BackgroundThe white mold fungus Sclerotinia sclerotiorum is a devastating necrotrophic plant pathogen with a remarkably broad host range. The interaction of necrotrophs with their hosts is more complex than initially thought, and still poorly understood.ResultsWe combined bioinformatics approaches to determine the repertoire of S. sclerotiorum effector candidates and conducted detailed sequence and expression analyses on selected candidates. We identified 486 S. sclerotiorum secreted protein genes expressed in planta, many of which have no predicted enzymatic activity and may be involved in the interaction between the fungus and its hosts. We focused on those showing (i) protein domains and motifs found in known fungal effectors, (ii) signatures of positive selection, (iii) recent gene duplication, or (iv) being S. sclerotiorum-specific. We identified 78 effector candidates based on these properties. We analyzed the expression pattern of 16 representative effector candidate genes on four host plants and revealed diverse expression patterns.ConclusionsThese results reveal diverse predicted functions and expression patterns in the repertoire of S. sclerotiorum effector candidates. They will facilitate the functional analysis of fungal pathogenicity determinants and should prove useful in the search for plant quantitative disease resistance components active against the white mold.
Only few fungal effectors have been described to be delivered into the host cell during obligate biotrophic interactions. RTP1p, from the rust fungi Uromyces fabae and U. striatus, was the first fungal protein for which localization within the host cytoplasm could be demonstrated directly. We investigated the occurrence of RTP1 homologues in rust fungi and examined the structural and biochemical characteristics of the corresponding gene products. The analysis of 28 homologues showed that members of the RTP family are most likely to occur ubiquitously in rust fungi and to be specific to the order Pucciniales. Sequence analyses indicated that the structure of the RTPp effectors is bipartite, consisting of a variable N-terminus and a conserved and structured C-terminus. The characterization of Uf-RTP1p mutants showed that four conserved cysteine residues sustain structural stability. Furthermore, the C-terminal domain exhibits similarities to that of cysteine protease inhibitors, and it was shown that Uf-RTP1p and Us-RTP1p are able to inhibit proteolytic activity in Pichia pastoris culture supernatants. We conclude that the RTP1p homologues constitute a rust fungi-specific family of modular effector proteins comprising an unstructured N-terminal domain and a structured C-terminal domain, which exhibit protease inhibitory activity possibly associated with effector function during biotrophic interactions.
Fungi occupy a plethora of niches and play essential roles in diverse environments through decomposition of organic material as saprophytes or through establishment of symbiotic relationships with plants and animals that range from mutually beneficial to pathogenic. During colonization of their niches, fungi secrete proteins that include carbohydrate-degrading enzymes to feed on complex molecules and effectors that mediate the establishment of interactions with host organisms. Although effectors are typically thought to be species- or even lineage-specific, some effectors are widespread among pathogens, such as the necrosis- and ethylene-inducing-like proteins (NLPs) that are widely spread in bacteria, fungi, and oomycetes. Several studies have shown that NLPs contribute to pathogen virulence through phytotoxic activity, but more recent work has revealed that some NLPs act in processes other than pathogenicity, such as fungal growth and sporulation]. A more recently identified class of conserved effectors are LysM effectors: fungal effectors that carry no recognizable protein domains other than lysin motifs (LysMs). Intriguingly, like NLPs, LysM effectors occur in both pathogenic and in nonpathogenic fungi.
PubMed comprises more than 23 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Breeding agricultural crops for resistance against pathogens is essential to secure global food production. Despite efforts to control crop diseases, pathogens are estimated to account for losses of 15% of global food production. It is suggested that losses would be almost twice as much without disease control measures, such as crop resistance breeding . There are now opportunities to improve the effectiveness of breeding crops for resistance against damaging pathogens by exploiting new molecular and genetic insights to improve understanding of the defence system of crop plants against pathogens. In this opinion, we focus on the resistance of crops against foliar fungal pathogens that exploit the host apoplast for retrieval of nutrients. Some of these pathogens are globally widespread and of considerable economic importance. They include pathogens that penetrate the host leaf cuticle and then exploit a niche underneath it (e.g., Pyrenopeziza brassicae, oilseed rape light leaf spot; Venturia inaequalis, apple scab; and Rhynchosporium commune, barley leaf blotch, global losses of approximately US$3.5 billion per year). Others enter leaves through stomata, then grow between host mesophyll cells (e.g., Cladosporium fulvum, tomato leaf mould; Leptosphaeria maculans, oilseed rape phoma stem canker, global losses of approximately US$1 billion per year; and Zymoseptoria tritici, wheat septoria leaf blotch, with a global loss of approximately US$5 billion per year) (Table 1, Figure 1). These apoplastic pathogens are all ascomycetes and many of them are dothideomycetes .
$2.5 million research grant to help plants fight fungal pathogens agprofessional.com Much of the research centers on effectors, or proteins secreted by the powdery mildew fungus that sabotage or weaken plant defense.
Hemibiotrophic plant pathogens first establish a biotrophic interaction with the host plant and later switch to a destructive necrotrophic lifestyle. Studies of biotrophic pathogens have shown that they actively suppress plant defenses after an initial microbe-associated molecular pattern-triggered activation. In contrast, studies of the hemibiotrophs suggest that they do not suppress plant defenses during the biotrophic phase, indicating that while there are similarities between the biotrophic phase of hemibiotrophs and biotrophic pathogens, the two lifestyles are not analogous. We performed transcriptomic, histological, and biochemical studies of the early events during the infection of maize (Zea mays) with Colletotrichum graminicola, a model pathosystem for the study of hemibiotrophy. Time-course experiments revealed that mRNAs of several defense-related genes, reactive oxygen species, and antimicrobial compounds all begin to accumulate early in the infection process and continue to accumulate during the biotrophic stage. We also discovered the production of maize-derived vesicular bodies containing hydrogen peroxide targeting the fungal hyphae. We describe the fungal respiratory burst during host infection, paralleled by superoxide ion production in specific fungal cells during the transition from biotrophy to a necrotrophic lifestyle. We also identified several novel putative fungal effectors and studied their expression during anthracnose development in maize. Our results demonstrate a strong induction of defense mechanisms occurring in maize cells during C. graminicola infection, even during the biotrophic development of the pathogen. We hypothesize that the switch to necrotrophic growth enables the fungus to evade the effects of the plant immune system and allows for full fungal pathogenicity.
Fungal effectors have often been referred as a ‘sea of diversity’, but recently, experiments have shed some light onto effector biology, including discovery that unrelated fungi utilize some common methods for creating a more compatible host environment. A wheat pathogen and a rice pathogen, for example, have evolved mechanisms to suppress chitin-mediated basal defenses in their respective plant hosts. Smut fungi, on the other hand, might have evolved a unique mechanism to manipulate their host environment by altering cell metabolism. Genome mining and bioinformatics pipelines have streamlined the suite of effectors in important pathogen genomes, so researchers can make more targeted strikes on potentially important effectors. This combination of informatics and empirical studies will allow greater insight into effector function.
Sharing your scoops to your social media accounts is a must to distribute your curated content. Not only will it drive traffic and leads through your content, but it will help show your expertise with your followers.
How to integrate my topics' content to my website?
Integrating your curated content to your website or blog will allow you to increase your website visitors’ engagement, boost SEO and acquire new visitors. By redirecting your social media traffic to your website, Scoop.it will also help you generate more qualified traffic and leads from your curation work.
Distributing your curated content through a newsletter is a great way to nurture and engage your email subscribers will developing your traffic and visibility.
Creating engaging newsletters with your curated content is really easy.