Nitric oxide prevents wound-induced browning and delays senescence through inhibition of hydrogen peroxide accumulation in fresh-cut lettuce
Iakimova, E.T. ; Woltering, E.J. - \ 2015
Innovative Food Science and Emerging Technologies 30 (2015). - ISSN 1466-8564 - p. 157 - 169.
programmed cell-death - short-term exposure - lactuca-sativa l. - disease resistance response - processed romaine lettuce - ammonia-lyase activity - phenolic metabolism - iceberg lettuce - shelf-life - postharvest senescence
As a source of bioactive ingredients, lettuce is a preferable component of a healthy diet. In recent years the production of fresh-cut produce has become a fast growing business. However, the shreds are highly sensitive to wound-induced browning and premature senescence that substantially reduces the visual and sensory qualities and shortens the shelf life. To improve the fresh-cut quality, in this work, short pre-storage exposure of shreds from butterhead and iceberg lettuce to nitric oxide (NO) gas was applied. It was found that fumigation with 100 and 200 ppm NO for 1 or 2 h remarkably inhibited the browning of the cut surface and of other injured leaf areas; NO treatment delayed the senescence and substantially prolonged the shelf life upon storage at 4 °C and 12 °C. To obtain information on the physiological processes involved in the wound response, the generation of hydrogen peroxide (H2O2) and the occurrence of cell death were analyzed. The results revealed that the wounding stimulated the accumulation of H2O2 thus generating oxidative stress leading to cell death. A correlation between elevated H2O2 levels, cut surface browning, senescence and storability of the fresh-cuts was established. In comparison to mature leaves, younger leaves expressed a lesser susceptibility to wound-induced browning and the associated oxidative stress. Applied NO strongly inhibited the H2O2 accumulation which may explain its beneficial effects.
Proteome catalog of Zymoseptoria tritici captured during pathogenesis in wheat
M'Barek, S. Ben; Cordewener, J.H.G. ; Lee, T.A.J. van der; America, A.H.P. ; Mirzadi Gohari, A. ; Mehrabi, R. ; Hamza, S. ; Wit, P.J.G.M. de; Kema, G.H.J. - \ 2015
Fungal Genetics and Biology 79 (2015)June. - ISSN 1087-1845 - p. 42 - 53.
wall-degrading enzymes - fungus mycosphaerella-graminicola - programmed cell-death - cladosporium-fulvum - septoria-tritici - plant-pathogen - magnaporthe-grisea - disease resistance - hydrogen-peroxide - blotch pathogen
Zymoseptoria tritici is an economically important pathogen of wheat. However, the molecular basis of pathogenicity on wheat is still poorly understood. Here, we present a global survey of the proteins secreted by this fungus in the apoplast of resistant (cv. Shafir) and susceptible (cv. Obelisk) wheat cultivars after inoculation with reference Z. tritici strain IPO323. The fungal proteins present in apoplastic fluids were analyzed by gel electrophoresis and by data-independent acquisition liquid chromatography/mass spectrometry (LC/MS(E)) combined with data-dependent acquisition LC-MS/MS. Subsequent mapping mass spectrometry-derived peptide sequence data against the genome sequence of strain IPO323 identified 665 peptides in the MS(E) and 93 in the LC-MS/MS mode that matched to 85 proteins. The identified fungal proteins, including cell-wall degrading enzymes and proteases, might function in pathogenicity, but the functions of many remain unknown. Most fungal proteins accumulated in cv. Obelisk at the onset of necrotrophy. This inventory provides an excellent basis for future detailed studies on the role of these genes and their encoded proteins during pathogenesis in wheat
Enhancing crop resilience to combined abiotic and biotic stress through the dissection of physiological and molecular crosstalk
Kissoudis, C. ; Wiel, C.C.M. van de; Visser, R.G.F. ; Linden, C.G. van der - \ 2014
Frontiers in Plant Science 5 (2014). - ISSN 1664-462X - 20 p.
