Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elicitation of cultured chickpea (Cicer arietinum L.) cells stimulates a signal transduction pathway leading to several rapid responses: (1) oxidative burst, (2) extracellular alkalinisation, (3) extracellular acidification, (4) transient K+ efflux, and (5) activation of defence related genes all within 2 hours. Induced genes are encoding acidic and basic chitinases, a thaumatin-like protein and isoflavone reductase. All these elicitor-induced responses are inhibited by the Ser/Thr protein kinase inhibitor staurosporine and the anion channel blocker anthracene-9-carboxylic acid but stimulated by the Ser/Thr protein phosphatase 2A inhibitor cantharidin. The oxidative burst leads to a transient extracellular H2O2 accumulation which seems to be preceded by O2- production, indicating dismutation of O2- to H2O2. The oxidative burst is accompanied by transient alkalinisation of the culture medium which is followed by long-lasting extracellular acidification. An 80 percent inhibition of the alkalinisation after complete inhibition of the H2O2 burst with diphenylene iodonium indicates that the elicitor induced increase of extracellular pH is mainly based on a proton consumption for O2-dismutation. A simultaneous deactivation of the plasma membrane H+-ATPase during oxidative burst and extracellular alkalinisation is also suggested. The elicitor-stimulated extracellular acidification is inhibited by the plasma membrane H+-ATPase inhibitor N, N'-dicyclohexylcarbodiimide assuming a reactivation of the H+-ATPase 25 min after elicitation. Extracellular acidification seems not to be necessary for elicitor-induced activation of defence related genes. Opposite modulation of K+ and proton fluxes after elicitation and/or treatment with the H+-ATPase effectors fusicoccin or N, N'-dicyclohexylcarbodiimide indicate that the elicitor induced transient K+ efflux is regulated by a K+/H+ exchange reaction.
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PMID:Early elicitor-induced events in chickpea cells: functional links between oxidative burst, sequential occurrence of extracellular alkalinisation and acidification, K+/H+ exchange and defence-related gene activation. 1130 17

This study investigates the stress-mitigating effects of endophytic Penicillium funiculosum LHL06 on soybean roots via modulation of physio-biochemical, molecular, and proteomic responses to combined heavy metal (Ni, Cu, Pb, Cr, and Al) toxicity. Preliminary screening revealed that LHL06 can tolerate and remediate combined heavy metal contamination in its media and upregulate gibberellins (GA1, GA3, GA4, GA7 and GA9) and indole-3-acetic acid (IAA) production. Inoculation of LHL06 resulted in marked reduction of metals uptake in roots and shoots by downregulating heavy metal ATPase genes (GmHMA13, GmHMA14, GmHMA19) and GmMATE1 compared to non-inoculated plants; in turn, this decreased abscisic acid and jasmonic acid levels. Moreover, triggering of free amino acid metabolism in LHL06-inoculated roots significantly upregulated expression of stress-related proteins (glutathione S-transferase L3, isoflavone reductase-like, chalcone isomerase A, NAD(P)H dehydrogenase (quinone), FQR1-like 1 isoform X2, and Peroxidase 3) to combat metals toxicity. Compared to non-inoculated-plants, LHL06-inoculated-plants exhibited higher antioxidant activity and transcript accumulation of glutathione S-transferase (GmGST8 and GmGST3), G6PDH, and GmSOD1[Cu-Zn], which decreased metal-induced reactive oxygen species. Therefore, LHL06-inoculation remediate combined metal contamination in soil, activate signaling network of stress-responsive hormones and antioxidant systems for promoting growth and tolerance, and reduce metal-accumulation, thereby making plants safer for consumption.
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PMID:Phytohormones enabled endophytic Penicillium funiculosum LHL06 protects Glycine max L. from synergistic toxicity of heavy metals by hormonal and stress-responsive proteins modulation. 3127 35