Herbivore Oral Secreted Bacteria Trigger Distinct Defense Responses in Preferred and Non-Preferred Host Plants

2016 ◽  
Vol 42 (6) ◽  
pp. 463-474 ◽  
Author(s):  
Jie Wang ◽  
Seung Ho Chung ◽  
Michelle Peiffer ◽  
Cristina Rosa ◽  
Kelli Hoover ◽  
...  
2018 ◽  
Vol 116 (2) ◽  
pp. 496-505 ◽  
Author(s):  
Hiroki Irieda ◽  
Yoshihiro Inoue ◽  
Masashi Mori ◽  
Kohji Yamada ◽  
Yuu Oshikawa ◽  
...  

Plant pathogens have optimized their own effector sets to adapt to their hosts. However, certain effectors, regarded as core effectors, are conserved among various pathogens, and may therefore play an important and common role in pathogen virulence. We report here that the widely distributed fungal effector NIS1 targets host immune components that transmit signaling from pattern recognition receptors (PRRs) in plants. NIS1 from two Colletotrichum spp. suppressed the hypersensitive response and oxidative burst, both of which are induced by pathogen-derived molecules, in Nicotiana benthamiana. Magnaporthe oryzae NIS1 also suppressed the two defense responses, although this pathogen likely acquired the NIS1 gene via horizontal transfer from Basidiomycota. Interestingly, the root endophyte Colletotrichum tofieldiae also possesses a NIS1 homolog that can suppress the oxidative burst in N. benthamiana. We show that NIS1 of multiple pathogens commonly interacts with the PRR-associated kinases BAK1 and BIK1, thereby inhibiting their kinase activities and the BIK1-NADPH oxidase interaction. Furthermore, mutations in the NIS1-targeting proteins, i.e., BAK1 and BIK1, in Arabidopsis thaliana also resulted in reduced immunity to Colletotrichum fungi. Finally, M. oryzae lacking NIS1 displayed significantly reduced virulence on rice and barley, its hosts. Our study therefore reveals that a broad range of filamentous fungi maintain and utilize the core effector NIS1 to establish infection in their host plants and perhaps also beneficial interactions, by targeting conserved and central PRR-associated kinases that are also known to be targeted by bacterial effectors.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Volker Hegenauer ◽  
Peter Slaby ◽  
Max Körner ◽  
Julien-Alexander Bruckmüller ◽  
Ronja Burggraf ◽  
...  

Abstract Parasitic plants of the genus Cuscuta penetrate shoots of host plants with haustoria and build a connection to the host vasculature to exhaust water, solutes and carbohydrates. Such infections usually stay unrecognized by the host and lead to harmful host plant damage. Here, we show a molecular mechanism of how plants can sense parasitic Cuscuta. We isolated an 11 kDa protein of the parasite cell wall and identified it as a glycine-rich protein (GRP). This GRP, as well as its minimal peptide epitope Crip21, serve as a pathogen-associated molecular pattern and specifically bind and activate a membrane-bound immune receptor of tomato, the Cuscuta Receptor 1 (CuRe1), leading to defense responses in resistant hosts. These findings provide the initial steps to understand the resistance mechanisms against parasitic plants and further offer great potential for protecting crops by engineering resistance against parasitic plants.


2021 ◽  
Vol 22 (16) ◽  
pp. 9022
Author(s):  
Jitendra Kumar ◽  
Ayyagari Ramlal ◽  
Kamal Kumar ◽  
Anita Rani ◽  
Vachaspati Mishra