systemic acquired-resistance - activated protein-kinase - programmed cell-death - regulated gene-expression - plant immune-responses - abscisic-acid - salicylic-acid - disease resistance - arabidopsis-thaliana - transcription factor
Plants growing in their natural habitats are often challenged simultaneously by multiple stress factors, both abiotic and biotic. Research has so far been limited to responses to individual stresses, and understanding of adaptation to combinatorial stress is limited, but indicative of non-additive interactions. Omics data analysis and functional characterization of individual genes has revealed a convergence of signaling pathways for abiotic and biotic stress adaptation. Taking into account that most data originate from imposition of individual stress factors, this review summarizes these findings in a physiological context, following the pathogenesis timeline and highlighting potential differential interactions occurring between abiotic and biotic stress signaling across the different cellular compartments and at the whole plant level. Potential effects of abiotic stress on resistance components such as extracellular receptor proteins, R-genes and systemic acquired resistance will be elaborated, as well as crosstalk at the levels of hormone, reactive oxygen species, and redox signaling. Breeding targets and strategies are proposed focusing on either manipulation and deployment of individual common regulators such as transcription factors or pyramiding of non- (negatively) interacting components such as R-genes with abiotic stress resistance genes. We propose that dissection of broad spectrum stress tolerance conferred by priming chemicals may provide an insight on stress cross regulation and additional candidate genes for improving crop performance under combined stress. Validation of the proposed strategies in lab and field experiments is a first step toward the goal of achieving tolerance to combinatorial stress in crops.
PIRIN2 stabilizes cysteine protease XCP2 and increases susceptibility to the vascular pathogen Ralstonia solanacearum in Arabidopsis
Zhang, B. ; Tremousaygue, D. ; Denancé, N. ; Esse, H.P. van; Hörger, A.C. ; Dabos, P. ; Goffner, D. ; Thomma, B.P.H.J. ; Hoorn, R.A.L. van der; Tuominen, H. - \ 2014
The Plant Journal 79 (2014)6. - ISSN 0960-7412 - p. 1009 - 1019.
programmed cell-death - nf-kappa-b - disease resistance - phytophthora-infestans - gene-expression - plants - xylem - thaliana - effector - defense
PIRIN (PRN) is a member of the functionally diverse cupin protein superfamily. There are four members of the Arabidopsis thaliana PRN family, but the roles of these proteins are largely unknown. Here we describe a function of the Arabidopsis PIRIN2 (PRN2) that is related to susceptibility to the bacterial plant pathogen Ralstonia solanacearum. Two prn2 mutant alleles displayed decreased disease development and bacterial growth in response to R. solanacearum infection. We elucidated the underlying molecular mechanism by analyzing PRN2 interactions with the papain-like cysteine proteases (PLCPs) XCP2, RD21A, and RD21B, all of which bound to PRN2 in yeast two-hybrid assays and in Arabidopsis protoplast co-immunoprecipitation assays. We show that XCP2 is stabilized by PRN2 through inhibition of its autolysis on the basis of PLCP activity profiling assays and enzymatic assays with recombinant protein. The stabilization of XCP2 by PRN2 was also confirmed in planta. Like prn2 mutants, an xcp2 single knockout mutant and xcp2 prn2 double knockout mutant displayed decreased susceptibility to R. solanacearum, suggesting that stabilization of XCP2 by PRN2 underlies susceptibility to R. solanacearum in Arabidopsis.
Dynamic hydrolase activities precede hypersensitive tissue collapse in tomato seedlings
Sueldo, D. ; Ali, A. ; Misas-Villamil, J. ; Colby, T. ; Tameling, W.I.L. ; Joosten, M.H.A.J. ; Hoorn, R. van der - \ 2014
New Phytologist 203 (2014)3. - ISSN 0028-646X - p. 913 - 925.
programmed cell-death - vacuolar processing enzyme - pathogenesis-related proteins - disease resistance - cysteine proteases - defense responses - plant-pathogen - gene-expression - arabidopsis - activation
Hydrolases such as subtilases, vacuolar processing enzymes (VPEs) and the proteasome play important roles during plant programmed cell death (PCD). We investigated hydrolase activities during PCD using activity-based protein profiling (ABPP), which displays the active proteome using probes that react covalently with the active site of proteins. We employed tomato (Solanum lycopersicum) seedlings undergoing synchronized hypersensitive cell death by co-expressing the avirulence protein Avr4 from Cladosporium fulvum and the tomato resistance protein Cf-4. Cell death is blocked in seedlings grown at high temperature and humidity, and is synchronously induced by decreasing temperature and humidity. ABPP revealed that VPEs and the proteasome are not differentially active, but that activities of papain-like cysteine proteases and serine hydrolases, including Hsr203 and P69B, increase before hypersensitive tissue collapse, whereas the activity of a carboxypeptidase-like enzyme is reduced. Similar dynamics were observed for these enzymes in the apoplast of tomato challenged with C. fulvum. Unexpectedly, these challenged plants also displayed novel isoforms of secreted putative VPEs. In the absence of tissue collapse at high humidity, the hydrolase activity profile is already altered completely, demonstrating that changes in hydrolase activities precede hypersensitive tissue collapse.
