, the identity of eNAD+-binding receptors still remains elusive. Here, we identify a lectin receptor kinase (LecRK), LecRK-I.8, as a potential eNAD+ receptor in Arabidopsis. The extracellular lectin domain of LecRK-I.8 binds NAD+ with a dissociation constant of 436.5 ± 104.8 nM, although much higher concentrations are needed to trigger in vivo responses. Mutations in LecRK-I.8 inhibit NAD+-induced immune responses, whereas overexpression of LecRK-I.8 enhances the Arabidopsis response to NAD+. Furthermore, LecRK-I.8 is required for basal resistance against bacterial pathogens, substantiating a role for eNAD+ in plant immunity. Our results demonstrate that lectin receptors can potentially function as eNAD+-binding receptors and provide direct evidence for eNAD+ being an endogenous signaling molecule in plants.

scholarly journals Extracellular pyridine nucleotides trigger plant systemic immunity through a lectin receptor kinase/BAK1 complex

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Chenggang Wang ◽  
Xiaoen Huang ◽  
Qi Li ◽  
Yanping Zhang ◽  
Jian-Liang Li ◽  
...  
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Systemic Acquired Resistance ◽  
Plant Immunity ◽  
Acquired Resistance ◽  
Receptor Complex ◽  
Pyridine Nucleotides ◽  
Receptor Kinase ◽  
Systemic Immunity ◽  
Lectin Receptor

Abstract Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant immunity induced by mobile signals produced in the local leaves where the initial infection occurs. Although multiple structurally unrelated signals have been proposed, the mechanisms responsible for perception of these signals in the systemic leaves are unknown. Here, we show that exogenously applied nicotinamide adenine dinucleotide (NAD+) moves systemically and induces systemic immunity. We demonstrate that the lectin receptor kinase (LecRK), LecRK-VI.2, is a potential receptor for extracellular NAD+ (eNAD+) and NAD+ phosphate (eNADP+) and plays a central role in biological induction of SAR. LecRK-VI.2 constitutively associates with BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1) in vivo. Furthermore, BAK1 and its homolog BAK1-LIKE1 are required for eNAD(P)+ signaling and SAR, and the kinase activities of LecR-VI.2 and BAK1 are indispensable to their function in SAR. Our results indicate that eNAD+ is a putative mobile signal, which triggers SAR through its receptor complex LecRK-VI.2/BAK1 in Arabidopsis thaliana.

scholarly journals Metastatic potential severely altered by changes in tumor cell adhesiveness and cell-surface sialylation.

1983 ◽  
Vol 157 (1) ◽  
pp. 371-376 ◽  
Author(s):  
M Fogel ◽  
P Altevogt ◽  
V Schirrmacher
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Tumor Cell ◽  
Metastatic Potential ◽  
Lectin Receptors ◽  
Lectin Receptor ◽  
Receptor Sites ◽  
Variant Line

A plastic adherent variant line (ESb-M) of a highly invasive and metastatic murine T cell lymphoma (ESb) was found to have lost its metastatic potential while still being tumorigenic in normal syngeneic hosts. The variant retained most of its ESb-derived antigenic and biochemical characteristics but differed at binding sites for certain lectins with specificity for terminal N-acetylgalactosamine residues. Whereas such sites were masked by sialic acid on metastatic ESb cells, they became unmasked on the adherent variant line. Metastatic revertants of ESb-M cells did not express the respective lectin receptor sites because these were again masked by sialic acid. It is suggested that the masking of specific lectin receptors sites on the tumor cell surface is of crucial importance for metastatis. If freely exposed, these sites may change adherence characteristics of the cells possibly not only in vitro (to plastic) but also in vivo.

scholarly journals New Chemical Probe Targeting Bacterial NAD Kinase

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 4893
Author(s):  
David A. Clément ◽  
Clarisse Leseigneur ◽  
Muriel Gelin ◽  
Dylan Coelho ◽  
Valérie Huteau ◽  
...  
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Kinase Inhibitors ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Infection Model ◽  
Detailed Knowledge ◽  
Nad Kinase ◽  
Chemical Probe ◽  
Covalent Coupling

Nicotinamide adenine dinucleotide (NAD) kinases are essential and ubiquitous enzymes involved in the tight regulation of NAD/nicotinamide adenine dinucleotide phosphate (NADP) levels in many metabolic pathways. Consequently, they represent promising therapeutic targets in cancer and antibacterial treatments. We previously reported diadenosine derivatives as NAD kinase inhibitors with bactericidal activities on Staphylococcus aureus. Among them, one compound (namely NKI1) was found effective in vivo in a mouse infection model. With the aim to gain detailed knowledge about the selectivity and mechanism of action of this lead compound, we planned to develop a chemical probe that could be used in affinity-based chemoproteomic approaches. Here, we describe the first functionalized chemical probe targeting a bacterial NAD kinase. Aminoalkyl functional groups were introduced on NKI1 for further covalent coupling to an activated SepharoseTM matrix. Inhibitory properties of functionalized NKI1 derivatives together with X-ray characterization of their complexes with the NAD kinase led to identify candidate compounds that are amenable to covalent coupling to a matrix.

NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia

1982 ◽  
Vol 243 (4) ◽  
pp. H619-H627 ◽  
Author(s):  
L. Gyulai ◽  
E. Dora ◽  
A. G. Kovach
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Redox State ◽  
Redox System ◽  
Inhibitory Effect ◽  
Nadh Oxidation ◽  
Nicotinamide Adenine ◽  
Direct Inhibitory Effect ◽  
Anterior Suprasylvian Gyrus ◽  
Reduced Nicotinamide Adenine Dinucleotide

The redox state of the anterior suprasylvian gyrus of cats was measured during electrical stimulation and under hypercapnia on cast immobilized and artificially respirated. The state of the nicotinamide adenine dinucleotide-reduced nicotinamide adenine dinucleotide (NAD/NADH) redox system was monitored by in vivo fluorometry. Hypercapnia was produced by inhalation of 10, 15, and 30% CO2, respectively. Hypercapnic acidosis led to NADH oxidation. The NADH oxidation under 30% CO2 inhalation was significantly larger (-14.9 +/- 2.9%) than that observed under 10% (-6.5 +/- 1.9%) and 15% CO2 (-7.0 +/- 1.6%) inhalation. Under normocapnic conditions, stimulation induced NAD reduction to NADH (5.5 +/- 0.8%). The magnitude of the NAD reductive response to stimulation was unaffected by 10% CO2 inhalation, but it was decreased by 15 and 30% CO2 inhalation. The increased concentration of NADH upon stimulation is interpreted as resulting from an increased rate of substrate mobilization. The cause of the oxidation of the NADH pool of the cell during hypercapnia is partly due to the direct inhibitory effect of CO2 on the carbohydrate metabolism, but the role of other mechanisms cannot be neglected either.

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