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Biotrophic Pathogens (biotrophic + pathogen)
Selected AbstractsInfection of Arabidopsis thaliana leaves with Albugo candida (white blister rust) causes a reprogramming of host metabolismMOLECULAR PLANT PATHOLOGY, Issue 2 2000Hsueh-Mei Chou Albugo candida (Pers.) (O.) Kunze is a biotrophic pathogen which infects the crucifer Arabidopsis thaliana (L.) Heynh forming discrete areas of infection. Eight days after inoculation of leaves, white blisters became visible on the under surface of the leaf although no symptoms were apparent on the upper surface. By day 14, the region of leaf invaded by fungal mycelium had become chlorotic. Recently it has been hypothesized that an accumulation of soluble carbohydrates, following an increase in invertase activity, may trigger sugar signal transduction pathways leading to the repression of photosynthetic gene expression and to the induction of defence proteins. This hypothesis was investigated by quantifying localized changes in carbohydrate and photosynthetic metabolism and the expression of genes encoding photosynthetic and defence proteins. Quantitative imaging of chlorophyll fluorescence revealed that the rate of photosynthesis declined progressively in the invaded regions of the leaf. However, in uninfected regions of the infected leaf the rate of photosynthesis was similar to that measured in the control leaf until late on during the infection cycle when it declined. Images of nonphotochemical fluorescence quenching (NPQ) suggested that the capacity of the Calvin cycle had been reduced in infected regions and that there was a complex metabolic heterogeneity within the infected leaf. A. candida also caused localized changes in the carbohydrate metabolism of the leaf; soluble carbohydrates accumulated in the infected region whereas the amount of starch declined. The reverse was seen in uninfected regions of the infected leaf; carbohydrates did not accumulate until late on during infection and the amount of starch increased as the infection progressed. There was an increase in the activity of invertases which was confined to regions of the leaf invaded by the fungal mycelium. The increase in apoplastic invertase activity was of host origin, as mRNA levels of the AT,FRUCT1 gene (measured by semiquantitative RT-PCR) increased 40-fold in the infected region. The increase in soluble invertase activity resulted from the appearance of a new isoform in the invaded region of the leaf. Current evidence suggests that this was of fungal origin. Northern blot analysis of cab and rbcS showed that photosynthetic gene expression was repressed in the infected leaf from 6 days after inoculation (DAI) when compared to control leaves. In contrast, there was no detectable induction of defence proteins in the infected leaf. These data are discussed in the context of the sugar-sensing hypothesis presented above. [source] Avirulence proteins from haustoria-forming pathogensFEMS MICROBIOLOGY LETTERS, Issue 2 2007Ann-Maree Catanzariti Abstract A major insight that has emerged in the study of haustoria-forming plant pathogens over the last few years is that these eukaryotic biotrophs deliver suites of secreted proteins into host cells during infection. This insight has largely derived from successful efforts to identify avirulence (Avr) genes and their products from these pathogens. These Avr genes, identified from a rust and a powdery mildew fungus and three oomycete species, encode small proteins that are recognized by resistance proteins in the host plant cytoplasm, suggesting that they are transported inside plant cells during infection. These Avr proteins probably represent examples of fungal and oomycete effector proteins with important roles in subverting host cell biology during infection. In this respect, they represent a new opportunity to understand the basis of disease caused by these biotrophic pathogens. Elucidating how these pathogen proteins gain entry into plant cells and their biological function will be key questions for future research. [source] Fine-Tuning Plant Defence Signalling: Salicylate versus JasmonatePLANT BIOLOGY, Issue 1 2006G. J. M. Beckers Abstract: Plant defences against pathogens and herbivorous insects form a comprehensive network of interacting signal transduction pathways. The signalling molecules salicylic acid (SA) and jasmonic acid (JA) play important roles in this network. SA is involved in signalling processes providing systemic acquired resistance (SAR), protecting the plant from further infection after an initial pathogen attack. SAR is long-lasting and provides broad spectrum resistance to biotrophic pathogens that feed on a living host cell. The regulatory protein NPR1 is a central positive regulator of SAR. SA-activated NPR1 localizes to the nucleus where it interacts with TGA transcription factors to induce the expression of a large set of pathogenesis-related proteins that contribute to the enhanced state of resistance. In a distinct signalling process, JA protects the plant from insect infestation and necrotrophic pathogens that kill the host cell before feeding. JA activates the regulatory protein COI1 that is part of the E3 ubiquitin ligase-containing complex SCFCOI1, which is thought to derepress JA-responsive genes involved in plant defence. Both synergistic and antagonistic interactions have been observed between SA- and JA-dependent defences. NPR1 has emerged as a critical modulator of cross-talk between the SA and JA signal and is thought to aid in fine tuning defence responses specific to the encountered attacker. Here we review SA- and JA-dependent signal transduction and summarize our current understanding of the molecular mechanisms of cross-talk between these defences. [source] Arabidopsis thaliana class-II TGA transcription factors are essential activators of jasmonic acid/ethylene-induced defense responsesTHE PLANT JOURNAL, Issue 2 2010Mark Zander Summary The three closely related Arabidopsis basic leucine zipper (bZIP) transcription factors TGA2, TGA5 and TGA6 are required for the establishment of the salicylic acid (SA)-dependent plant defense response systemic acquired resistance, which is effective against biotrophic pathogens. Here we show that the same transcription factors are essential for the activation of jasmonic acid (JA)- and ethylene (ET)-dependent defense mechanisms that counteract necrotrophic pathogens: the tga256 triple mutant is impaired in JA/ET-induced PDF1.2 and b-CHI expression, which correlates with a higher susceptibility against the necrotroph Botrytis cinerea. JA/ET induction of the trans -activators ERF1 and ORA59, which act upstream of PDF1.2, was slightly increased (ERF1) or unaffected (ORA59). PDF1.2 expression can be restored in the tga256 mutant by increased expression of ORA59, as observed in the tga256 jin1 quadruple mutant, which lacks the transcription factor JIN1/AtMYC2 that functions as a negative regulator of the JA/ET-dependent anti-fungal defense program. Whereas JA/ET-induced PDF1.2 expression is strongly suppressed by SA in wild-type plants, no negative effect of SA on PDF1.2 expression was observed in the tga256 jin1 quadruple mutant. These results imply that the antagonistic effects of TGA factors and JIN1/AtMYC2 on the JA/ET pathway are necessary to evoke the SA-mediated suppression of JA/ET-induced defense responses. [source] | ||||||||||