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Kalachova, Tetiana; Leontovycova, Hana; Iakovenko, Oksana; Pospichalova, Romana; Marsik, Petr; Kloucek, Pavel; Janda, Martin; Valentova, Olga; Kocourkova, Daniela; Martinec, Jan; Burketova, Lenka; Ruelland, Eric (2019): Interplay between phosphoinositides and actin cytoskeleton in the regulation of immunity related responses in Arabidopsis thaliana seedlings. In: Environmental and Experimental Botany, Vol. 167, 103867
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Actin cytoskeleton is indispensable for plant cell integrity. Besides, increasing evidences illustrate its crucial role in plant responses to environment, including defence against pathogens. Recently, we have demonstrated that pre-treatment with actin disrupting drugs latrunculin B (latB) and cytochalasin E can enhance plant resistance against bacterial and fungal pathogens via activation of salicylic acid (SA) pathway. Here, we show that actin depolymerization in Arabidopsis thaliana seedlings not only triggers SA biosynthesis by ICS1, but also induces callose deposition via callose synthase PMR4. This effect is SA-independent since still present in mutants that do not accumulate SA. LatB also triggers the expression of several defence related genes. We could distinguish genes, induced in a SA-dependent manner (PR1, WRKY38, ICS1) and those that are SA-independent (PR2, PAD4, BAP1). As actin cytoskeleton is tightly connected with membrane trafficking, we assayed the effect of latB on mutant plants invalidated in phosphatidylinositol 4-kinase beta1 and beta2 (PI4K beta 1 beta 2). Deficiency in PI4K beta 1 beta 2 enhanced latB-triggered actin filaments depolymerisation. Yet, it did not lead to a stronger callose deposition or SA biosynthesis in response to latB. Surprisingly, introduction of NahG construct or pad4 mutation in pi4k beta 1 beta 2 background had much lower effect on SA induction and SA-dependent gene expression changes than it has in wild type. We can thus conclude that actin disruption itself triggers immune-like responses: there is an induction of SA via PAD4 coupled to ICS1;it leads to the induction of PR1 and WRKY38, and this requires a functional PI4K beta 1 beta 2 to be properly regulated. However, an alternative, SA-independent pathway also exists that leads to the enhanced expression of PR2 and to callose accumulation.