Molecular Plant Pathology (Mol Plant Pathol)
Description
Published for the British Society for Plant Pathology.Molecular Plant Pathology is published bi-monthly and welcomes submissions from all areas of molecular plant pathology including research on diseases caused by fungi, oomycetes, viruses, nematodes, bacteria, insects, parasitic plants and other organisms.Molecular Plant Pathology is especially interested in manuscripts emphasizing molecular analyses of pathogens, determinants affecting host response to plant pathogens or the interaction of both. In addition to the principal content of full length and short research papers, Molecular Plant Pathology will also include technical advances, along with major and micro reviews on areas of particular interest and importance. The journal is dedicated to minimising the time between submission, review and publication and to providing a high quality forum for original research in molecular plant pathology.
- Impact factor3.9
- WebsiteMolecular Plant Pathology website
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Other titlesMolecular plant pathology online, MPPOL
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ISSN1364-3703
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OCLC37263706
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Material typeDocument, Periodical, Internet resource
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Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
Publisher details
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Pre-print
- Author can archive a pre-print version
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Restrictions
- Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
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Conditions
- See Wiley-Blackwell entry for articles after February 2007
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- 'Blackwell Publishing' is an imprint of 'Wiley-Blackwell'
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Classification yellow
Publications in this journal
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Article: The bacterial effector DspA/E is toxic in Arabidopsis thaliana and is required for multiplication and survival of fire blight pathogen.
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ABSTRACT: The type III effector DspA/E is an essential pathogenicity factor of the phytopathogenic bacterium Erwinia amylovora. We showed that DspA/E was required for transient bacterial growth in nonhost Arabidopsis thaliana leaves, as an E. amylovora dspA/E mutant was unable to grow. We expressed DspA/E in A. thaliana transgenic plants under the control of an oestradiol-inducible promoter, and found that DspA/E expressed in planta restored the growth of a dspA/E mutant. DspA/E expression in these transgenic plants led to the modulation by at least two-fold of the expression of 384 genes, mostly induced (324 genes). Both induced and repressed genes contained high proportions of defence genes. DspA/E expression ultimately resulted in plant cell death without requiring a functional salicylic acid signalling pathway. Analysis of A. thaliana transgenic seedlings expressing a green fluorescent protein (GFP):DspA/E fusion indicated that the fusion protein could only be detected in a few cells per seedling, suggesting the degradation or absence of accumulation of DspA/E in plant cells. Consistently, we found that DspA/E repressed plant protein synthesis when injected by E. amylovora or when expressed in transgenic plants. Thus, we conclude that DspA/E is toxic to A. thaliana: it promotes modifications, among which the repression of protein synthesis could be determinant in the facilitation of necrosis and bacterial growth.Molecular Plant Pathology 06/2013; 14(5):506-17. -
Article: HrpE3 is a type III effector protein required for full virulence of Xanthomonas oryzae pv. oryzicola in rice.
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ABSTRACT: Xanthomonas oryzae pv. oryzicola (Xoc) is the causal agent of bacterial leaf streak, a devastating disease in rice. Xoc uses a type III secretion (T3S) system, which is encoded by the hrp-hrc-hpa (hypersensitive response and pathogenicity, hrp-conserved and hrp-associated) genes, to inject repertoires of T3S effectors (T3Es) into plant cells. Many of the hrp-hrc-hpa genes have roles in pathogenesis, but the role of hrpE3, which shows homology to hpaE in X. campestris pv. vesicatoria (Xcv), is poorly understood. In this study, hrpE3 was shown to be transcribed independent of the hrpD operon, and its expression was dependent on a promoter within hpaB. The expression of hrpE3 was positively regulated by HrpG and HrpX, a finding probably caused by an imperfect plant-inducible promoter (PIP) box (TTCGT-N16 -TTCGA) in the hrpE3 promoter. The secretion of HrpE3 was dependent on T3S, and subcellular localization of HrpE3 was cytoplasmic and nuclear in plant cells. A mutation in hrpE3 reduced the virulence of Xoc by decreasing disease lesion length and bacterial growth in planta. Full virulence was restored to the mutant when Xoc hrpE3, but not Xcv hpaE, was expressed in trans. The differences in transcription, secretion via the T3S system and bacterial virulence in plants were attributed to N-terminal amino acid differences between Xoc HrpE3 and Xcv HpaE. Collectively, the results demonstrate that hrpE3 encodes a T3E protein which is delivered into the plant cell through the T3S system, localizes to the cytoplasm and nucleus, and is required for full virulence in rice.Molecular Plant Pathology 05/2013; -
Article: Pepino mosaic virus triple gene block protein 1 (TGBp1) interacts with and increases tomato catalase 1 activity to enhance virus accumulation.
