Abnormal callose response phenotype and hypersusceptibility to Peronosporaparasitica in defense-compromised Arabidopsis nim1-1 and salicylate hydroxylase-expressing plants

To investigate the impact of induced host defenses on the virulence of a co mpatible Peronospora parasitica strain on Arabidopsis thaliana, we examined growth and development of this pathogen in nim1-1 mutants and transgenic s alicylate hydroxylase plants. These plants are unable to respond to or accu mulate salicylic acid (SA), respectively, are defective in expression of sy stemic acquired resistance (SAR), and permit partial growth of some normall y avirulent pathogens. We dissected the P. parasitica life cycle into nine stages and compared its progression through these stages in the defense-com promised hosts and in wild-type plants, NahG plants supported the greatest accumulation of pathogen biomass and conidiophore production, followed by n im1-1 and then wild-type plants. Unlike the wild type, NahG and nim1-1 plan ts showed little induction of the SAR gene PR-1 after colonization with P, parasitica, which is similar to our previous observations. We examined the frequency and morphology of callose deposits around parasite haustoria and found significant differences between the three hosts. NahG plants showed a lower fraction of haustoria surrounded by thick callose encasements and a much higher fraction of haustoria with callose limited to thin collars arou nd haustorial necks compared to wild type, whereas nim1-1 plants were inter mediate between NahG and wild type. Chemical induction of SAR in plants col onized by P, parasitica converted the extrahaustorial. callose phenotype in NahG to resemble closely the wild-type pattern, but had no effect on nim1- 1 plants. These results suggest that extrahaustorial callose deposition is influenced by the presence or lack of SA and that this response may be sens itive to the NIM1/NPR1 pathway. Additionally, the enhanced susceptibility d isplayed by nim1-1 and NahG plants shows that even wild-type susceptible ho sts exert defense functions that reduce disease severity and pathogen fitne ss.