Rhizosphere filamentous fungi of the genus
, a dominant component of various soil ecosystem mycobiomes, are characterized by the ability to colonize plant roots. Detailed knowledge of the properties ...of
, including metabolic activity and the type of interaction with plants and other microorganisms, can ensure its effective use in agriculture. The growing interest in the application of
results from their direct and indirect biocontrol potential against a wide range of soil phytopathogens. They act through various complex mechanisms, such as mycoparasitism, the degradation of pathogen cell walls, competition for nutrients and space, and induction of plant resistance. With the constant exposure of plants to a variety of pathogens, especially filamentous fungi, and the increased resistance of pathogens to chemical pesticides, the main challenge is to develop biological protection alternatives. Among non-pathogenic microorganisms,
seems to be the best candidate for use in green technologies due to its wide biofertilization and biostimulatory potential. Most of the species from the genus
belong to the plant growth-promoting fungi that produce phytohormones and the 1-aminocyclopropane-1-carboxylate (ACC) deaminase enzyme. In the present review, the current status of
is gathered, which is especially relevant in plant growth stimulation and the biocontrol of fungal phytopathogens.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Two classes of genes are used for breeding rust resistant wheat. The first class, called R (for resistance) genes, are pathogen race specific in their action, effective at all plant growth stages and ...probably mostly encode immune receptors of the nucleotide binding leucine rich repeat (NB-LRR) class. The second class is called adult plant resistance genes (APR) because resistance is usually functional only in adult plants, and, in contrast to most R genes, the levels of resistance conferred by single APR genes are only partial and allow considerable disease development. Some but not all APR genes provide resistance to all isolates of a rust pathogen species and a subclass of these provides resistance to several fungal pathogen species. Initial indications are that APR genes encode a more heterogeneous range of proteins than R proteins. Two APR genes, Lr34 and Yr36, have been cloned from wheat and their products are an ABC transporter and a protein kinase, respectively. Lr34 and Sr2 have provided long lasting and widely used (durable) partial resistance and are mainly used in conjunction with other R and APR genes to obtain adequate rust resistance. We caution that some APR genes indeed include race specific, weak R genes which may be of the NB-LRR class. A research priority to better inform rust resistance breeding is to characterize further APR genes in wheat and to understand how they function and how they interact when multiple APR and R genes are stacked in a single genotype by conventional and GM breeding. An important message is do not be complacent about the general durability of all APR genes.
The efficacy of disease resistance genes in plants decreases over time because of the selection of virulent pathogen genotypes. A key goal of crop protection programs is to increase the durability of ...the resistance conferred by these genes. The spatial and temporal deployment of plant disease resistance genes is considered to be a major factor determining their durability. In the literature, four principal strategies combining resistance genes over time and space have been considered to delay the evolution of virulent pathogen genotypes. We reviewed this literature with the aim of determining which deployment strategy results in the greatest durability of resistance genes. Although theoretical and empirical studies comparing deployment strategies of more than one resistance gene are very scarce, they suggest that the overall durability of disease resistance genes can be increased by combining their presence in the same plant (pyramiding). Retrospective analyses of field monitoring data also suggest that the pyramiding of disease resistance genes within a plant is the most durable strategy. By extension, we suggest that the combination of disease resistance genes with other practices for pathogen control (pesticides, farming practices) may be a relevant management strategy to slow down the evolution of virulent pathogen genotypes.
SUMMARY
Plants sense various pathogens and activate immunity responses through receptor‐like kinases (RLKs). Cysteine‐rich receptor‐like kinases (CRKs) are involved in massive transduction pathways ...upon perception of a pathogen. However, the roles of CRKs in response to stripe rust are unclear. In the present study, we identified a CRK gene (designated TaCRK10) from wheat variety Xiaoyan 6 (XY6) that harbors high‐temperature seedling‐plant (HTSP) resistance to stripe rust caused by fungal pathogen Puccinia striiformis f. sp. tritici (Pst). The expression level of TaCRK10 was induced by Pst inoculation and high temperature treatment. Knockdown of TaCRK10 by virus‐induced gene silencing resulted in attenuated wheat HTSP resistance to Pst, whereas there is no effect on Pst development and host responses under normal temperatures. Notably, overexpression of TaCRK10 in susceptible variety Fielder provided resistance only under normal temperatures at 14 days with reactive oxygen species accumulation and defense‐related gene expression of the salicylic acid pathway. Moreover, TaCRK10 physically interacted with and phosphorylated a histone variant TaH2A.1, which belongs to the H2A.W group. Silencing of TaH2A.1 suppressed wheat resistance to Pst, indicating that TaH2A.1 plays a positive role in wheat resistance to Pst. Thus, TaCRK10 serves as an important sensor of Pst infection and high temperatures, and it activates wheat resistance to Pst through regulating nuclear processes. This knowledge helps elucidate the molecular mechanism of wheat HTSP resistance to Pst and promotes efforts in developing wheat varieties with resistance to stripe rust.
