scholarly journals Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lukas Hunziker ◽  
Mariana Tarallo ◽  
Keiko Gough ◽  
Melissa Guo ◽  
Cathy Hargreaves ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Plants ◽  
Effector Proteins ◽  
Host Immune System ◽  
Natural Forests ◽  
Forest Pathogen ◽  
Immune Receptors ◽  
Forest Pathogens ◽  
Dothistroma Needle Blight ◽  
Trigger Cell Death

AbstractForests are under threat from pests, pathogens, and changing climate. A major forest pathogen worldwide is the hemibiotroph Dothistroma septosporum, which causes dothistroma needle blight (DNB) of pines. While D. septosporum uses effector proteins to facilitate host infection, it is currently unclear whether any of these effectors are recognised by immune receptors to activate the host immune system. Such information is needed to identify and select disease resistance against D. septosporum in pines. We predicted and investigated apoplastic D. septosporum candidate effectors (DsCEs) using bioinformatics and plant-based experiments. We discovered DsCEs that trigger cell death in the angiosperm Nicotiana spp., indicative of a hypersensitive defence response and suggesting their recognition by immune receptors in non-host plants. In a first for foliar forest pathogens, we developed a novel protein infiltration method to show that tissue-cultured pine shoots can respond with a cell death response to a DsCE, as well as to a reference cell death-inducing protein. The conservation of responses across plant taxa suggests that knowledge of pathogen–angiosperm interactions may also be relevant to pathogen–gymnosperm interactions. These results contribute to our understanding of forest pathogens and may ultimately provide clues to disease immunity in both commercial and natural forests.

scholarly journals Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants

2021 ◽  
Author(s):  
Lukas Hunziker ◽  
Mariana Tarallo ◽  
Keiko Gough ◽  
Melissa Guo ◽  
Cathy Hargreaves ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Plants ◽  
Secreted Proteins ◽  
Natural Forests ◽  
Crop Species ◽  
Forest Pathogen ◽  
Immune Receptors ◽  
Forest Pathogens ◽  
Dothistroma Needle Blight ◽  
Trigger Cell Death

Forests are under threat from pests, pathogens, and changing climate. One of the major forest pathogens worldwide is Dothistroma septosporum, which causes dothistroma needle blight (DNB) of pines. D. septosporum is a hemibiotrophic fungus related to well-studied Dothideomycete pathogens, such as Cladosporium fulvum. These pathogens use small secreted proteins, termed effectors, to facilitate the infection of their hosts. The same effectors, however, can be recognised by plants carrying corresponding immune receptors, resulting in resistance responses. Hence, effectors are increasingly being exploited to identify and select disease resistance in crop species. In gymnosperms, however, such research is scarce. We predicted and investigated apoplastic D. septosporum candidate effectors (DsCEs) using bioinformatics and plant-based experiments. We discovered secreted proteins that trigger cell death in the angiosperm Nicotiana spp., suggesting their recognition by immune receptors in non-host plants. In a first for foliar forest pathogens, we also developed a novel protein infiltration method to show that tissue-cultured pine shoots can respond with a cell death response to one of our DsCEs, as well as to a reference cell death-inducing protein. These results contribute to our understanding of forest pathogens and may ultimately provide clues to disease immunity in both commercial and natural forests.

scholarly journals The barley powdery mildew effectors CSEP0139 and CSEP0182 suppress cell death and promote B. graminis fungal virulence in plants

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Xue Li ◽  
Cong Jin ◽  
Hongbo Yuan ◽  
Wanting Huang ◽  
Fang Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Powdery Mildew ◽  
Host Plants ◽  
Host Immunity ◽  
Effector Proteins ◽  
Fungal Virulence ◽  
Cell Death Pathways ◽  
Barley Powdery Mildew ◽  
Powdery Mildew Fungi ◽  
Transient Overexpression

