<p>Cytoplasmic Ca²⁺ ([Ca²⁺]_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 <i>Piriformospora indica</i> requires the MALECTIN-DOMAIN CONTAINING CELLOOLIGOMER RECEPTOR KINASE1 (CORK1) and the mitochondrial POLY(A)-SPECIFIC RIBONUCLASE AtPARN for [Ca²⁺]_cyt elevation in Arabidopsis roots. Here, we show that CW extracts from beneficial and pathogenic <i>Fusarium</i> strains, in particular <i>Fusarium incarnatum</i> strain K23, require AtPARN, but not CORK1 for [Ca²⁺]_cyt elevation and the activation of Ca²⁺-dependent downstream responses. [Ca²⁺]_cyt elevation by the <i>F. incarnatum</i> strain K23 extract does not require the BRASSINOSTEROID INSENSITIVE1-ASSOCIATED RECEPTOR KINASE1 (BAK1) co-receptor or the TWO-PORE Ca²⁺ 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 <i>P. indica</i> and K23 at AtPARN prior to the increase in [Ca²⁺]_cyt ~ 90&#xa0;s after the stimulus. Furthermore, the elevated [Ca²⁺]_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.</p>