Significance Statement
Wheat high‐temperature seedling‐plant (HTSP) resistance to Puccinia striiformis f. sp. tritici (Pst) is non‐race specific and is induced by exposure of wheat plants to high temperatures. Here, high temperature treatment and Pst inoculation induced the high expression of TaCRK10, which activates wheat resistance to Pst through interacting with and phosphorylating a histone variant TaH2A.1 that belongs to the H2A.W group. Overexpression of TaCRK10 in susceptible variety Fielder provided resistance only under normal temperatures. These findings can elucidate the molecular mechanism of wheat HTSP resistance to Pst, and will make contributions to improving and utilizing this kind of resistance.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
SUMMARY
Resistance to Pseudomonas syringae pv. maculicola 1 (RPM1)‐induced protein kinase (RIPK) in Arabidopsis belongs to the receptor‐like cytoplasmic kinase (RLCK) family and plays a vital role in ...immunity. However, the role of RLCKs in the high‐temperature seedling‐plant (HTSP) resistance of wheat (Triticum aestivum) to Puccinia striiformis f. sp. tritici (Pst), the stripe rust pathogen, remains unclear. Here, we identified a homologous gene of RIPK in wheat, namely TaRIPK. Expression of TaRIPK was induced by Pst inoculation and high temperatures. Silencing of TaRIPK reduced the expression level of TaRPM1, resulting in weaker HTSP resistance. Moreover, TaRIPK interacts with and phosphorylates papain‐like cysteine protease 1 (TaPLCP1). Meanwhile, we found that the Pst‐secreted protein PSTG_01766 targets TaPLCP1. Transient expression of PSTG_01766 inhibited basal immunity in tobacco (Nicotiana benthamiana) and wheat. The role of PSTG_01766 as an effector involved in HTSP resistance was further supported by host‐induced gene silencing and bacterial type three secretion system‐mediated delivery into wheat. PSTG_01766 inhibited the TaRIPK‐induced phosphorylation of TaPLCP1. Furthermore, PSTG_01766 has the potential to influence the subcellular localization of TaPLCP1. Overall, we suggest that the TaRIPK–TaPLCP1–TaRPM1 module fits the guard model for disease resistance, participating in HTSP resistance. PSTG_01766 decreases HTSP resistance via targeting TaPLCP1. Guarded by wheat and attacked by Pst, TaPLCP1 may serve as a central hub of the defense response. Our findings improve the understanding of the molecular mechanism of wheat HTSP resistance, which may be an important strategy for controlling stripe rust in the face of global warming.
Significance Statement
This work focuses on the molecular mechanisms of the high‐temperature seedling‐plant resistance against stripe rust in wheat cultivar Xiaoyan 6, which contains the resistance for over 40 years in the field. With global warming, the importance of breeding wheat cultivars carrying high‐temperature resistance is becoming more obvious.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Summary
Stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is a devastating disease of wheat (Triticum aestivum) worldwide. Wheat high‐temperature seedling plant (HTSP) resistance to ...Pst is non‐race‐specific and durable. WRKY transcription factors have been proven to play important roles in plant defence responses to attacks by several pathogens. However, there is no direct evidence as to whether WRKY transcription factors play a role in HTSP resistance to Pst. We isolated a WRKY gene, named TaWRKY70, from wheat cultivar Xiaoyan 6. The expression level of TaWRKY70 was increased significantly when exposed to high temperatures (HTs) during the initial symptom expression stage of Pst infection. The expression of this gene increased in plants treated with ethylene (ET), salicylic acid (SA) and cold (4°C) stresses, but decreased in plants treated with methyl jasmonate (MeJA) and heat (40°C) stresses. Silencing of TaWRKY70 led to greater susceptibility to Pst (in terms of the increase in length of uredinial pustules and the decrease in the number of necrotic cells) compared with non‐silenced plants when exposed to HT during the initial symptom expression stage of Pst infection, coinciding with expression changes of the ET‐ and SA‐responsive genes TaPIE1 and TaPR1.1. In contrast, the expression level of the jasmonic acid (JA)‐responsive gene TaAOS was not affected by TaWRKY70. These results indicate that TaWRKY70 is positively involved in HTSP resistance, during which SA and ET signalling are probably activated.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UILJ, UKNU, UL, UM, UPUK
Wheat cultivar Xiaoyan 6 (XY6) has high‐temperature seedling‐plant (HTSP) resistance to Puccinia striiformis f. sp. tritici (Pst). However, the molecular mechanism of Pst effectors involved in HTSP ...resistance remains unclear. In this study, we determined the interaction between two Pst effectors, PstCEP1 and PSTG_11208, through yeast two‐hybrid (Y2H), bimolecular fluorescence complementation (BiFC), and pull‐down assays. Transient overexpression of PSTG_11208 enhanced HTSP resistance in different temperature treatments. The interaction between PstCEP1 and PSTG_11208 inhibited the resistance enhancement by PSTG_11208. Furthermore, the wheat apoplastic thaumatin‐like protein 1 (TaTLP1) appeared to recognize Pst invasion by interacting with PSTG_11208 and initiate the downstream defence response by the pathogenesis‐related protein TaPR1. Silencing of TaTLP1 and TaPR1 separately or simultaneously reduced HTSP resistance to Pst in XY6. Moreover, we found that PstCEP1 targeted wheat ferredoxin 1 (TaFd1), a homologous protein of rice OsFd1. Silencing of TaFd1 affected the stability of photosynthesis in wheat plants, resulting in chlorosis on the leaves and reducing HTSP resistance. Our findings revealed the synergistic mechanism of effector proteins in the process of pathogen infection.
