Apoptosis-like programmed cell death in the grey mould fungus Botrytis cinerea: genes and their role in pathogenicity

2011 ◽  
Vol 39 (5) ◽  
pp. 1493-1498 ◽  
Author(s):  
Neta Shlezinger ◽  
Adi Doron ◽  
Amir Sharon
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Botrytis Cinerea ◽  
Fungal Pathogens ◽  
Grey Mould ◽  
Fungal Species ◽  
Fungal Virulence ◽  
Mould Fungus ◽  
Apoptosis Protein ◽  
Result Show

A considerable number of fungal homologues of human apoptotic genes have been identified in recent years. Nevertheless, we are far from being able to connect the different pieces and construct a primary structure of the fungal apoptotic regulatory network. To get a better picture of the available fungal components, we generated an automatic search protocol that is based on protein sequences together with a domain-centred approach. We used this protocol to search all the available fungal databases for domains and homologues of human apoptotic proteins. Among all known apoptotic domains, only the BIR [baculovirus IAP (inhibitor of apoptosis protein) repeat] domain was found in fungi. A single protein with one or two BIR domains is present in most (but not all) fungal species. We isolated the BIR-containing protein from the grey mould fungus Botrytis cinerea and determined its role in apoptosis and pathogenicity. We also isolated and analysed BcNMA, a homologue of the yeast NMA11 gene. Partial knockout or overexpression strains of BcBIR1 confirmed that BcBir1 is anti-apoptotic and this activity was assigned to the N′-terminal part of the protein. Plant infection assays showed that the fungus undergoes massive PCD (programmed cell death) during early stages of infection. Further studies showed that fungal virulence was fully correlated with the ability of the fungus to cope with plant-induced PCD. Together, our result show that BcBir1 is a major regulator of PCD in B. cinerea and that proper regulation of the host-induced PCD is essential for pathogenesis in this and other similar fungal pathogens.

A tomato metacaspase gene is upregulated during programmed cell death in Botrytis cinerea-infected leaves

Planta ◽  
2003 ◽  
Vol 217 (3) ◽  
pp. 517-522 ◽  
Author(s):  
Frank A. Hoeberichts ◽  
Arjen ten Have ◽  
Ernst J. Woltering
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Botrytis Cinerea

Macromolecular Toxins Secreted by Botrytis cinerea Induce Programmed Cell Death in Arabidopsis Leaves

2018 ◽  
Vol 65 (4) ◽  
pp. 579-587 ◽  
Author(s):  
D. Huo ◽  
J. Wu ◽  
Q. Kong ◽  
G. B. Zhang ◽  
Y. Y. Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Botrytis Cinerea

scholarly journals A novel Botrytis cinerea‐ specific gene BcHBF1 enhances virulence of the grey mould fungus via promoting host penetration and invasive hyphal development

2019 ◽  
Vol 20 (5) ◽  
pp. 731-747 ◽  
Author(s):  
Yue Liu ◽  
Jiane‐Kang Liu ◽  
Gui‐Hua Li ◽  
Ming‐Zhe Zhang ◽  
Ying‐Ying Zhang ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Grey Mould ◽  
Specific Gene ◽  
Mould Fungus ◽  
Hyphal Development ◽  
Host Penetration

scholarly journals Fungicide-Driven Evolution and Molecular Basis of Multidrug Resistance in Field Populations of the Grey Mould Fungus Botrytis cinerea

2009 ◽  
Vol 5 (12) ◽  
pp. e1000696 ◽  
Author(s):  
Matthias Kretschmer ◽  
Michaela Leroch ◽  
Andreas Mosbach ◽  
Anne-Sophie Walker ◽  
Sabine Fillinger ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Botrytis Cinerea ◽  
Molecular Basis ◽  
Grey Mould ◽  
Mould Fungus

scholarly journals CTIM-10. PHASE II STUDY OF PEMBROLIZUMAB PLUS SurVaxM FOR GLIOBLASTOMA AT FIRST RECURRENCE

