Full Text Available
Note: Clicking the button above will open the full text document at the original institutional repository in a new window.
An investigation into the role of cytosolic free Ca2+ in Salicylic acid mediation of disease resistance in Arabidopsis
Salicylic acid (SA) accumulation upon pathogen attack is a fundamental requirement for the activation of numerous plant defence mechansms. Cytosolic free Ca2+ ([Ca2+]c) is a ubiquitous signalling molecule involved in a host of cellular processes. Using transgenic Arabidopsis thaliana seedlings expre...
Saved in:
| Main Author: | |
|---|---|
| Other Authors: | |
| Format: | Thesis |
| Language: | English |
| Published: |
Department of Molecular and Cell Biology
2024
|
| Subjects: | |
| Tags: |
No Tags, Be the first to tag this record!
|
| Summary: | Salicylic acid (SA) accumulation upon pathogen attack is a fundamental requirement for the activation of numerous plant defence mechansms. Cytosolic free Ca2+ ([Ca2+]c) is a ubiquitous signalling molecule involved in a host of cellular processes. Using transgenic Arabidopsis thaliana seedlings expressing the Ca2+-sensitive photoprotein aequorin, we previously reported a rapid and transient increase in [Ca2+]c upon application of exogenous SA. We now investigated the characteristics of the SA-induced [Ca2+]c increase and report that the majority of the response is derived from internal stores. It appears likely that SA triggers Ca2+-induced Ca2+-release. Preliminary evidence suggests a role for the SA-induced [Ca2+]c increase in the regulation of NPR1 expression since modulation of the SA-induced [Ca2+]c response with the extracellular Ca2+ chelator BAPTA causes a reduction in NPR1 mRNA levels. We have isolated two putative mutants that are defective in their ability to produce a SA-induced [Ca2+]c increase. Characterisation of these mutants is underway and will prove invaluable in identifying the components or events that cause the SA-induced [Ca2+]c transient, thereby aiding in the understanding of the role of [Ca2+]c in SA-mediated signal transduction. |
|---|