Effector-triggered defence against apoplastic fungal pathogens
Stotz, H.U. ; Mitrousia, G.K. ; Wit, P.J.G.M. de; Fitt, B.D.L. - \ 2014
Trends in Plant Science 19 (2014)8. - ISSN 1360-1385 - p. 491 - 500.
programmed cell-death - plant immune-system - cf-2-dependent disease resistance - leptosphaeria-maculans - cladosporium-fulvum - brassica-napus - mycosphaerella-graminicola - avirulence gene - rhynchosporium-secalis - oilseed rape
R gene-mediated host resistance against apoplastic fungal pathogens is not adequately explained by the terms pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) or effector-triggered immunity (ETI). Therefore, it is proposed that this type of resistance is termed 'effector-triggered defence' (ETD). Unlike PTI and ETI, ETD is mediated by R genes encoding cell surface-localised receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1. In contrast to this extracellular recognition, ETI is initiated by intracellular detection of pathogen effectors. ETI is usually associated with fast, hypersensitive host cell death, whereas ETD often triggers host cell death only after an elapsed period of endophytic pathogen growth. In this opinion, we focus on ETD responses against foliar fungal pathogens of crops.
System-Wide Hypersensitive Response-Associated Transcriptome and Metabolome Reprogramming in Tomato
Etalo, D.W. ; Stulemeijer, I.J.E. ; Esse, H.P. van; Vos, R.C.H. de; Bouwmeester, H.J. ; Joosten, M.H.A.J. - \ 2013
Plant Physiology 162 (2013)3. - ISSN 0032-0889 - p. 1599 - 1617.
programmed cell-death - pathogen pseudomonas-syringae - campestris pv. vesicatoria - glutathione s-transferases - amino-acid catabolism - leaf rust resistance - higher-plant cells - mass-spectrometry - cladosporium-fulvum - functional-analysis
The hypersensitive response (HR) is considered to be the hallmark of the resistance response of plants to pathogens. To study HR-associated transcriptome and metabolome reprogramming in tomato (Solanum lycopersicum), we used plants that express both a resistance gene to Cladosporium fulvum and the matching avirulence gene of this pathogen. In these plants, massive reprogramming occurred, and we found that the HR and associated processes are highly energy demanding. Ubiquitin-dependent protein degradation, hydrolysis of sugars, and lipid catabolism are used as alternative sources of amino acids, energy, and carbon skeletons, respectively. We observed strong accumulation of secondary metabolites, such as hydroxycinnamic acid amides. Coregulated expression of WRKY transcription factors and genes known to be involved in the HR, in addition to a strong enrichment of the W-box WRKY-binding motif in the promoter sequences of the coregulated genes, point to WRKYs as the most prominent orchestrators of the HR. Our study has revealed several novel HR-related genes, and reverse genetics tools will allow us to understand the role of each individual component in the HR.
Structural Determinants at the Interface of the ARC2 and LRR Domains Control the Activation of the NB-LRR Plant Immune Receptors Rx1 and Gpa2
Slootweg, E.J. ; Spiridon, L.N. ; Roosien, J. ; Butterbach, P.B.E. ; Pomp, H. ; Westerhof, L.B. ; Wilbers, R.H.P. ; Bakker, E.H. ; Bakker, J. ; Petrescu, A.J. ; Smant, G. ; Goverse, A. - \ 2013
Plant Physiology 162 (2013)3. - ISSN 0032-0889 - p. 1510 - 1528.