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ABSTRACT: Various plant factors are co-opted by virus elements (RNA, proteins) and have been shown to act in pathways affecting virus accumulation and plant defence. Here, an interaction between Pepino mosaic virus (PepMV) triple gene block protein 1 (TGBp1; p26) and tomato catalase 1 (CAT1), a crucial enzyme in the decomposition of toxic hydrogen peroxide (H2 O2 ), was identified using the yeast two-hybrid assay, and confirmed via an in vitro pull-down assay and bimolecular fluorescent complementation (BiFC) in planta. Each protein was independently localized within loci in the cytoplasm and nuclei, sites at which their interaction had been visualized by BiFC. Following PepMV inoculation, CAT mRNA and protein levels in leaves were unaltered at 0, 3 and 6 days (locally) and 8 days (systemically) post-inoculation; however, leaf extracts from the last two time points contained increased CAT activity and lower H2 O2 levels. Overexpression of PepMV p26 in vitro and in planta conferred the same effect, suggesting an additional involvement of TGBp1 in potexvirus pathogenesis. The accumulation of PepMV genomic and subgenomic RNAs and the expression of viral coat protein in noninoculated (systemic) leaves were reduced significantly in CAT-silenced plants. It is postulated that, during PepMV infection, a p26-CAT1 interaction increases H2 O2 scavenging, thus acting as a negative regulator of plant defence mechanisms to promote PepMV infections.Molecular Plant Pathology 05/2013; -
Article: Salicylic acid: an old hormone up to new tricks.
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ABSTRACT: Salicylic acid (SA) acts as a signalling molecule in plant defence against biotrophic and hemibiotrophic phytopathogens. The biosynthesis of SA on pathogen detection is essential for local and systemic acquired resistance, as well as the accumulation of pathogenesis-related (PR) proteins. SA biosynthesis can occur via several different substrates, but is predominantly accomplished by isochorismate synthase (ICS1) following pathogen recognition. The roles of BTB domain-containing proteins, NPR1, NPR3 and NPR4, in SA binding and signal transduction have been re-examined recently and are elaborated upon in this review. The pathogen-mediated manipulation of SA-dependent defences, as well as the crosstalk between the SA signalling pathway, other plant hormones and defence signals, is also discussed in consideration of recent research. Furthermore, the recent links established between SA, pathogen-triggered endoplasmic reticulum stress and the unfolded protein response are highlighted.Molecular Plant Pathology 04/2013; -
Article: Inhibition of in vivo Slicer activity of Argonaute protein 1 by the viral 2b protein independent of its dsRNA-binding function.
