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 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 Identification and Characterization of Plant Cell Death–Inducing Secreted Proteins From Ustilaginoidea virens

2016 ◽  
Vol 29 (5) ◽  
pp. 405-416 ◽  
Author(s):  
Anfei Fang ◽  
Yanqing Han ◽  
Nan Zhang ◽  
Min Zhang ◽  
Lijuan Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Active Sites ◽  
Secreted Proteins ◽  
Ustilaginoidea Virens ◽  
Induce Cell Death ◽  
Functional Studies ◽  
Secretion Signal ◽  
Villosiclava Virens ◽  
Catalytic Active Sites ◽  
Trigger Cell Death

Ustilaginoidea virens (Cooke) Takah (telemorph Villosiclava virens) is an ascomycetous fungus that causes rice false smut, one of the most important rice diseases. Fungal effectors often play essential roles in host-pathogen coevolutionary interactions. However, little is known about the functions of U. virens effectors. Here, we performed functional studies on putative effectors in U. virens and demonstrated that 13 of 119 putative effectors caused necrosis or necrosis-like phenotypes in Nicotiana benthamiana. Among them, 11 proteins were confirmed to be secreted, using a yeast secretion system, and the corresponding genes are all highly induced during infection, except UV_44 and UV_4753. Eight secreted proteins were proven to trigger cell death or defenses in rice protoplasts and the secretion signal of these proteins is essential for their cell death–inducing activity. The ability of UV_44 and UV_1423 to trigger cell death is dependent on the predicted serine peptidase and ribonuclease catalytic active sites, respectively. We demonstrated that UV_1423 and UV_6205 are N-glycosylated proteins, which glycosylation has different impacts on their abilities to induce cell death. Collectively, the study identified multiple secreted proteins in U. virens with specific structural motifs that induce cell death or defense machinery in nonhost and host plants.

scholarly journals Erwinia amylovora Type Three–Secreted Proteins Trigger Cell Death and Defense Responses in Arabidopsis thaliana

2008 ◽  
Vol 21 (8) ◽  
pp. 1076-1086 ◽  
Author(s):  
A. Degrave ◽  
M. Fagard ◽  
C. Perino ◽  
M. N. Brisset ◽  
S. Gaubert ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Host Plants ◽  
Erwinia Amylovora ◽  
Disease Process ◽  
Defense Responses ◽  
Secreted Proteins ◽  
Relative Importance ◽  
Callose Deposition ◽  
Ros Accumulation

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.

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 Genetic Analysis Reveals Three Novel QTLs Underpinning a Butterfly Egg-Induced Hypersensitive Response-Like Cell Death in Brassica Rapa

2021 ◽  
Author(s):  
Niccolò Bassetti ◽  
Lotte Caarls ◽  
Gabriella Bukovinszkine’Kiss ◽  
Mohamed El-Soda ◽  
Jeroen van Veen ◽  
...  
Keyword(s):  
Cell Death ◽  
Brassica Rapa ◽  
Hypersensitive Response ◽  
Genetic Basis ◽  
Plant Immunity ◽  
Egg Survival ◽  
Crop Species ◽  
Germplasm Screening ◽  
Resistance To Herbivory ◽  
Crop Resistance

Abstract Background Cabbage white butterflies (Pieris spp.) can be severe pests of Brassica crops such as Chinese cabbage, Pak choi (Brassica rapa) or cabbages (B. oleracea). Eggs of Pieris spp. can induce a hypersensitive response-like (HR-like) cell death which reduces egg survival in the wild black mustard (B. nigra). Unravelling the genetic basis of this egg-killing trait in Brassica crops could improve crop resistance to herbivory, reducing major crop losses and pesticides use. Here we investigated the genetic architecture of a HR-like cell death induced by P. brassicae eggs in B. rapa. Results A germplasm screening of B. rapa 56 accessions, representing the genetic and geographical diversity of a B. rapa core collection, showed phenotypic variation for cell death. An image-based phenotyping protocol was developed to accurately measure size of HR-like cell death and was then used to identify two accessions that consistently showed weak (R-o-18) or strong cell death response (L58). Screening of 160 RILs derived from these two accessions resulted in three novel QTLs for Pieris brassicae-induced cell death on chromosomes A02 (Pbc1), A03 (Pbc2), and A06 (Pbc3). The three QTLs Pbc1-3 contain cell surface receptors, intracellular receptors and other genes involved in plant immunity processes, such as ROS accumulation and cell death formation. Synteny analysis with A. thaliana suggested that Pbc1 and Pbc2 are novel QTLs associated with this trait, while Pbc3 contains also LecRK-I.1, a gene of A. thaliana previously associated with cell death induced by a P. brassicae egg extract. Conclusions This study provides the first genomic regions associated with the Pieris egg-induced HR-like cell death in a Brassica crop species. It is a step closer towards unravelling the genetic basis of an egg-killing crop resistance trait, paving the way for breeders to further fine-map and validate candidate genes.

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.

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