secondary structure prediction - disease resistance genes - protein-protein interactions - programmed cell-death - nbs-lrr protein - coiled-coil - pathogen interactions - physical association - multiple alignments - self-association
Many plant and animal immune receptors have a modular NB-LRR architecture in which a nucleotide-binding switch domain (NB-ARC) is tethered to a leucine-rich repeat sensor domain (LRR). The cooperation between the switch and sensor domains, which regulates the activation of these proteins, is poorly understood. Here we report structural determinants governing the interaction between the NB-ARC and LRR in the highly homologous plant immune receptors Gpa2 and Rx1, which recognize the potato cyst nematode Globodera pallida and Potato Virus X, respectively. Systematic shuffling of polymorphic sites between Gpa2 and Rx1 showed that a minimal region in the ARC2 and the N-terminal repeats of the LRR domain coordinate the activation state of the protein. We identified two closely spaced amino acid residues in this region of the ARC2 (position 401 and 403) that distinguish between autoactivation and effector-triggered activation. Furthermore, a highly acidic loop region in the ARC2 domain and basic patches in the N-terminal end of the LRR domain were demonstrated to be required for the physical interaction between the ARC2 and LRR. The NB-ARC and LRR domains dissociate upon effector-dependent activation and the complementary charged regions are predicted to mediate a fast re-association enabling multiple rounds of activation. Finally, we present a mechanistic model showing how the ARC2, NB and N-terminal half of the LRR form a clamp, which regulates the dissociation and re-association of the switch and sensor domains in NB-LRR proteins.
The molecular mechanism of zinc and cadmium stress response in plants
Lin, Y.F. ; Aarts, M.G.M. - \ 2012
Cellular and Molecular Life Sciences 69 (2012)19. - ISSN 1420-682X - p. 3187 - 3206.
hyperaccumulator thlaspi-caerulescens - heavy-metal detoxification - sedum-alfredii hance - arbuscular mycorrhizal fungi - wrky53 transcription factor - quantitative trait locus - induced oxidative stress - programmed cell-death - arabidopsis-thaliana - nicotianam
When plants are subjected to high metal exposure, different plant species take different strategies in response to metal-induced stress. Largely, plants can be distinguished in four groups: metal-sensitive species, metal-resistant excluder species, metal-tolerant non-hyperaccumulator species, and metal-hypertolerant hyperaccumulator species, each having different molecular mechanisms to accomplish their resistance/tolerance to metal stress or reduce the negative consequences of metal toxicity. Plant responses to heavy metals are molecularly regulated in a process called metal homeostasis, which also includes regulation of the metal-induced reactive oxygen species (ROS) signaling pathway. ROS generation and signaling plays an important duel role in heavy metal detoxification and tolerance. In this review, we will compare the different molecular mechanisms of nutritional (Zn) and non-nutritional (Cd) metal homeostasis between metal-sensitive and metal-adapted species. We will also include the role of metal-induced ROS signal transduction in this comparison, with the aim to provide a comprehensive overview on how plants cope with Zn/Cd stress at the molecular level.
Functional analysis of two inhibitor of apoptosis (iap) orthologs from Helicoverpa armigera nucleopolyhedrovirus
Liang, Ch.Y. ; Lange, J. de; Chen, X.W. ; Oers, M.M. van; Vlak, J.M. ; Westenberg, M. - \ 2012
Virus Research 165 (2012)1. - ISSN 0168-1702 - p. 107 - 111.
programmed cell-death - baculovirus gene - insect cells - p35 gene - proteins - lines - identification - establishment - expression - tolerance
Baculoviruses induce apoptotic responses in cultured insect cells, which can severely limit viral replication. To overcome this host response baculoviruses carry anti-apoptotic genes, including members of the p35 and inhibitor of apoptosis (iap) gene families. The baculovirus Helicoverpa armigera nucleopolyhedrovirus (HearNPV) carries two putative apoptosis suppressor genes (iap2 and iap3), which we studied in more detail. IAPs are believed to be functional in the cytoplasm, but surprisingly, when transiently expressed as EGFP fusions, IAP2 was evenly distributed throughout the cell, while IAP3 was mainly found in the nucleus. The latter became evenly distributed in both compartments in HearNPV infected cells. When iap2 was deleted, HearNPV could be propagated in Hz2e5 cells, while an iap3 deletion was lethal. The HearNPV ¿iap3 mutant could be rescued by reinsertion of the HearNPV iap3 gene and by the well-studied anti-apoptotic genes Autographa californica (Ac)MNPV p35 or Orgyia pseudotsugata (Op)MNPV iap3. RNAi analysis showed that HearNPV induced apoptosis in Hz2e5 cells transfected with iap3 dsRNA, while silencing of iap2 did not lead to apoptosis. Finally, IAP3 was able to inhibit actinomycin-D induced apoptosis when transiently expressed in Sf21 cells. These results together indicate that HearNPV IAP3 is a functional apoptosis suppressor, while the function of IAP2 remains elusive.