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ABSTRACT: The 2b protein of Cucumber mosaic virus (CMV) has several unique properties, such as targeting to the nucleolus and interaction with both Argonautes (AGOs) and short and long double-stranded RNA (dsRNA). We have recently uncoupled the domain requirements for dsRNA binding and nucleolar targeting from the physical interactions with AGO proteins, and have found that the direct 2b-AGO interaction is sufficient to inhibit the in vitro AGO1 Slicer function independent of the other biochemical properties of 2b. Because the AGO binding activity of 2b is not required for its suppressor function in vivo, this raises the question of whether in vivo 2b-AGO interaction is possible to inhibit the in vivo AGO Slicer function. In this study, by taking advantage of a technology for the production of artificial trans-acting small interfering RNA (tasiRNA), a process uniquely associated with AGO1-mediated in vivo Slicer activity, we demonstrated that the expression of the 2b protein in planta interfered with the production of tasiRNA. Through further detailed analysis with deletion mutants of 2b proteins, we found that the inhibition of in vivo AGO1 Slicer function required the nucleolar localization signal (NoLS), in addition to the AGO-binding domain, of the 2b protein. Our finding demonstrates that in vivo 2b-AGO1 interaction is sufficient to inhibit AGO1 Slicer function independent of the dsRNA-binding activity of the 2b protein.Molecular Plant Pathology 04/2013; -
Article: Geminivirus protein structure and function.
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ABSTRACT: Geminiviruses are a family of plant viruses that cause economically important plant diseases worldwide. These viruses have circular single-stranded DNA genomes and four to eight genes that are expressed from both strands of the double-stranded DNA replicative intermediate. The transcription of these genes occurs under the control of two bidirectional promoters and one monodirectional promoter. The viral proteins function to facilitate virus replication, virus movement, the assembly of virus-specific nucleoprotein particles, vector transmission and to counteract plant host defence responses. Recent research findings have provided new insights into the structure and function of these proteins and have identified numerous host interacting partners. Most of the viral proteins have been shown to be multifunctional, participating in multiple events during the infection cycle and have, indeed, evolved coordinated interactions with host proteins to ensure a successful infection. Here, an up-to-date review of viral protein structure and function is presented, and some areas requiring further research are identified.Molecular Plant Pathology 04/2013; -
Article: The noncanonical type III secretion system of Xanthomonas translucens pv. graminis is essential for forage grass infection.
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ABSTRACT: Xanthomonas translucens pv. graminis (Xtg) is a gammaproteobacterium that causes bacterial wilt on a wide range of forage grasses. To gain insight into the host-pathogen interaction and to identify the virulence factors of Xtg, we compared a draft genome sequence of one isolate (Xtg29) with other Xanthomonas spp. with sequenced genomes. The type III secretion system (T3SS) encoding a protein transport system for type III effector (T3E) proteins represents one of the most important virulence factors of Xanthomonas spp. In contrast with other Xanthomonas spp. assigned to clade 1 on the basis of phylogenetic analyses, we identified an hrp (hypersensitive response and pathogenicity) gene cluster encoding T3SS components and a representative set of 35 genes encoding putative T3Es in the genome of Xtg29. The T3SS was shown to be divergent from the hrp gene clusters of other sequenced Xanthomonas spp. Xtg mutants deficient in T3SS regulating and structural genes were constructed to clarify the role of the T3SS in forage grass colonization. Italian ryegrass infection with these mutants led to significantly reduced symptoms (P < 0.05) relative to plants infected with the wild-type strain. This showed that the T3SS is required for symptom evocation. In planta multiplication of the T3SS mutants was not impaired significantly relative to the wild-type, indicating that the T3SS is not required for survival until 14 days post-infection. This study represents the first major step to understanding the bacterial colonization strategies deployed by Xtg and may assist in the identification of resistance (R) genes in forage grasses.Molecular Plant Pathology 04/2013; -
Article: Unrelated viral suppressors of RNA silencing mediate the control of ARGONAUTE1 level.
