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Projekt Druckansicht

Einfluss veränderter pflanzlicher Zellwände auf den Jasmonsäure-Signalweg in der Wurzel

Antragstellerin Dr. Debora Gasperini
Fachliche Zuordnung Pflanzenphysiologie
Genetik und Genomik der Pflanzen
Förderung Förderung von 2018 bis 2022
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 395537511
 
Erstellungsjahr 2023

Zusammenfassung der Projektergebnisse

Plant cells are surrounded by cell walls that support, protect and act as the immediate contact surface between cells and the extracellular environment. Perturbations in cell walls often lead to misregulated hormonal responses, including jasmonate (JA) accumulation, a crucial regulator of plant defense and growth responses. However, it remained unclear which cellular processes arising from cell wall perturbations are involved in transducing the signal intracellularly and initiate JA production in plastids. In this project, we used Arabidopsis cellulose-deficient mutants in KORRIGAN1 (KOR1) to unveil such processes. Kor1 mutants exhibit strong induction of JA marker genes and elevated levels of the bioactive hormone conjugate JA-Ile in endodermal and pericycle cells of seedling roots, which is caused by cell-non-autonomous signals deriving from adjacent cortex cells. To identify components involved in initiating JA-Ile production upon cell wall alterations, we screened for suppressors of JA-Ile in kor1, and isolated 12 putative candidates. Among those, mutations in the putative glycosyltransferase ESMERALDA 1 (ESMD1) suppressed elevated JA-Ile production in kor1 roots, as well as reduced kor1 root cell expansion by putatively modifying cell wall composition and properties. Consistently, restoring KOR1 function specifically in cortex cells also restored the JA-Ile phenotype in kor1. Subsequent hyperosmotic treatments phenocopied the suppression of kor1 root morphology as well as ectopic JA-Ile production. Conversely, hypoosmotic treatments activated JA-Ile signalling in WT plants at similar locations. This ultimately led to a model in which the equilibrium of plant cell walls containing the intracellular hydrostatic water pressure is disturbed. As a consequence, altered cortex cell morphology may exert mechanical stress towards inner tissues, triggering ectopic JA-Ile production. Hence, changes in turgor pressure leading to mechanical compression may be a crucial elicitor of JA-Ile biosynthesis and could occur during other mechanical stresses such as wounding or herbivory. Remarkably, the consequences of ectopic JA-Ile signalling in kor1 roots were neither to affect root growth nor canonical defense responses, but were found to be important to redirect root growth towards sites with higher water availability. Collectively, these results provide new perspectives towards understanding how plants sense and decode extracellular stimuli to initiate acclimation responses. The forward genetic screen was instrumental to generate a new hypothesis that turgordriven mechanical compression of cells embedded in inner tissues could be a causative force driving JA-Ile production and signalling. If we undertook only the reverse genetics approach, it would not have been possible to move the field forward, highlighting the need to combine complementary approaches to mitigate project risks and ensure scientific advancement.

Projektbezogene Publikationen (Auswahl)

 
 

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