AbstractThe powdery mildew fungi secrete numerous Candidate Secreted Effector Proteins (CSEPs) to manipulate host immunity during infection of host plants. However, the function of most of these CSEPs in cell death suppression has not yet been established. Here, we identified several CSEPs from Blumeria graminis f. sp. hordei (Bgh) that have the potential to suppress BAX- and NtMEK2DD-triggered cell death in Nicotiana benthamiana. We further characterized two effector candidates, CSEP0139 and CSEP0182, from family six and thirty-two, respectively. CSEP0139 and CSEP0182 contain a functional signal peptide and are likely secreted effectors. Expression of either CSEP0139 or CSEP0182 suppressed cell death triggered by BAX and NtMEK2DD but not by the AVRa13/MLA13 pair in N. benthamiana. Transient overexpression of CSEP0139 or CSEP0182 also inhibited BAX-induced cell death and collapse of cytoplasm in barley cells. Furthermore, overexpression of either CSEPs significantly increased Bgh haustorial formation in barley, whereas host-induced gene silencing (HIGS) of the CSEP genes reduced haustorial formation, suggesting both CSEPs promote Bgh virulence in barley. In addition, expression of CSEP0139 and CSEP0182 reduced size of the lesions caused by the necrotrophic Botrytis cinerea in N. benthamiana. Our findings suggest that CSEP0139 and CSEP0182 may target cell death components in plants to promote fungal virulence, which extends the current understanding of the functions of Bgh CSEPs and provides an opportunity for further investigation of fungal virulence in relation to cell death pathways in host plants.

Inhibition of Autophagy Potentiated Hippocampal Cell Death Induced by Endoplasmic Reticulum Stress and its Activation by Trehalose Failed to be Neuroprotective

2019 ◽  
Vol 16 (1) ◽  
pp. 3-11
Author(s):  
Luisa Halbe ◽  
Abdelhaq Rami
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Er Stress ◽  
Cell Damage ◽  
Protective Mechanism ◽  
Unfolded Proteins ◽  
Neuronal Viability ◽  
Hippocampal Cell ◽  
Trigger Cell Death ◽  
Autophagy Inhibition

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.

scholarly journals Short-term intense Bcr–Abl kinase inhibition with nilotinib is adequate to trigger cell death in BCR-ABL+ cells

Leukemia ◽  
2009 ◽  
Vol 23 (6) ◽  
pp. 1205-1206 ◽  
Author(s):  
D K Hiwase ◽  
D L White ◽  
V A Saunders ◽  
S Kumar ◽  
J V Melo ◽  
...  
Keyword(s):  
Cell Death ◽  
Short Term ◽  
Kinase Inhibition ◽  
Abl Kinase ◽  
Trigger Cell Death

Stilbene–Chalcone Hybrids: Design, Synthesis, and Evaluation as a New Class of Antimalarial Scaffolds That Trigger Cell Death through Stage Specific Apoptosis

2011 ◽  
Vol 55 (1) ◽  
pp. 297-311 ◽  
Author(s):  
Naina Sharma ◽  
Dinesh Mohanakrishnan ◽  
Amit Shard ◽  
Abhishek Sharma ◽  
Saima ◽  
...  
Keyword(s):  
Cell Death ◽  
Design Synthesis ◽  
New Class ◽  
Trigger Cell Death

PPE11 of Mycobacterium tuberculosis can alter host inflammatory response and trigger cell death

2019 ◽  
Vol 126 ◽  
pp. 45-55 ◽  
Author(s):  
Xuan Peng ◽  
Tao Luo ◽  
Xiaoqian Zhai ◽  
Chunxi Zhang ◽  
Jing Suo ◽  
...  
Keyword(s):  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Inflammatory Response ◽  
Trigger Cell Death ◽  
Host Inflammatory Response

scholarly journals Secretome Analysis and In Planta Expression of Salivary Proteins Identify Candidate Effectors from the Brown Planthopper Nilaparvata lugens