JUNGBRUNNEN1, a Reactive Oxygen Species–Responsive NAC Transcription Factor, Regulates Longevity in Arabidopsis
Wu, A. ; Devi Allu, A. ; Garapati, P. ; Siddiqui, H. ; Dortay, H. ; Zanor, M.I. ; Amparo Asensi-Fabado, M. ; Munne´ -Bosch, S. ; Antonio, C. ; Tohge, T. ; Fernie, A.R. ; Kaufmann, K. ; Xue, G.P. ; Mueller-Roeber, B. ; Balazadeh, S. - \ 2012
The Plant Cell 24 (2012)2. - ISSN 1040-4651 - p. 482 - 506.
programmed cell-death - heat-stress response - leaf senescence - gene-expression - hydrogen-peroxide - oxidative stress - glucosinolate biosynthesis - comprehensive analysis - environmental-stress - functional-genomics
The transition from juvenility through maturation to senescence is a complex process that involves the regulation of longevity. Here, we identify JUNGBRUNNEN1 (JUB1), a hydrogen peroxide (H2O2)-induced NAC transcription factor, as a central longevity regulator in Arabidopsis thaliana. JUB1 overexpression strongly delays senescence, dampens intracellular H2O2 levels, and enhances tolerance to various abiotic stresses, whereas in jub1-1 knockdown plants, precocious senescence and lowered abiotic stress tolerance are observed. A JUB1 binding site containing a RRYGCCGT core sequence is present in the promoter of DREB2A, which plays an important role in abiotic stress responses. JUB1 transactivates DREB2A expression in mesophyll cell protoplasts and transgenic plants and binds directly to the DREB2A promoter. Transcriptome profiling of JUB1 overexpressors revealed elevated expression of several reactive oxygen species–responsive genes, including heat shock protein and glutathione S-transferase genes, whose expression is further induced by H2O2 treatment. Metabolite profiling identified elevated Pro and trehalose levels in JUB1 overexpressors, in accordance with their enhanced abiotic stress tolerance. We suggest that JUB1 constitutes a central regulator of a finely tuned control system that modulates cellular H2O2 level and primes the plants for upcoming stress through a gene regulatory network that involves DREB2A
DNA damage in plant herbarium tissue.
Staats, M. ; Cuenca, A. ; Richardson, J.E. ; Ginkel, R.V. ; Petersen, G. ; Seberg, O. ; Bakker, F.T. - \ 2011
PLoS ONE 6 (2011)12. - ISSN 1932-6203 - 9 p.
programmed cell-death - ancient dna - miscoding lesions - enzymatic amplification - specimens - repair - preservation - extraction - sequences - reveals
Dried plant herbarium specimens are potentially a valuable source of DNA. Efforts to obtain genetic information from this source are often hindered by an inability to obtain amplifiable DNA as herbarium DNA is typically highly degraded. DNA post-mortem damage may not only reduce the number of amplifiable template molecules, but may also lead to the generation of erroneous sequence information. A qualitative and quantitative assessment of DNA post-mortem damage is essential to determine the accuracy of molecular data from herbarium specimens. In this study we present an assessment of DNA damage as miscoding lesions in herbarium specimens using 454-sequencing of amplicons derived from plastid, mitochondrial, and nuclear DNA. In addition, we assess DNA degradation as a result of strand breaks and other types of polymerase non-bypassable damage by quantitative real-time PCR. Comparing four pairs of fresh and herbarium specimens of the same individuals we quantitatively assess post-mortem DNA damage, directly after specimen preparation, as well as after long-term herbarium storage. After specimen preparation we estimate the proportion of gene copy numbers of plastid, mitochondrial, and nuclear DNA to be 2.4–3.8% of fresh control DNA and 1.0–1.3% after long-term herbarium storage, indicating that nearly all DNA damage occurs on specimen preparation. In addition, there is no evidence of preferential degradation of organelle versus nuclear genomes. Increased levels of C¿T/G¿A transitions were observed in old herbarium plastid DNA, representing 21.8% of observed miscoding lesions. We interpret this type of post-mortem DNA damage-derived modification to have arisen from the hydrolytic deamination of cytosine during long-term herbarium storage. Our results suggest that reliable sequence data can be obtained from herbarium specimens.