The Puccinia striiformis f. sp. tritici effector PstCEP1 interacts with PSTG_11208 to disturb recognition by TaTLP1; PstCEP1 could target TaFd1 to inhibit the high‐temperature seedling‐plant resistance of wheat.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UILJ, UKNU, UL, UM, UPUK
The inheritance of resistance to sunflower downy mildew (SDM) derived from HA-R5 conferring resistance to nine races of the pathogen has been determined and the new source has been designated as Pl ...₁₃ . The F₂ individuals and F₃ families of the cross HA-R5 (resistant) x HA 821 (susceptible) were screened against the four predominant SDM races 300, 700, 730, and 770 in separate tests which indicated dominant control by a single locus or a cluster of tightly linked genes. Bulked segregant analysis (BSA) was carried out on 116 F₂ individuals with 500 SSR primer pairs that resulted in the identification of 10 SSR markers of linkage groups 1 (9 markers) and 10 (1 marker) of the genetic map (Tang et al. in Theor Appl Genet 105:1124-1136, 2002) that distinguished the bulks. Of these, the SSR marker ORS 1008 of linkage group 10 was tightly linked (0.9 cM) to the Pl ₁₃ gene. Genotyping the F₂ population and linkage analysis with 20 polymorphic primer pairs located on linkage group 10 failed to show linkage of the markers with downy mildew resistance and the ORS 1008 marker. Nevertheless, validation of polymorphic SSR markers of linkage group 1 along with six RFLP-based STS markers of linkage group 12 of the RFLP map of Jan et al. (Theor Appl Genet 96:15-22, 1998) corresponding to linkage group 1 of the SSR map, mapped seven SSR markers (ORS 965-1, ORS 965-2, ORS 959, ORS 371, ORS 716, and ORS 605) including ORS 1008 and one STS marker (STS10D6) to linkage group 1 covering a genetic distance of 65.0 cM. The Pl ₁₃ gene, as a different source with its location on linkage group 1, was flanked by ORS 1008 on one side at a distance of 0.9 cM and ORS 965-1 on another side at a distance of 5.8 cM. These closely linked markers to the Pl ₁₃ gene provide a valuable basis for marker-assisted selection in sunflower breeding programs.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Schematic representation of an integrated approach for pre-harvest aflatoxin management.
•Novel biotechnologies needed for pre-harvest host–plant resistance to aflatoxin.•New strategies for ...resistance to aflatoxin open up horizons for practical solutions.•Reduced aflatoxin can have a significant positive impact on health and economics.
Aflatoxins are toxic, carcinogenic, mutagenic, teratogenic and immunosuppressive byproducts of Aspergillus spp. that contaminate a wide range of crops such as maize, peanut, and cotton. Aflatoxin not only affects crop production but renders the produce unfit for consumption and harmful to human and livestock health, with stringent threshold limits of acceptability. In many crops, breeding for resistance is not a reliable option because of the limited availability of genotypes with durable resistance to Aspergillus. Understanding the fungal/crop/environment interactions involved in aflatoxin contamination is therefore essential in designing measures for its prevention and control. For a sustainable solution to aflatoxin contamination, research must be focused on identifying and improving knowledge of host–plant resistance factors to aflatoxin accumulation. Current advances in genetic transformation, proteomics, RNAi technology, and marker-assisted selection offer great potential in minimizing pre-harvest aflatoxin contamination in cultivated crop species. Moreover, developing effective phenotyping strategies for transgenic as well as precision breeding of resistance genes into commercial varieties is critical. While appropriate storage practices can generally minimize post-harvest aflatoxin contamination in crops, the use of biotechnology to interrupt the probability of pre-harvest infection and contamination has the potential to provide sustainable solution.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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