Dynamic reorganization of microfilaments and microtubules is necessary for the expression of non‐host resistance in barley coleoptile cells

Abstract

SummaryTo show the involvement of microfilaments and microtubules in non-host resistance of barley, partially dissected coleoptiles which had been inoculated with a non-pathogen, Erysiphe pisi, were treated with several actin and tubulin inhibitors. If the coleoptiles were not treated with any of the inhibitors, the non-pathogen always failed to penetrate the coleoptile cells. However, when coleoptiles were treated with actin or tubulin polymerization or depolymerization inhibitors, the non-pathogen was able to penetrate successfully and to form haustoria in coleoptlie cells of a non-host plant, barley. Actin polymerization inhibitors, cytochalasins, were more effective in causing an increase in penetration efficiency of E. pisithan tubulin inhibitors. The effects of cytochalasins depended on the kind of cytochalasin; the strength of the actin depolymerizing activity correlated significantly with the efficiency of increasing the penetration of the non-pathogen. When both actin and tubulin inhibitors were added simultaneously, the polarization of defense-related responses, such as massive cytoplasmic aggregation, deposition of papillae and accumulation of autofluorescent compounds, at fungal penetration sites was suppressed. Actin inhibitors did not affect arrangement and stability of microtubules and vice versa, and a double treatment of coleoptile cells with both microfilament and microtubule inhibitors showed an additive effect in increasing the penetration efficiency of E. pisL Furthermore, cytochalasin A treatment allowed other non-pathogens, Colletotrichum lagenarium and Alternaria alternata, to penetrate successfully into the non-host barley cells. These results strongly suggest that microfilaments and microtubules might play important roles in the expression of non-host resistance of barley.

Functional analysis of barley RAC/ROP G‐protein family members in susceptibility to the powdery mildew fungus

“…Some members of the closely related type I subgroup (AtROP1±AtROP6, HvRACB, HvRACD) are known to be regulators of the actin cytoskeleton (Fu et al, 2001;Gu et al, 2003) that is rearranged during the attack of powdery mildew fungi on barley (Kobayashi et al, 1997; K. Opalsky and R. Hu È ckelhoven unpublished results).…”

“…The regulation of cell polarity might be of special interest, because invagination of the host PM during haustoria establishment within barley epidermal cells may represent a kind of`inverted' tip growth induced by Bgh possibly via HvRACB. Alternatively, CA HvRACB such as other CA type I RAC/ROPs could induce isotropic cell growth, which antagonizes polar cytoskeleton focusing to site of attempted penetration crucial for penetration resistance (Kobayashi et al, 1997).…”

“…This leads further cytoplasma aggregation and migration of the nucleus. These types of subcellular processes are assumed to be important for early defence and penetration resistance (Kobayashi et al, 1997;Schmelzer, 2002). Inhibition of cytoskeleton rearrangement leads to facilitated parasitic access to plant cells.…”

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

“…Formation of these cell wall appositions (CWAs) or papillae is usually accompanied by a co-localised accumulation of phenolics and reactive oxygen species [2][3][4][5][6]. The complex process of sub-cellular cell wall remodelling is tightly linked to the rapid disassembly and subsequent focal reassembly of the plant cytoskeleton at fungal entry sites, which is indicative of a pathogen-triggered cell polarisation [6][7][8][9]. There has been a long-standing controversy, however, over whether CWAs function in disease resistance or facilitate the entry of fungal pathogens into host cells by providing a structural collar for the intruder.…”

Myosins XI modulate host cellular responses and penetration resistance to fungal pathogens

“…In addition to the deposition of cell wall reinforcements and focal accumulation of penetration-related proteins such as PEN3, the accretion of cytoplasm and organelles at sites of attempted fungal penetration involves reorganization of actin cytoskeleton, which forms a radial array focused on penetration site (10,11,(14)(15)(16)(17)(18). Consistent with this finding, disruption of AFs hampers penetration resistance, leading to increased penetration frequency by various fungal and oomycete pathogens (15)(16)(17)19). However, the mechanisms that drive AF dynamics and active transport of cellular components toward sites of attempted pathogen penetration remain elusive.…”