2019 ◽  
Vol 32 (2) ◽  
pp. 227-239 ◽  
Author(s):  
Weiwei Rao ◽  
Xiaohong Zheng ◽  
Bingfang Liu ◽  
Qin Guo ◽  
Jianping Guo ◽  
...  
Keyword(s):  
Cell Death ◽  
Expression Analysis ◽  
Plant Pathogens ◽  
Critical Role ◽  
Brown Planthopper ◽  
Ectopic Expression ◽  
Nilaparvata Lugens ◽  
Effector Proteins ◽  
Salivary Proteins ◽  
Secretome Analysis

The brown planthopper (BPH), Nilaparvata lugens (Stål), is a phloem sap-feeding insect. During feeding on rice plants, BPH secretes salivary proteins with potential effector functions, which may play a critical role in the plant–insect interactions. However, a limited number of BPH effector proteins have been identified to date. Here, we sequenced the salivary gland transcriptomes of five BPH populations and subsequently established a N. lugens secretome consisting of 1,140 protein-encoding genes. Secretome analysis revealed the presence of both conserved and rapidly evolving salivary proteins. A screen for potential effectors that elicit responses in the plant was performed via the transient expression analysis of 64 BPH salivary proteins in Nicotiana benthamiana leaves and rice protoplasts. The salivary proteins Nl12, Nl16, Nl28, and Nl43 induced cell death, whereas Nl40 induced chlorosis and Nl32 induced a dwarf phenotype in N. benthamiana, indicating effector properties of these proteins. Ectopic expression of the six salivary proteins in N. benthamiana upregulated expression of defense-related genes and callose deposition. Tissue expression analysis showed a higher expression level of the six candidate effectors in salivary glands than in other tissues. Subcellular localization and analysis of the domain required for cell death showed a diverse structure of the six effectors. Nl28, Nl40, and Nl43 are N. lugens specific; in contrast, Nl12, Nl16, and Nl32 are conserved among insects. The Nl40 family has numerous isoforms produced by alternative splicing, exemplifying rapid evolution and expansion of effector proteins in the BPH. Our results suggest a potential large effector repertoire in BPH and a higher level of effector conservation exist in BPH compared with that in plant pathogens.

scholarly journals Reaction of wheat plants and alternative hosts to Magnaporthe oryzae

2018 ◽  
Vol 85 (0) ◽  
Author(s):  
Lucas Gustavo Yock Durante ◽  
Lilian Maria Arruda Bacchi ◽  
Jessica Evangelista de Souza ◽  
Felipe André Sganseria Graichen
Keyword(s):  
Cell Death ◽  
Magnaporthe Oryzae ◽  
Plant Pathogen ◽  
Host Plants ◽  
Blast Disease ◽  
Plant Responses ◽  
Defensive Response ◽  
Species Pair ◽  
Digitaria Sanguinalis ◽  
Plant Pathogen Interactions

ABSTRACT: Blast disease, caused by the fungus Magnaporthe oryzae, has a major impact on wheat farming. The study of plant responses to pathogens has improved the management of this disease. Moreover, it is important to identify potential host plants in the crops’ vicinity and to understand reactions caused by plant-pathogen interactions. The objective of this study was to assess the histopathology of wheat plants, Digitaria insularis and Digitaria sanguinalis inoculated with M. oryzae isolates obtained either rice or wheat plants. Thirty-three days after sowing, greenhouse-grown plants of all three species were inoculated with each M. oryzae isolate. The observed effects (48 hours after inoculation) differed depending on the particular interaction between each pathogen isolate-plant species pair. For instance, wheat and D. sanguinalis had the weakest defensive response against spore germination, production of melanized appressoria, and appressorial penetration, with average values above 87, 90, and 43%, respectively, for these events in these plants. Furthermore, germination and appressoria melanization were more aggressive in the rice isolate than in the wheat isolate. Additionally, evidence for a defensive response (such as cell death) was observed in wheat plants inoculated with rice isolates. However, such a response was absent in plants inoculated using wheat isolates, presumably because pathogen recognition failed.

scholarly journals WtsE, an AvrE-Family Effector Protein from Pantoea stewartii subsp. stewartii, Causes Disease-Associated Cell Death in Corn and Requires a Chaperone Protein for Stability