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ABSTRACT: Various plant viruses ubiquitously mediate the induction of miR168, resulting in the control of ARGONAUTE 1 (AGO1), which is the pivotal component of the microRNA (miRNA) regulation pathway and can also exhibit antiviral function. Here, we demonstrate that miR168-driven control of AGO1 can persist for a long time in virus-infected plants and can be an important component of symptom development. We also show that infection of RNA viruses belonging to various genera is associated with the transcriptional induction of the MIR168 precursor gene. Moreover, in a transient expression study, we reveal that different unrelated viral suppressors of RNA silencing (VSRs) are responsible for the enhanced accumulation of miR168. The induction of miR168 accumulation is an early function of VSRs and this activity is associated with the control of the endogenous AGO1 protein level. The common ability of unrelated VSRs to induce the miR168 level implies that this activity might be a component of the host defence suppression in plant-virus interactions.Molecular Plant Pathology 04/2013; -
Article: Citrus leaf blotch virus invades meristematic regions in Nicotiana benthamiana and citrus.
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ABSTRACT: To invade systemically host plants, viruses need to replicate in the infected cells, spread to neighbouring cells through plasmodesmata and move to distal parts of the plant via sieve tubes to start new infection foci. To monitor the infection of Nicotiana benthamiana plants by Citrus leaf blotch virus (CLBV), leaves were agroinoculated with an infectious cDNA clone of the CLBV genomic RNA expressing green fluorescent protein (GFP) under the transcriptional control of a duplicate promoter of the coat protein subgenomic RNA. Fluorescent spots first appeared in agroinfiltrated leaves 11-12 days after infiltration, indicating CLBV replication. Then, after entering the phloem vascular system, CLBV was unloaded in the upper parts of the plant and invaded all tissues, including flower organs and meristems. GFP fluorescence was not visible in citrus plants infected with CLBV-GFP. Therefore, to detect CLBV in meristematic regions, Mexican lime (Citrus aurantifolia) plants were graft inoculated with CLBV, with Citrus tristeza virus (CTV), a virus readily eliminated by shoot-tip grafting in vitro, or with both simultaneously. Although CLBV was detected by hybridization and real-time reverse transcription-polymerase chain reaction (RT-PCR) in 0.2-mm shoot tips in all CLBV-inoculated plants, CTV was not detected. These results explain the difficulty in eliminating CLBV by shoot-tip grafting in vitro.Molecular Plant Pathology 04/2013; -
Article: TGBp3 triggers the unfolded protein response and SKP1-dependent programmed cell death.
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ABSTRACT: The Potato virus X (PVX) triple gene block protein 3 (TGBp3), an 8-kDa membrane binding protein, aids virus movement and induces the unfolded protein response (UPR) during PVX infection. TGBp3 was expressed from the Tobacco mosaic virus (TMV) genome (TMV-p3), and we noted the up-regulation of SKP1 and several endoplasmic reticulum (ER)-resident chaperones, including the ER luminal binding protein (BiP), protein disulphide isomerase (PDI), calreticulin (CRT) and calmodulin (CAM). Local lesions were seen on leaves inoculated with TMV-p3, but not TMV or PVX. Such lesions were the result of TGBp3-elicited programmed cell death (PCD), as shown by an increase in reactive oxygen species, DNA fragmentation and induction of SKP1 expression. UPR-related gene expression occurred within 8 h of TMV-p3 inoculation and declined before the onset of PCD. TGBp3-mediated cell death was suppressed in plants that overexpressed BiP, indicating that UPR induction by TGBp3 is a pro-survival mechanism. Anti-apoptotic genes Bcl-xl, CED-9 and Op-IAP were expressed in transgenic plants and suppressed N gene-mediated resistance to TMV, but failed to alleviate TGBp3-induced PCD. However, TGBp3-mediated cell death was reduced in SKP1-silenced Nicotiana benthamiana plants. The combined data suggest that TGBp3 triggers the UPR and elicits PCD in plants.Molecular Plant Pathology 04/2013; 14(3):241-55. -
Article: Identification of the amino acid residues and domains in the cysteine-rich protein of Chinese wheat mosaic virus that are important for RNA silencing suppression and subcellular localization.
