The role of calcium in signal transduction pathways leading to the plant oxidative burst
Abstract
The plant oxidative burst, the rapid production of reactive oxygen species during pathogen defense and resistance responses, is stimulated by a multi-step intracellular signal transduction cascade. While several previous studies have suggested that Ca2+ may serve as a second messenger in this cascade, the cytosolic Ca2+ fluxes involved previously had not been scrutinized carefully. Here we demonstrate that every stimulant of the oxidative burst activates a transient Ca2+ flux in Nicotiana tabacum cells. Similar results were also found when measurements were made at the single cell level. The Ca2+ pulses required to stimulate oxidant production derive from the release of Ca2+ from an internal Ca2+ store. These burst-inducing Ca 2+ fluxes invariably require the prior activation of a protein kinase(s) and trans-membrane anion fluxes. Furthermore, we have used our knowledge of Ca2+ fluxes activated during the oxidative burst to assess the interaction between plant cells and the oxalate-secreting fungal plant pathogen Sclerotinia sclerotiorum. Oxalate was found to inhibit the oxidative burst in concentrations consistent with those measured in S. sclerotiorum infected plants. This inhibition appeared to occur independently of oxalate's acidity or, remarkably, its affinity for Ca 2+. Finally, in the course of these explorations we have discovered that depletion of extra-cellular Ca2+ with externally applied Ca2+ chelators stimulates release of Ca2+ from internal stores. These chelator-activated Ca2+ fluxes appear to be regulated by discrete signaling pathways, and may aid the plant by filling alternative Ca2+ stores.
Degree
Ph.D.
Advisors
Low, Purdue University.
Subject Area
Biochemistry|Botany|Cellular biology
Off-Campus Purdue Users:
To access this dissertation, please log in to our
proxy server.