Plants and Microbes

It has been reported that filament forming surface proteins like hydrophobins are important virulence determinants in fungi and are secreted during pathogenesis. In obligate biotrophic pathogens like rust fungi, such proteins have not yet been identified. Rust transferred protein 1 (RTP1p), a rust protein that is transferred into the host cytoplasm, accumulates around the haustorial complex. To investigate RTP1p structure and function, we used immuno cytological, biochemical and computational approaches. We revealed that RTP1p accumulates in protuberances of the extrahaustorial matrix, a compartment that is surrounding the haustorium and separated from the plant cytoplasm by a modified host plasma membrane. Our analyses reveal RTP1p being capable of forming filamentous structures in vitro and in vivo. We present evidence that filament formation is due to ß-aggregation similar to what is known from amyloid like proteins. Our findings reveal RTP1p being a member of a new class of structural effectors. We hypothesize that RTP1p is transferred into the host to stabilise the host cell and protect the haustorium from degradation in later stages of the interaction. We report first evidence for an amyloid like protein being transferred into the host cell giving high potential for new resistance mechanisms against rust fungi.

Plant pathogens secrete effector proteins to promote host colonization. During infection of tomato xylem vessels, Fusarium oxysporum f. sp.lycopersici (Fol) secretes the Avr2 effector protein. Besides being a virulence factor, Avr2 is recognized intracellularly by the tomato I-2 resistance protein, resulting in the induction of host defenses. Here, we show that AVR2 is highly expressed in root- and xylem-colonizing hyphae three days post inoculation of roots. Co-expression of I-2 with AVR2deletion constructs using agroinfiltration in Nicotiana benthamianaleaves revealed that, except for the N-terminal 17 amino acids, the entireAVR2 protein is required to trigger I-2-mediated cell death. The truncated Avr2 variants are still able to form homo-dimers, showing that the central region of Avr2 is required for dimerization. Simultaneous production of I-2 and Avr2 chimeras carrying various subcellular localization signals in N. benthamiana leaves revealed that a nuclear localization of Avr2 is required to trigger I-2-dependent cell death. Nuclear exclusion of Avr2 prevented its activation of I-2, suggesting that Avr2 is recognized by I-2 in the nucleus.

Population genetic and phylogenetic studies have shown that Phaeosphaeria nodorum is a member of a species complex that probably shares its center of origin with wheat (Triticum aestivum and Triticum durum). We examined the evolutionary histories of three known necrotrophic effectors (NEs) produced by P. nodorum and compared them with neutral loci.

We screened over 1000 individuals for the presence/absence of each effector and assigned each individual to a multi-effector genotype. Diversity at each NE locus was assessed by sequencing c. 200 individuals for each locus.

We found significant differences in effector frequency among populations. We propose that these differences reflect the presence/absence of the corresponding susceptibility gene in wheat cultivars. The population harboring the highest sequence diversity was different for each effector locus and never coincided with populations harboring the highest diversity at neutral loci. Coalescent and phylogenetic analyses showed a discontinuous presence of all three NEs among nine closely related Phaeosphaeria species. Only two of the nine species were found to harbor NEs.

We present evidence that the three described NEs of P. nodorum were transmitted to its sister species, Phaeosphaeria avenaria tritici 1, via interspecific hybridization.