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ABSTRACT: Cysteine-rich proteins (CRPs) encoded by some plant viruses in diverse genera function as RNA silencing suppressors. Within the N-terminal portion of CRPs encoded by furoviruses, there are six conserved cysteine residues and a Cys-Gly-X-X-His motif (Cys, cysteine; Gly, glycine; His, histidine; X, any amino acid residue) with unknown function. The central domains contain coiled-coil heptad amino acid repeats that usually mediate protein dimerization. Here, we present evidence that the conserved cysteine residues and Cys-Gly-X-X-His motif in the CRP of Chinese wheat mosaic virus (CWMV) are critical for protein stability and silencing suppression activity. Mutation of a leucine residue in the third coiled-coil heptad impaired CWMV CRP activity for suppression of local silencing, but not for the promotion of cell-to-cell movement of Potato virus X (PVX). In planta and in vitro analysis of wild-type and mutant proteins indicated that the ability of the CRP to self-interact was correlated with its suppression activity. Deletion of up to 40 amino acids at the C-terminus did not abolish suppression activity, but disrupted the association of CRP with endoplasmic reticulum (ER), and reduced its activity in the enhancement of PVX symptom severity. Interestingly, a short region in the C-terminal domain, predicted to form an amphipathic α-helical structure, was responsible for the association of CWMV CRP with ER. Overall, our results demonstrate that the N-terminal and central regions are the functional domains for suppression activity, whereas the C-terminal region primarily functions to target CWMV CRP to the ER.Molecular Plant Pathology 04/2013; 14(3):265-78. -
Article: A pepper (Capsicum annuum L.) metacaspase 9 (Camc9) plays a role in pathogen-induced cell death in plants.
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ABSTRACT: Metacaspases, which belong to the cysteine-type C14 protease family, are most structurally similar to mammalian caspases than any other caspase-like protease in plants. Atmc9 (Arabidopsis thaliana metacaspase 9) has a unique domain structure, and distinct biochemical characteristics, such as Ca(2+) binding, pH, redox status, S-nitrosylation and specific protease inhibitors. However, the biological roles of Atmc9 in plant-pathogen interactions remain largely unknown. In this study, a metacaspase gene present as a single copy in the pepper genome, and sharing 54% amino acid sequence identity with Atmc9, was isolated and named Capsicum annuum metacaspase 9 (Camc9). Camc9 encodes a 318-amino-acid polypeptide with an estimated molecular weight of 34.6 kDa, and shares approximately 40% amino acid sequence identity with known type II metacaspases in plants. Quantitative reverse transcription-polymerase chain reaction analyses revealed that the expression of Camc9 was induced by infections of Xanthomonas campestris pv. vesicatoria race 1 and race 3 and treatment with methyl jasmonate. Suppression of Camc9 expression using virus-induced gene silencing enhanced disease resistance and suppressed cell death symptom development following infection with virulent bacterial pathogens. By contrast, overexpression of Camc9 by transient or stable transformation enhanced disease susceptibility and pathogen-induced cell death by regulation of reactive oxygen species production and defence-related gene expression. These results suggest that Camc9 is a possible member of the metacaspase gene family and plays a role as a positive regulator of pathogen-induced cell death in the plant kingdom.Molecular Plant Pathology 03/2013; -
Article: Similar and distinct roles of NADPH oxidase components in the tangerine pathotype of Alternaria alternata.
