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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catalase and hydrogen peroxide (H(2)O(2)) have been extensively studied for their roles in various stress responses. However, little is known about the triggering mechanisms for stress-induced catalase gene expression or about H(2)O(2) production as a stress signal. It is reported here that ABA-, drought-, and salt stress-induced gene expression of CAT1 catalase is mediated by AtMEK1, an Arabidopsis MAPK kinase, by triggering H(2)O(2) signal production. Both CAT1 expression and AtMEK1 activity were activated by ABA, drought, and salt stresses. The mek1 mutant totally blocked stress-induced CAT1 expression and, interestingly, stress-induced H(2)O(2) production was also blocked. Over-expression of AtMEK1 significantly promoted stress-induced CAT1 expression, and also promoted H(2)O(2) production. These results conclusively indicate that stress-induced CAT1 expression is mediated by AtMEK1 and, furthermore, that the triggering of H(2)O(2) production might be involved in this process, as further proved by the observation that CAT1 expression was induced by applied H(2)O(2.) Surprisingly, the signalling mechanisms for stress-induced gene expression of CAT2 and CAT3 were very different from that of CAT1. Except for drought stress, expression of CAT2 or CAT3 was also activated by salt stress or ABA treatment, and AtMEK1 was not proved to be involved in the drought-induced expression of CAT2 or CAT3. Further studies showed that stomatal movement was much less sensitive to ABA in AtMEK1 mutant (mek1), and over-expression of AtMEK1 in Arabidopsis increased plant resistance to drought or salt stress, which further demonstrated that AtMEK1 is a crucial mediator in plant stress signal transduction.
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PMID:AtMEK1 mediates stress-induced gene expression of CAT1 catalase by triggering H2O2 production in Arabidopsis. 1772 92

Periods of carbohydrate deprivation are commonly encountered by plant cells. Plants respond to this nutrient stress by the mobilization of stored carbohydrates and the reallocation of other cellular macromolecules to degradative pathways. Previously we identified a number of metabolic genes that are upregulated in Arabidopsis thaliana cells during sucrose starvation. One of the genes identified encodes acyl-CoA oxidase-4 (ACX4, EC 1.3.3.6), a peroxisomal acyl-CoA oxidase that is unique to plants and involved in beta-oxidation of short-chain fatty acids. Here we demonstrate that ACX4 activity increases during sucrose starvation, indicating a shift to a catabolic breakdown of fatty acids as a source of available carbon. This suggests a role for degradation of short-chain fatty acids in the response to sucrose starvation, leading in turn to the production of toxic H2O2. Catalase-3 (CAT3, EC 1.11.1.6) activity also increases during starvation as a direct response to the increase in oxidative stress caused by the rapid activation of alternative catabolic pathways, including a specific increase in ACX4 activity. Any disruption in ACX4 expression or in beta-oxidation of fatty acids in general prevents this increase in catalase activity and expression. We hypothesize that CAT3 activity increases to remove the H2O2 produced by alternative catabolic processes induced during the carbohydrate shortages caused by extended periods of low-light conditions.
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PMID:Increase in catalase-3 activity as a response to use of alternative catabolic substrates during sucrose starvation. 2013 75