Glycerol-3-phosphate and cell wall integrity maintenance mechanism - two sides to the same story?
Master thesis
Permanent lenke
http://hdl.handle.net/11250/2615477Utgivelsesdato
2018Metadata
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- Institutt for biologi [2616]
Sammendrag
Plants and pathogens are in a constant "arms-race", with the plant cell wall as one of the main battlefields. This arms-race have evolved to complex defense responses in plants against primary infections in local infected tissue. Moreover, local resistance induce systemic acquired resistance (SAR), a broad-spectrum and long lasting resistance in systemic tissue, with glycerol-3-phosphate (G3P) as a central signal metabolite. A well-known response to pathogen infections is reinforcement of the cell wall. The cell wall´s functional integrity is also maintained by the cell wall integrity (CWI) maintenance mechanism. Pathogen resistance and the CWI maintenance mechanism show overlapping responses to cell wall damage (CWD), but limited knowledge of their connections is available. However, pattern-triggered immunity (PTI), involved in local resistance, was recently shown to inhibit the CWI maintenance mechanism by e.g. downregulation of phytohormone synthesis. In this project, various CWD-induced responses (by Isoxaben) were studied in KO-mutants impaired in G3P-metabolism to investigate G3P-signalling´s association with CWI maintenance in Arabidposis thaliana. Moreover, sorbitol cotreatment was performed to examine how hyperosmotic conditions affected the responses. It was shown that genes involved in G3P-metabolism, or the resulting impairment of G3P-metabolism does not seem to be involved in ISX-induced CWD responses such as lignin biosynthesis and growth inhibition. However, the genes seem to act as negative regulators of ISX-induced phytohormone accumulation. Since G3P is a central signal metabolite in SAR, and there is a known interconnection between SAR and PTI, this raises the questions of a possible CWI maintenance-suppressing role of SAR, either directly, through G3P-metabolism gene activity or G3P-flux modulations, or indirectly, through activation of PTI.