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ABSTRACT: The fungal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) complex, which has been implicated in the production of low-level reactive oxygen species (ROS), contains mainly NoxA, NoxB (gp91(phox) homologues) and NoxR (p67(phox) homologue). Here, we report the developmental and pathological functions of NoxB and NoxR in the tangerine pathotype of Alternaria alternata. Loss-of-function genetics revealed that all three Nox components are required for the accumulation of cellular hydrogen peroxide (H2 O2 ). Alternaria alternata strains lacking NoxA, NoxB or NoxR also displayed an increased sensitivity to H2 O2 and many ROS-generating oxidants. These phenotypes are highly similar to those previously seen for the Δyap1 mutant lacking a YAP1 transcriptional regulator and for the Δhog1 mutant lacking a HOG1 mitogen-activated protein (MAP) kinase, implicating a possible link among them. A fungal strain carrying a NoxA NoxB or NoxA NoxR double mutation was more sensitive to the test compounds than the strain mutated at a single gene, implicating a synergistic function among Nox components. The ΔnoxB mutant strain failed to produce any conidia; both ΔnoxA and ΔnoxR mutant strains showed a severe reduction in sporulation. Mutant strains carrying defective NoxB had higher chitin content than the wild-type and were insensitive to calcofluor white, Congo red and the fungicides vinclozolin and fludioxonil. Virulence assays revealed that all three Nox components are required for the elaboration of the penetration process. The inability to penetrate the citrus host, observed for Δnox mutants, could be overcome by wounding and by reacquiring a dominant Nox gene. The A. alternata NoxR did not influence the expression of NoxB, but negatively regulated NoxA. Importantly, the expression of both YAP1 and HOG1 genes, whose products are involved in resistance to ROS, was down-regulated in fungi carrying defective NoxA, NoxB or NoxR. Our results highlight the requirement of Nox in ROS resistance and provide insights into its critical role in regulating both YAP1 and HOG1 in A. alternata.Molecular Plant Pathology 03/2013; -
Article: Potato virus Y: a major crop pathogen that has provided major insights into the evolution of viral pathogenicity.
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ABSTRACT: TAXONOMY: Potato virus Y (PVY) is the type member of the genus Potyvirus in the family Potyviridae. VIRION AND GENOME PROPERTIES: PVY virions have a filamentous, flexuous form, with a length of 730 nm and a diameter of 12 nm. The genomic RNA is single stranded, messenger sense, with a length of 9.7 kb, covalently linked to a viral-encoded protein (VPg) at the 5' end and to a 3' polyadenylated tail. The genome is expressed as a polyprotein of approximately 3062 amino acid residues, processed by three virus-specific proteases into 11 mature proteins. HOSTS: PVY is distributed worldwide and has a broad host range, consisting of cultivated solanaceous species and many solanaceous and nonsolanaceous weeds. It is one of the most economically important plant pathogens and causes severe diseases in cultivated hosts, such as potato, tobacco, tomato and pepper, as well as in ornamental plants. TRANSMISSION: PVY is transmitted from plant to plant by more than 40 aphid species in a nonpersistent manner and, in potato, by planting contaminated seed tubers. DIVERSITY: Five major clades, named C1, C2, Chile, N and O, have been described within the PVY species. In recent decades, a strong increase in prevalence of N × O recombinant isolates has been observed worldwide. A correlation has been observed between PVY phylogeny and certain pathogenicity traits. GENETIC CONTROL OF PVY: Resistance genes against PVY have been used widely in breeding programmes and deployed in the field. These resistance genes show a large diversity of spectrum of action, durability and genetic determinism. Notably, recessive and dominant major resistance genes show highly contrasting patterns of interaction with PVY populations, displaying rapid co-evolution or stable relationships, respectively.Molecular Plant Pathology 03/2013; -
Article: The influence of cis-acting P1 protein and translational elements on the expression of Potato virus Y helper-component proteinase (HCPro) in heterologous systems and its suppression of silencing activity.