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii34-ii35
Author(s):  
Manmeet Ahluwalia ◽  
David Peereboom ◽  
Yasmeen Rauf ◽  
Cathy Schilero ◽  
Marci Ciolfi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Phase Ii ◽  
Phase Ii Study ◽  
Progression Free Survival ◽  
Microtubule Organizing Center ◽  
Free Survival ◽  
Apoptosis Protein ◽  
Secondary Endpoints ◽  
First Recurrence

Abstract BACKGROUND Pembrolizumab is a potent humanized immunoglobulin G4 monoclonal antibody with high specificity of binding to the programmed cell death 1 (PD-1) receptor, thus inhibiting its interaction with programmed cell death ligand 2 (PD-L2). Survivin is a 16.5 kDa intracellular protein that belongs to the inhibitor of apoptosis protein (IAP) family. It acts in concert with the mitotic spindle apparatus to regulate cell division and localizes to the spindle microtubule organizing center (MTOC) during the G2/M phase of cell cycle progression. Survivin has also been shown to modulate the function of a number of terminal effector cell death proteases (caspases) leading to an inhibition of apoptosis. METHODS This is a Phase II study of two arms in patients with recurrent glioblastoma. Arm A is patients with first recurrence of glioblastoma who have failed prior chemotherapy and radiation but have not received any immunotherapy. Arm B is an exploratory arm of 10 patients who have failed prior anti-PD1 therapy. The ongoing study is a phase II clinical study with a 10 patient, toxicity run-in. All patients will receive the study drug combination consisting of SurVaxM and pembrolizumab with no randomization, stratification or dose escalation. RESULTS So far ten patients have been enrolled on the study as safety run in. Primary endpoint is Progression free survival at 6 months. Safety and tolerability of Pembrolizumab and SurVaxM, Response rates of Pembrolizumab and SurVaxM determined using RANO criteria are secondary endpoints. Additional secondary endpoints include Overall survival and Progression Free survival Exploratory endpoints include Cellular and humoral immune responses during concurrent administration of Pembrolizumab and SurVaxM. CONCLUSION This is an ongoing clinical trial.

scholarly journals Antileukemic Natural Product Induced Both Apoptotic and Pyroptotic Programmed Cell Death and Differentiation Effect

2021 ◽  
Vol 22 (20) ◽  
pp. 11239
Author(s):  
Wohn-Jenn Leu ◽  
Hsun-Shuo Chang ◽  
Ih-Sheng Chen ◽  
Jih-Hwa Guh ◽  
She-Hung Chan
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Electron Microscopic Examination ◽  
Leukemic Cells ◽  
Caspase 8 ◽  
Electron Microscopic ◽  
Medical Needs ◽  
Response To Chemotherapy ◽  
Apoptosis Protein ◽  
Induced Apoptosis

Acute myeloid leukemia (AML) is one of the most common forms of leukemia. Despite advances in the management of such malignancies and the progress of novel therapies, unmet medical needs still exist in AML because of several factors, including poor response to chemotherapy and high relapse rates. Ardisianone, a plant-derived natural component with an alkyl benzoquinone structure, induced apoptosis in leukemic HL-60 cells. The determination of dozens of apoptosis-related proteins showed that ardisianone upregulated death receptors and downregulated the inhibitor of apoptosis protein (IAPs). Western blotting showed that ardisianone induced a dramatic increase in tumor necrosis factor receptor 2 (TNFR2) protein expression. Ardisianone also induced downstream signaling by activating caspase-8 and -3 and degradation in Bid, a caspase-8 substrate. Furthermore, ardisianone induced degradation in DNA fragmentation factor 45 kDa (DFF45), a subunit of inhibitors of caspase-activated DNase (ICAD). Q-VD-OPh (a broad-spectrum caspase inhibitor) significantly diminished ardisianone-induced apoptosis, confirming the involvement of caspase-dependent apoptosis. Moreover, ardisianone induced pyroptosis. Using transmission electron microscopic examination and Western blot analysis, key markers including gasdermin D, high mobility group box1 (HMGB1), and caspase-1 and -5 were detected. Notably, ardisianone induced the differentiation of the remaining survival cells, which were characterized by an increase in the expression of CD11b and CD68, two markers of macrophages and monocytes. Wright–Giemsa staining also showed the differentiation of cells into monocyte and macrophage morphology. In conclusion, the data suggested that ardisianone induced the apoptosis and pyroptosis of leukemic cells through downregulation of IAPs and activation of caspase pathways that caused gasdermin D cleavage and DNA double-stranded breaks and ultimately led to programmed cell death. Ardisianone also induced the differentiation of leukemic cells into monocyte-like and macrophage-like cells. The data suggested the potential of ardisianone for further antileukemic development.