Genome analysis of the necrotrophic fungal pathogens Sclerotinia sclerotiorum and Botrytis cinerea
Amselem, J. ; Cuomo, C.A. ; Kan, J.A.L. van; Viaud, M. ; Benito, E.P. ; Couloux, A. ; Coutinho, P.M. ; Vries, R.P. de; Dyer, P.S. ; Fillinger, S. ; Fournier, E. ; Gout, L. ; Hahn, M. ; Kohn, L. ; Lapalu, N. ; Plummer, K.M. ; Pradier, J.M. ; Quévillon, E. ; Sharon, A. ; Simon, A. ; Have, A. ten; Tudzynski, B. ; Tudzynski, P. ; Wincker, P. ; Andrew, M. ; Anthouard, V. ; Beever, R.E. ; Beffa, R. ; Benoit, I. ; Bouzid, O. ; Brault, B. ; Chen, Z. ; Choquer, M. ; Collemare, J. ; Cotton, P. ; Danchin, E.G. ; Silva, C. Da; Gautier, A. ; Giraud, C. ; Giraud, T. ; Gonzalez, C. ; Grossetete, S. ; Güldener, U. ; Henrissat, B. ; Howlett, B.J. ; Kodira, C. ; Kretschmer, M. ; Lappartient, A. ; Leroch, M. ; Levis, C. ; Mauceli, E. ; Neuvéglise, C. ; Oeser, B. ; Pearson, M. ; Poulain, J. ; Poussereau, N. ; Quesneville, H. ; Rascle, C. ; Schumacher, J. ; Ségurens, B. ; Sexton, A. ; Silva, E. ; Sirven, C. ; Soanes, D.M. ; Talbot, N.J. ; Templeton, M. ; Yandava, C. ; Yarden, O. ; Zeng, Q. ; Rollins, J.A. ; Lebrun, M.H. ; Dickman, M. - \ 2011
Plos Genetics 7 (2011)8. - ISSN 1553-7404 - 27 p.
rice blast fungus - development-specific protein - expressed sequence tags - programmed cell-death - mating-type loci - oxalic-acid - neurospora-crassa - arabidopsis-thaliana - secondary metabolism - molecular phylogeny
Sclerotinia sclerotiorum and Botrytis cinerea are closely related necrotrophic plant pathogenic fungi notable for their wide host ranges and environmental persistence. These attributes have made these species models for understanding the complexity of necrotrophic, broad host-range pathogenicity. Despite their similarities, the two species differ in mating behaviour and the ability to produce asexual spores. We have sequenced the genomes of one strain of S. sclerotiorum and two strains of B. cinerea. The comparative analysis of these genomes relative to one another and to other sequenced fungal genomes is provided here. Their 38–39 Mb genomes include 11,860–14,270 predicted genes, which share 83% amino acid identity on average between the two species. We have mapped the S. sclerotiorum assembly to 16 chromosomes and found large-scale co-linearity with the B. cinerea genomes. Seven percent of the S. sclerotiorum genome comprises transposable elements compared to
Plants under continuous light
Velez Ramirez, A.I. ; Ieperen, W. van; Vreugdenhill, D. ; Millenaar, F.F. - \ 2011
Trends in Plant Science 16 (2011)6. - ISSN 1360-1385 - p. 310 - 318.
programmed cell-death - clock gene-expression - arabidopsis-thaliana - circadian clock - continuous irradiation - constant-light - leaf chlorosis - maize leaves - photosynthetic characteristics - carbohydrate accumulation
Continuous light is an essential tool for understanding the plant circadian clock. Additionally, continuous light might increase greenhouse food production. However, using continuous light in research and practice has its challenges. For instance, most of the circadian clock-oriented experiments were performed under continuous light; consequently, interactions between the circadian clock and the light signaling pathway were overlooked. Furthermore, in some plant species continuous light induces severe injury, which is only poorly understood so far. In this review paper, we aim to combine the current knowledge with a modern conceptual framework. Modern genomic tools and rediscovered continuous light-tolerant tomato species (Solanum spp.) could boost the understanding of the physiology of plants under continuous light
Death proteases: alive and kicking
Woltering, E.J. - \ 2010
Trends in Plant Science 15 (2010)4. - ISSN 1360-1385 - p. 185 - 188.