Parasitic organisms account for a large portion of living species. They have arisen on multiple independent occasions in many phyla, and thus encompass a huge biological diversity. This review uses several lines of evidence to argue that this vast diversity can be reduced to a few evolutionary end points that transcend phylogenetic boundaries. These represent peaks in the adaptive landscape reached independently by different lineages undergoing convergent evolution. Among eukaryotic parasites living in or on animals, six basic parasitic strategies are identified based on the number of hosts used per parasite generation, the fitness loss incurred by the host, and the transmission routes used by the parasites. They are parasitoids, parasitic castrators, directly transmitted parasites, trophically transmitted parasites, vector-transmitted parasites and micropredators. These show evidence of convergence in morphology, physiology, reproduction, life cycles and transmission patterns. Parasite–host body size ratios, and the relationship between virulence and intensity of infection, are also associated with the different parasitic strategies, but not consistently so. At the population level, patterns of parasite distribution among hosts are not uniform across all parasitic strategies, but are distinctly different for parasitoids and castrators than for other parasites. To demonstrate that the above six strategies defined for animal parasites are universal, comparisons are made with parasites of plants, in particular, plant–parasitic nematodes and parasitic angiosperms; these are shown to follow the same evolutionary trajectories seen among animal parasites, despite huge physiological and ecological differences between animals and plants. Beyond demonstrating the inevitable convergence of disparate lineages across biological hyperspace towards a limited set of adaptive strategies, this synthesis also provides a unifying framework for the study of parasitism.

Welcome to the website of the Trujillo laboratory at the Leibniz Institute of Plant Biochemistry. We are a plant research group interested in ubiquitination and its roles in plant immunity. The molecular machinery that mediates ubiquitination offers great possibilities for the improvement of crop plants. It is of particular importance to widen our understanding of the ubiquitination process and to identify the proteins targetted by this machinery. We combine several approaches including reverse genetics, cell-biology and biochemical methods to analyze the components of the ubiquitination process and to identify and characterize target proteins. Our work is mainly performed using the model plant Arabidopsis thaliana and to study the immune response in plants we employ several plant pathogens, e.g. the bacterial pathogen Pseudomonas syringe or the oomycete Hyaloperonospora arabidopsidis.

NAIROBI (Thomson Reuters Foundation) – The future of cassava, one of the most climate-resilient crops in Africa, may be under threat because rising temperatures have led to a dramatic increase in the number of whiteflies, tiny insects that spread the deadly cassava brown steak virus.

Previously seen as a major problem, but one confined to eastern and central Africa, the virus is spreading, alarming scientists who say new outbreaks suggest the disease is heading west towards the world’s largest cassava producer – Nigeria.

So far, according to James Legg, a plant virologist at the International Institute for Tropical Agriculture (IITA), new countries such as Angola, Gabon and Central African Republic have been hit by the virus. Legg has done extensive research on the disease and its causes in East Africa.

Scientists have already successfully tackled an equally lethal virus – cassava mosaic disease - transmitted by the same whitefly,Bemisia tabaci. This was done by developing a variety that is resistant to the virus.

But by a cruel twist of nature, both the improved and the unaltered varieties have succumbed to a ‘new’ pandemic of cassava brown streak virus, and scientists have yet to develop a resistant variety.

The biggest worry now is that as the whitefly population hugely increases, the insects could spread across the entire African continent.

FLAGELLIN-SENSING 2 (FLS2) is a leucine-rich repeat/transmembrane domain/protein kinase (LRR-RLK) that is the plant receptor for bacterial flagellin or the flagellin-derived flg22 peptide. Previous work has shown that after flg22 binding, FLS2 releases BIK1 kinase and homologs and associates with BAK1 kinase, and that FLS2 kinase activity is critical for FLS2 function. However, the detailed mechanisms for activation of FLS2 signaling remain unclear. The present study initially identified multiple FLS2 in vitro phosphorylation sites and found that Serine-938 is important for FLS2 function in vivo. FLS2-mediated immune responses are abolished in transgenic plants expressing FLS2S938A, while the acidic phosphomimic mutants FLS2S938D and FLS2S938E conferred responses similar to wild-type FLS2. FLS2-BAK1 association and FLS2-BIK1 disassociation after flg22 exposure still occur with FLS2S938A, demonstrating that flg22-induced BIK1 release and BAK1 binding are not sufficient for FLS2 activity, and that Ser-938 controls other aspects of FLS2 activity. Purified BIK1 still phosphorylated purified FLS2S938A and FLS2S938D mutant kinase domains in vitro. Phosphorylation of BIK1 and homologs after flg22 exposure was disrupted in transgenicArabidopsis thaliana plants expressing FLS2S938A or FLS2D997A (a kinase catalytic site mutant), but was normally induced in FLS2S938D plants. BIK1 association with FLS2 required a kinase-active FLS2, but FLS2-BAK1 association did not. Hence FLS2-BIK1 dissociation and FLS2-BAK1 association are not sufficient for FLS2-mediated defense activation, but the proposed FLS2 phosphorylation site Ser-938 and FLS2 kinase activity are needed both for overall defense activation and for appropriate flg22-stimulated phosphorylation of BIK1 and homologs.