2006 ◽  
Vol 19 (10) ◽  
pp. 1092-1102 ◽  
Author(s):  
Jong Hyun Ham ◽  
Doris R. Majerczak ◽  
Angel S. Arroyo-Rodriguez ◽  
David M. Mackey ◽  
David L. Coplin
Keyword(s):  
Cell Death ◽  
Sweet Corn ◽  
Coli Strain ◽  
Effector Proteins ◽  
Erwinia Chrysanthemi ◽  
Endoplasmic Reticulum Membrane ◽  
E Coli ◽  
Pantoea Stewartii ◽  
C Terminus ◽  
Efficient Delivery

The pathogenicity of Pantoea stewartii subsp. stewartii to sweet corn and maize requires a Hrp type III secretion system. In this study, we genetically and functionally characterized a disease-specific (Dsp) effector locus, composed of wtsE and wtsF, that is adjacent to the hrp gene cluster. WtsE, a member of the AvrE family of effector proteins, was essential for pathogenesis on corn and was complemented by DspA/E from Erwinia amylovora. An intact C-terminus of WtsE, which contained a putative endoplasmic reticulum membrane retention signal, was important for function of WtsE. Delivery of WtsE into sweet corn leaves by an Escherichia coli strain carrying the hrp cluster of Erwinia chrysanthemi caused water-soaking and necrosis. WtsE-induced cell death was not inhibited by cycloheximide treatment, unlike the hypersensitive response caused by a known Avr protein, AvrRxo1. WtsF, the putative chaperone of WtsE, was not required for secretion of WtsE from P. stewartii, and the virulence of wtsF mutants was reduced only at low inoculum concentrations. However, WtsF was required for full accumulation of WtsE within the bacteria at low temperatures. In contrast, WtsF was needed for efficient delivery of WtsE from E. coli via the Erwinia chrysanthemi Hrp system.

scholarly journals MultipleLegionella pneumophilaeffector virulence phenotypes revealed through high-throughput analysis of targeted mutant libraries

2017 ◽  
Vol 114 (48) ◽  
pp. E10446-E10454 ◽  
Author(s):  
Stephanie R. Shames ◽  
Luying Liu ◽  
James C. Havey ◽  
Whitman B. Schofield ◽  
Andrew L. Goodman ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Severe Pneumonia ◽  
Effector Proteins ◽  
Host Cells ◽  
Limiting Factor ◽  
Effector Protein ◽  
Host Immune System ◽  
Loss Of Function ◽  
High Throughput Analysis ◽  
Single Strain

Legionella pneumophilais the causative agent of a severe pneumonia called Legionnaires’ disease. A single strain ofL. pneumophilaencodes a repertoire of over 300 different effector proteins that are delivered into host cells by the Dot/Icm type IV secretion system during infection. The large number ofL. pneumophilaeffectors has been a limiting factor in assessing the importance of individual effectors for virulence. Here, a transposon insertion sequencing technology called INSeq was used to analyze replication of a pool of effector mutants in parallel both in a mouse model of infection and in cultured host cells. Loss-of-function mutations in genes encoding effector proteins resulted in host-specific or broad virulence phenotypes. Screen results were validated for several effector mutants displaying different virulence phenotypes using genetic complementation studies and infection assays. Specifically, loss-of-function mutations in the gene encoding LegC4 resulted in enhancedL. pneumophilain the lungs of infected mice but not within cultured host cells, which indicates LegC4 augments bacterial clearance by the host immune system. The effector proteins RavY and Lpg2505 were important for efficient replication within both mammalian and protozoan hosts. Further analysis of Lpg2505 revealed that this protein functions as a metaeffector that counteracts host cytotoxicity displayed by the effector protein SidI. Thus, this study identified a large cohort of effectors that contribute toL. pneumophilavirulence positively or negatively and has demonstrated regulation of effector protein activities by cognate metaeffectors as being critical for host pathogenesis.

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