programmed cell-death - caspase-like activity - plant embryogenesis - arabidopsis
Two recent discoveries significantly add to our understanding of plant programmed cell death (PCD). Hatsugai et al. showed that cell death is dependent on proper proteasome functioning. Sundström et al. showed that the in vivo substrate of a type II metacaspase is associated with cell viability. Both findings are major breakthroughs within the plant PCD field and highlight that the plant cell death machinery apparently employs a wide range of structurally unrelated proteases that, surprisingly, show a caspase-like preference for specific (evolutionarily conserved) substrates
The het-c heterokaryon incompatibility gene in Aspergillus niger
Diepeningen, A.D. van; Pal, K. ; Lee, T. ; Hoekstra, R.F. ; Debets, A.J.M. - \ 2009
Mycological Research 113 (2009)2. - ISSN 0953-7562 - p. 222 - 229.
programmed cell-death - neurospora-crassa - vegetative incompatibility - filamentous fungi - podospora-anserina - mating-type - locus - nidulans - sequence - protein
Heterokaryon incompatibility among Aspergillus niger strains is a widespread phenomenon that is observed as the inability to form stable heterokaryons. The genetic basis of heterokaryon incompatibility reactions is well established in some sexual filamentous fungi but largely unknown in presumed asexual species, such as A. niger. To test whether the genes that determine heterokaryon incompatibility in Neurospora crassa, such as het-c, vib-1 and pin-c, have a similar function in A. niger, we performed a short in silico search for homologues of these genes in the A. niger and several related genomes. For het-c, pin-c and vib-1 we did indeed identify putative orthologues. We then screened a genetically diverse worldwide collection of incompatible black Aspergilli for polymorphisms in the het-c orthologue. No size variation was observed in the variable het-c indel region that determines the specificity in N. crassa. Sequence comparison showed only minor variation in the number of glutamine coding triplets. However, introduction of one of the three N. crassa alleles (het-c2) in A. niger by transformation resulted in an abortive phenotype, reminiscent of the heterokaryon incompatibility in N. crassa. We conclude that although the genes required are present and the het-c homologue could potentially function as a heterokaryon incompatibility gene, het-c has no direct function in heterokaryon incompatibility in A. niger because the necessary allelic variation is absent
Quantitative phosphoproteomics of tomato mounting a hypersensitive response reveals a swift suppression of photosynthetic activity and a differential role for Hsp90 isoforms
Stulemeijer, I.J.E. ; Joosten, M.H.A.J. ; Jensen, O.N. - \ 2009
Journal of Proteome Research 8 (2009)3. - ISSN 1535-3893 - p. 1168 - 1182.
dependent protein-kinase - highly selective enrichment - plant-pathogen interactions - innate immune-responses - programmed cell-death - heat-shock-protein - cladosporium-fulvum - mass-spectrometry - plasma-membrane - functional-analysis
An important mechanism by which plants defend themselves against pathogens is the rapid execution of a hypersensitive response (HR). Tomato plants containing the Cf-4 resistance gene mount an HR that relies on the activation of phosphorylation cascades, when challenged with the Avr4 elicitor secreted by the pathogenic fungus Cladosporium fulvum. Phosphopeptides were isolated from tomato seedlings expressing both Cf-4 and Avr4 using titanium dioxide columns and LC-MS/MS analysis led to the identification of 50 phosphoproteins, most of which have not been described in tomato before. Phosphopeptides were quantified using a label-free approach based on the MS peak areas. We identified 12 phosphopeptides for which the abundance changed upon HR initiation, as compared to control seedlings. Our results suggest that photosynthetic activity is specifically suppressed in a phosphorylation-dependent way during the very early stages of HR development. In addition, phosphopeptides originating from four Hsp90 isoforms exhibited altered abundances in Cf-4/Avr4 seedlings compared to control seedlings, suggesting that the isoforms of this chaperone protein have a different function in defense signaling. We show that label-free relative quantification of the phosphoproteome of complex samples is feasible, allowing extension of our knowledge on the general physiology and defense signaling of plants mounting the HR.
Identification of the het-r vegetative incompatibility gene of Podospora anserina as a member of the fast evolving HNWD gene family
Chevanne, D. ; Bastiaans, E. ; Debets, A.J.M. ; Saupe, S.J. ; Clave, C. ; Paoletti, M. - \ 2009
Current Genetics 55 (2009)1. - ISSN 0172-8083 - p. 93 - 102.