To accomplish successful infection, pathogens deploy complex strategies to interfere with host defense systems and subterfuge host physiology to favor pathogen survival and multiplication. Modulation of plant auxin physiology and signaling is emerging as a common virulence strategy for phytobacteria to cause diseases. However, the underlying mechanisms remain largely elusive. We have previously shown that the Pseudomonas syringae type III effector AvrRpt2 alters Arabidopsis auxin physiology. Here we report that AvrRpt2 promotes auxin response by stimulating the turnover of Aux/IAA proteins, the key negative regulators in auxin signaling. AvrRpt2 acts additively with auxin to stimulate Aux/IAA turnover, suggesting distinct, yet proteasome-dependent mechanisms operated by AvrRpt2 and auxin to control Aux/IAA stability. The cysteine protease activity is required for AvrRpt2-stimulated auxin signaling and Aux/IAA degradation. Importantly, the transgenic plants expressing the dominant axr2-1 mutation recalcitrant to AvrRpt2-mediated degradation ameliorated virulence functions of AvrRpt2, but did not alter the avirulent function mediated by the corresponding RPS2 resistance protein. Thus, promoting auxin response via modulating the stability of key transcription repressors Aux/IAA is a mechanism used by bacterial type III effector AvrRpt2 to promote pathogenicity.

which are responsible for a wide range of diseases including malaria and toxoplasmosis. The primary barrier to understanding the early stages of evolution of these parasites has been the difficulty in finding parasites with closely related free-living lineages with which to make comparisons. Parasites found throughout the florideophyte red algal lineage, however, provide a unique and powerful model to investigate the genetic origins of a parasitic lifestyle. This is because they share a recent common ancestor with an extant free-living red algal species and parasitism has independently arisen over 100 times within this group. Here, we synthesize the relevant hypotheses with respect to how these parasites have proliferated. We also place red algal research in the context of recent developments in understanding the genome evolution of other eukaryotic photosynthesizers turned parasites.

Microbial plant pathogens have evolved a variety of strategies to enter plant hosts and cause disease. In particular, biotrophic pathogens, which parasitize living plant tissue, establish sophisticated interactions in which they modulate the plant's metabolism to their own good. The prime decision, whether or not a pathogen can accommodate itself in its host tissue, is made during the initial phase of infection. At this stage, the plant immune system recognizes conserved molecular patterns of the invading microbe, which initiate a set of basal immune responses. Induced plant defense proteins, toxic compounds and antimicrobial proteins encounter a broad arsenal of pathogen-derived virulence factors that aim to disarm host immunity. Crucial regulatory processes and protein–protein interactions take place in the apoplast, that is, intercellular spaces, plant cell walls and defined host–pathogen interfaces which are formed between the plant cytoplasm and the specialized infection structures of many biotrophic pathogens. This article aims to provide an insight into the most important principles and components of apoplastic plant immunity and its modulation by filamentous microbial pathogens.

PRG-Wiki is an open and daily update space about plant resistance gene, in which all information about this family is stored, curated and discussed. The purpose of our work is creating a worldwide community working on plant resistance genes with a constant update on all aspects of this research field and to encourage scientists to be actors of the discussion and of the data exchange. PRG-Wiki actually stores more than 112 reference resistance gene and 104335 putative disease resistance gene. Through the wiki pages any contributor can suggest changes to the PRG database and directly update it with new data, new information and with corrections of wrong information.