Apoplastic Venom Allergen‐like Proteins of Cyst Nematodes Modulate the Activation of Basal Plant Innate Immunity by Cell Surface Receptors
Poster Jan 26, 2015
Jose L. Lozano-Torresa, Ruud H.P. Wilbersa, SonjaWarmerdama, Anna Finkers-Tomczaka, Amalia Diaz-Granadosa, Casper C. van Schaika, Johannes Heldera, Jaap Bakkera,b, Aska Goversea,b, Arjen Schotsa and Geert Smanta,b
Despite causing considerable damage to host tissue during the onset of parasitism, nematodes establish remarkably persistent infections in both animals and plants. It is thought that an elaborate repertoire of effector proteins in nematode secretions suppresses damage-triggered immune responses of the host. However, the nature and mode of action of most immunomodulatory compounds in nematode secretions are not well understood. We have recently discovered that venom allergen-like proteins (VAPs) of plant-parasitic nematodes selectively suppress host immunity mediated by surface-localized immune receptors. VAPs are uniquely conserved in secretions of all animal- and plant-parasitic nematodes studied to date, but their role during the onset of parasitism has thus far remained elusive. Knocking-down the expression of Gr-VAP1 severely hampered the infectivity of the potato cyst nematode Globodera rostochiensis. By contrast, heterologous expression of Gr-VAP1 and VAPs from the beet cyst nematode Heterodera schachtii in plants resulted in the loss of basal immunity to multiple pathogens. The modulation of basal immunity by ectopic VAPs involves extracellular protease-based host defenses. Furthermore, the onset of programmed cell death was commonly suppressed by VAPs from G. rostochiensis, H. schachtii, and the root-knot nematode Meloidogyne incognita. Surprisingly, these VAPs only affected the programmed cell death mediated by surface-localized immune receptors. Furthermore, the delivery of VAPs into host tissue coincides with the enzymatic breakdown of plant cell walls by migratory nematodes. We, therefore, conclude that parasitic nematodes most likely utilize VAPs to suppress the activation of defenses by immunogenic breakdown products in damaged host tissue.