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ABSTRACT: In the Potyvirus genus, the P1 protein is the first N-terminal product processed from the viral polyprotein, followed by the helper-component proteinase (HCPro). In silencing suppression patch assays, we found that Potato virus Y (PVY) HCPro expressed from a P1-HCPro sequence increased the accumulation of a reporter gene, whereas protein expressed from an HCPro sequence did not, even with P1 supplied in trans. This enhancing effect of P1 has been noted in other potyviruses, but has remained unexplained. We analysed the accumulation of PVY HCPro in infiltrated tissues and found that it was higher when expressed from P1-HCPro than from HCPro sequences. Co-expression of heterologous suppressors increased the steady-state level of mRNA expressed from the HCPro sequence, but not that of protein. This suggests that, in the absence of P1 upstream, either HCPro acquires a conformation that affects negatively its activity or stability, or that its translation is reduced. To test these options, we purified HCPro expressed in the presence or absence of upstream P1, and found no difference in purification pattern and final soluble state. By contrast, alteration of the Kozak context in the HCPro mRNA sequence to favour translation increased partially suppressor accumulation and activity. Furthermore, protein activity was not lower than in protein expressed from P1-HCPro sequences. Thus, a direct role for P1 on HCPro suppressor activity or stability, by influencing its conformation during translation, can be excluded. However, P1 could still have an indirect effect favouring HCPro accumulation. Our data highlight the relevance of cis-acting translational elements in the heterologous expression of HCPro.Molecular Plant Pathology 03/2013; -
Article: Protein phosphatase 2A regulatory subunits perform distinct functional roles in the maize pathogen Fusarium verticillioides.
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ABSTRACT: Fusarium verticillioides is a pathogen of maize causing ear rot and stalk rot. The fungus also produces fumonisins, a group of mycotoxins linked to disorders in animals and humans. A cluster of genes, designated FUM genes, plays a key role in the synthesis of fumonisins. However, our understanding of the regulatory mechanism of fumonisin biosynthesis is still incomplete. We have demonstrated previously that Cpp1, a protein phosphatase type 2A (PP2A) catalytic subunit, negatively regulates fumonisin production and is involved in cell shape maintenance. In general, three PP2A subunits, structural A, regulatory B and catalytic C, make up a heterotrimer complex to perform regulatory functions. Significantly, we identified two PP2A regulatory subunits in the F. verticillioides genome, Ppr1 and Ppr2, which are homologous to Saccharomyces cerevisiae Cdc55 and Rts1, respectively. In this study, we hypothesized that Ppr1 and Ppr2 are involved in the regulation of fumonisin biosynthesis and/or cell development in F. verticillioides, and generated a series of mutants to determine the functional role of Ppr1 and Ppr2. The PPR1 deletion strain (Δppr1) resulted in drastic growth defects, but increased microconidia production. The PPR2 deletion mutant strain (Δppr2) showed elevated fumonisin production, similar to the Δcpp1 strain. Germinating Δppr1 conidia formed abnormally swollen cells with a central septation site, whereas Δppr2 showed early hyphal branching during conidia germination. A kernel rot assay showed that the mutants were slow to colonize kernels, but this is probably a result of growth defects rather than a virulence defect. Results from this study suggest that two PP2A regulatory subunits in F. verticillioides carry out distinct roles in the regulation of fumonisin biosynthesis and fungal development.Molecular Plant Pathology 03/2013; -
Article: Defence responses regulated by jasmonate and delayed senescence caused by ethylene receptor mutation contribute to the tolerance of petunia to Botrytis cinerea.
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ABSTRACT: Ethylene and jasmonate (JA) have powerful effects when plants are challenged by pathogens. The inducible promoter-regulated expression of the Arabidopsis ethylene receptor mutant ethylene-insensitive1-1 (etr1-1) causes ethylene insensitivity in petunia. To investigate the molecular mechanisms involved in transgenic petunia responses to Botrytis cinerea related to the ethylene and JA pathways, etr1-1-expressing petunia plants were inoculated with Botrytis cinerea. The induced expression of etr1-1 by a chemical inducer dexamethasone resulted in retarded senescence and reduced disease symptoms on detached leaves and flowers or intact plants. The extent of decreased disease symptoms correlated positively with etr1-1 expression. The JA pathway, independent of the ethylene pathway, activated petunia ethylene response factor (PhERF) expression and consequent defence-related gene expression. These results demonstrate that ethylene induced by biotic stress influences senescence, and that JA in combination with delayed senescence by etr1-1 expression alters tolerance to pathogens.Molecular Plant Pathology 02/2013;
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