programmed cell-death - chestnut blight fungus - non-self recognition - heterokaryon incompatibility - neurospora-crassa - filamentous fungi - virus transmission - protein - locus - domain
In fungi, vegetative incompatibility is a conspecific non-self recognition mechanism that restricts formation of viable heterokaryons when incompatible alleles of specific het loci interact. In Podospora anserina, three non-allelic incompatibility systems have been genetically defined involving interactions between het-c and het-d, het-c and het-e, het-r and het-v. het-d and het-e are paralogues belonging to the HNWD gene family that encode proteins of the STAND class. HET-D and HET-E proteins comprise an N-terminal HET effector domain, a central GTP binding site and a C-terminal WD repeat domain constituted of tandem repeats of highly conserved WD40 repeat units that define the specificity of alleles during incompatibility. The WD40 repeat units of the members of this HNWD family are undergoing concerted evolution. By combining genetic analysis and gain of function experiments, we demonstrate that an additional member of this family, HNWD2, corresponds to the het-r non-allelic incompatibility gene. As for het-d and het-e, allele specificity at the het-r locus is determined by the WD repeat domain. Natural isolates show allelic variation for het-r
RD19, an Arabidopsis cysteine protease required for RRS1-R-mediated resistance, is relocalized to the nucleus by the Ralstonia solanacearum PopP2 effector
Bernoux, M. ; Timmers, T. ; Jauneau, A. ; Brière, C. ; Wit, P.J.G.M. de; Marco, Y. ; Deslandes, L. - \ 2008
The Plant Cell 20 (2008)8. - ISSN 1040-4651 - p. 2252 - 2264.
agrobacterium-mediated transformation - cf-2-dependent disease resistance - tomato lycopersicon-esculentum - lifetime imaging microscopy - programmed cell-death - plant innate immunity - for-gene concept - iii effector - cladosporium-fulvum - hypersensitive respon
Bacterial wilt, a disease impacting cultivated crops worldwide, is caused by the pathogenic bacterium Ralstonia solanacearum. PopP2 (for Pseudomonas outer protein P2) is an R. solanacearum type III effector that belongs to the YopJ/AvrRxv protein family and interacts with the Arabidopsis thaliana RESISTANT TO RALSTONIA SOLANACEARUM 1-R (RRS1-R) resistance protein. RRS1-R contains the Toll/Interleukin1 receptor¿nucleotide binding site¿Leu-rich repeat domains found in several cytoplasmic R proteins and a C-terminal WRKY DNA binding domain. In this study, we identified the Arabidopsis Cys protease RESPONSIVE TO DEHYDRATION19 (RD19) as being a PopP2-interacting protein whose expression is induced during infection by R. solanacearum. An Arabidopsis rd19 mutant in an RRS1-R genetic background is compromised in resistance to the bacterium, indicating that RD19 is required for RRS1-R¿mediated resistance. RD19 normally localizes in mobile vacuole-associated compartments and, upon coexpression with PopP2, is specifically relocalized to the plant nucleus, where the two proteins physically interact. No direct physical interaction between RRS1-R and RD19 in the presence of PopP2 was detected in the nucleus as determined by Förster resonance energy transfer. We propose that RD19 associates with PopP2 to form a nuclear complex that is required for activation of the RRS1-R¿mediated resistance response.
The social evolution of somatic fusion
Aanen, D.K. ; Debets, A.J.M. ; Visser, J.A.G.M. de; Hoekstra, R.F. - \ 2008
Bioessays 30 (2008)11-12. - ISSN 0265-9247 - p. 1193 - 1203.
conidial anastomosis tubes - programmed cell-death - double-stranded-rna - vegetative incompatibility - heterokaryon incompatibility - neurospora-crassa - filamentous fungi - podospora-anserina - aspergillus-nidulans - allorecognition specificity
The widespread potential for somatic fusion among different conspecific multicellular individuals suggests that such fusion is adaptive. However, because recognition of non-kin (allorecognition) usually leads to a rejection response, successful somatic fusion is limited to close kin. This is consistent with kin-selection theory, which predicts that the potential cost of fusion and the potential for somatic parasitism decrease with increasing relatedness. Paradoxically, however, Crozier found that, in the short term, positive-frequency-dependent selection eliminates the required genetic polymorphism at allorecognition loci. The Crozier paradox may be solved if allorecognition is based on extrinsically balanced polymorphisms, for example at immune loci. Alternatively, the assumption of most models that self fusion is mutually beneficial is wrong. If fusion is on average harmful, selection will promote unconditional rejection. However, we propose that fusion within individuals is beneficial, selecting for the ability to fuse, but fusion between individuals on average costly, selecting for non-self recognition (rather than non-kin recognition)