Abstract
Cytoplasmic Ca(2+) ([Ca(2+)](cyt)) elevation is a rapid response of roots to colonizing beneficial and pathogenic fungi. We have previously demonstrated that the elicitor-active compound cellotriose from a cell wall (CW) extract of the beneficial fungus Piriformospora indica requires the MALECTIN-DOMAIN CONTAINING CELLOOLIGOMER RECEPTOR KINASE1 (CORK1) and the mitochondrial POLY(A)-SPECIFIC RIBONUCLASE AtPARN for [Ca(2+)](cyt) elevation in Arabidopsis roots. Here, we show that CW extracts from beneficial and pathogenic Fusarium strains, in particular Fusarium incarnatum strain K23, require AtPARN, but not CORK1 for [Ca(2+)](cyt) elevation and the activation of Ca(2+)-dependent downstream responses. [Ca(2+)](cyt) elevation by the F. incarnatum strain K23 extract does not require the BRASSINOSTEROID INSENSITIVE1-ASSOCIATED RECEPTOR KINASE1 (BAK1) co-receptor or the TWO-PORE Ca(2+) CHANNEL1 (TPC1) but operates synergistically with the cellotriose- and chitin-induced signaling pathways. We propose a convergence of the signaling pathways induced by the CW extracts from P. indica and K23 at AtPARN prior to the increase in [Ca(2+)](cyt) ~ 90 s after the stimulus. Furthermore, the elevated [Ca(2+)](cyt) levels activate a mild defense response which might be used by the roots to restrict fungal propagation and to balance beneficial and non-beneficial traits in the symbiosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12298-025-01600-7.