Phytopathogens, such as biotrophs, hemibiotrophs and necrotrophs, pose serious stress on the development of their host plants, compromising their yields. Plants are in constant interaction with such phytopathogens and hence are vulnerable to their attack. In order to counter these attacks, plants need to develop immunity against them. Consequently, plants have developed strategies of recognizing and countering pathogenesis through pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Pathogen perception and surveillance is mediated through receptor proteins that trigger signal transduction, initiated in the cytoplasm or at the plasma membrane (PM) surfaces. Plant hosts possess microbe-associated molecular patterns (P/MAMPs), which trigger a complex set of mechanisms through the pattern recognition receptors (PRRs) and resistance (R) genes. These interactions lead to the stimulation of cytoplasmic kinases by many phosphorylating proteins that may also be transcription factors. Furthermore, phytohormones, such as salicylic acid, jasmonic acid and ethylene, are also effective in triggering defense responses. Closure of stomata, limiting the transfer of nutrients through apoplast and symplastic movements, production of antimicrobial compounds, programmed cell death (PCD) are some of the primary defense-related mechanisms. The current article highlights the molecular processes involved in plant innate immunity (PII) and discusses the most recent and plausible scientific interventions that could be useful in augmenting PII.


2008 ◽  
Vol 21 (8) ◽  
pp. 1076-1086 ◽  
Author(s):  
A. Degrave ◽  
M. Fagard ◽  
C. Perino ◽  
M. N. Brisset ◽  
S. Gaubert ◽  
...  

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.


2020 ◽  
Author(s):  
Kevin R. Cope ◽  
Arjun Kafle ◽  
Jaya Krishna Yakha ◽  
Philip E. Pfeffer ◽  
Gary D. Strahan ◽  
...  

Arbuscular mycorrhizal (AM) fungi provide their host plants with greater access to limited mineral nutrients, but the amount they provide can be variable. Here, we evaluated the capacity of the high-benefit fungus Rhizophagus irregularis 09 and the low-benefit fungus Glomus aggregatum 165 to transfer nitrogen and phosphorus to the host plant Medicago truncatula, and identified putative molecular mechanisms regulating the physiological response of the host to these fungi. R. irregularis led to an increase in plant biomass and transferred more nitrogen and phosphate to the host than G. aggregatum. This increase was linked to elevated expression of known mycorrhiza-induced phosphate (PT8), ammonium (AMT2;3), and nitrate (NPF4.12) transporters in the roots, as well as the putative ammonium transporter NIP1;5. R. irregularis also stimulated the expression of photosynthesis related genes in the shoot and the upregulation of the mycorrhiza-induced sugar transporter SWEET1.2 and the lipid biosynthesis gene RAM2 in the roots, which is indicative of increased carbon flux to this fungus. In contrast, G. aggregatum induced biotic stress defense response genes (e.g., Medtr4g120760 and Medtr8g096900) in the shoots, and several genes associated with the GO term "response to water deprivation" in the roots of M. truncatula. This could indicate that the host perceives colonization by the low-benefit fungus as pathogen attack, or that G. aggregatum is more effective than R. irregularis at priming host defense responses. Our findings reveal novel insights into the molecular mechanisms by which host plants reward high- but sanction low-benefit arbuscular mycorrhizal symbionts.


1995 ◽  
Vol 73 (S1) ◽  
pp. 616-623 ◽  
Author(s):  
Michèle C. Heath

The rust fungi appear to have evolved a sophisticated complex of molecular interactions with their host plants that govern both plant resistance and susceptibility. It is suggested that many of these interactions relate to the maintenance and effective exploitation of biotrophy, and that host specificity and the obligacy of parasitism are a consequence of the resulting interactive molecular control of plant and fungal activities. For the dikaryon, plant signals are required for locating stomata and the formation of infection structures, haustorial mother cells, and haustoria. Host susceptibility to both the monokaryon and the dikaryon appears to involve the suppression of defensive secretory processes, the induction of cellular alterations in invaded cells, and, for the dikaryon at least, changes in nutrient translocation. Parasite-specific resistance involves cultivar-specific fungal signals (elicitors) of defense responses such as cell death and callose deposition. The nature of, and evidence for, the signals involved in these interactions are reviewed. Key words: biotrophy, elicitors, rust fungi, signal exchange.


Sign in / Sign up

Export Citation Format

Share Document