scholarly journals Changes in mycelial structure of Botrytis cinerea induced by removal of the glucan matrix

OENO One ◽  
2007 ◽  
Vol 41 (3) ◽  
pp. 149
Author(s):  
Nurit Bar-Nun ◽  
Annie L'Hyvernay ◽  
Bernard Donèche ◽  
Alfred M. Mayer
Keyword(s):  
Botrytis Cinerea ◽  
Fungal Pathogens ◽  
Extra Cellular Matrix ◽  
Fungal Mycelium ◽  
Fungal Virulence ◽  
Pathogenesis Related ◽  
Normal Diameter ◽  
Plant Pathogen Interactions ◽  
Related Proteins ◽  
Cellular Matrix

<p style="text-align: justify;"><strong>Aims</strong>: b-1,3-glucanase is one of the main pathogenesis related proteins of plants, involved in plant-pathogen interactions. Its effect on fungal pathogens is not entirely known. The hyphae of Botrytis cinerea are covered by an extra cellular matrix, mainly composed of a b-1,3-D-glucan. This matrix also contains a variety of enzymes, lipids and melanin which may play a role in fungal virulence.</p><p style="text-align: justify;"><strong>Methods and results</strong>: Cultures of Botrytis cinerea are made in presence of b-1,3-glucanase. The structure of the mycelium of Botrytis cinerea after exposure to b-1,3-glucanase during growth was examined by staining with Schiff's reagent and using the electron microscope. Without glucanase, hyphae have a normal diameter and were surrounded by a glucan matrix. Cytoplasm is dense and contains little vacuoles. The glucanase treatment removed most of the glucan sheath, but did not kill the fungus. The structure of the hyphae was changed by the treatment and their diameter increased. Membrane structure showed marked changes, the cytoplasm of the cells was less dense, but more inclusions were observed, including an increase in what appeared to be lipids.</p><p style="text-align: justify;"><strong>Conclusion</strong>: The appearance of the mycelium, whose glucan sheath has been removed, was that of cells under stress. The possible implications of the function of the glucan sheath during the interaction of Botrytis cinerea with its host during pathogenesis are discussed.</p><p style="text-align: justify;"><strong>Significance and impact of study</strong>: These changes following glucanase treatment would lead to a fungal mycelium which will be more sensitive to antifungal agents and might suggest ways of combating Botrytis infections by preventing the formation of the extra-cellular matrix.</p>

scholarly journals Multicopper Oxidases in Saccharomyces cerevisiae and Human Pathogenic Fungi

2020 ◽  
Vol 6 (2) ◽  
pp. 56
Author(s):  
Tanmoy Chakraborty ◽  
Renáta Tóth ◽  
Joshua D. Nosanchuk ◽  
Attila Gácser
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Environmental Conditions ◽  
Defense Mechanisms ◽  
Fungal Pathogens ◽  
Lignin Degradation ◽  
Pathogenic Fungi ◽  
Fungal Species ◽  
Multicopper Oxidases ◽  
Fungal Virulence ◽  
Physiological Processes

Multicopper oxidases (MCOs) are produced by microscopic and macroscopic fungal species and are involved in various physiological processes such as morphogenesis, lignin degradation, and defense mechanisms to stress inducing environmental conditions as well as fungal virulence. This review will summarize our current understanding regarding the functions of MCOs present in Saccharomyces cerevisiae and in different human fungal pathogens. Of the two main MCO groups, the first group of MCOs is involved in iron homoeostasis and the second includes laccases. This review will also discuss their role in the pathogenesis of human fungal pathogens.

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