Auxin, abscisic acid and jasmonate are the central players in rice sheath rot caused by Sarocladium oryzae and Pseudomonas fuscovaginae

Abstract Sheath rot is an emerging rice disease that causes severe yield losses worldwide. The main causal agents are the toxin producers Sarocladium oryzae and Pseudomonas fuscovaginae. The fungus S. oryzae produces helvolic acid and cerulenin and the bacterium P. fuscovaginae produces cyclic lipopeptides. Helvolic acid and the lipopeptide, fuscopeptin, inhibit membrane-bound H+-ATPase pumps in the rice plant. To manage rice sheath rot, a better understanding of the host response and virulence strategies of the pathogens is required. This study investigated the interaction of the sheath rot pathogens with their host and the role of their toxins herein. Japonica rice was inoculated with high- and low-helvolic acid-producing S. oryzae isolates or with P. fuscovaginae wild type and fuscopeptin mutant strains. During infection, cerulenin, helvolic acid and the phytohormones abscisic acid, jasmonate, auxin and salicylic acid were quantified in the sheath. In addition, disease severity and grain yield parameters were assessed. Rice plants responded to high-toxin-producing S. oryzae and P. fuscovaginae strains with an increase in abscisic acid, jasmonate and auxin levels. We conclude that, for both pathogens, toxins play a core role during sheath rot infection. S. oryzae and P. fuscovaginae interact with their host in a similar way. This may explain why both sheath rot pathogens cause very similar symptoms despite their different nature.

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Auxin, Abscisic Acid and Jasmonate Are the Central Players in Rice Sheath Rot Caused by Sarocladium oryzae and Pseudomonas fuscovaginae

Rice ◽

10.1186/s12284-020-00438-9 ◽

2020 ◽

Vol 13 (1) ◽

Author(s):

K. J. Peeters ◽

M. Ameye ◽

K. Demeestere ◽

K. Audenaert ◽

M. Höfte

Keyword(s):

Abscisic Acid ◽

Host Response ◽

Wild Type ◽

Yield Parameters ◽

Mutant Strains ◽

Rice Disease ◽

Membrane Bound ◽

Helvolic Acid ◽

Sheath Rot

AbstractSheath rot is an emerging rice disease that causes severe yield losses worldwide. The main causal agents are the toxin producers Sarocladium oryzae and Pseudomonas fuscovaginae. The fungus S. oryzae produces helvolic acid and cerulenin and the bacterium P. fuscovaginae produces cyclic lipopeptides. Helvolic acid and the lipopeptide, fuscopeptin, inhibit membrane-bound H+-ATPase pumps in the rice plant. To manage rice sheath rot, a better understanding of the host response and virulence strategies of the pathogens is required. This study investigated the interaction of the sheath rot pathogens with their host and the role of their toxins herein. Japonica rice was inoculated with high- and low-helvolic acid-producing S. oryzae isolates or with P. fuscovaginae wild type and fuscopeptin mutant strains. During infection, cerulenin, helvolic acid and the phytohormones abscisic acid, jasmonate, auxin and salicylic acid were quantified in the sheath. In addition, disease severity and grain yield parameters were assessed. Rice plants responded to high-toxin-producing S. oryzae and P. fuscovaginae strains with an increase in abscisic acid, jasmonate and auxin levels. We conclude that, for both pathogens, toxins play a core role during sheath rot infection. S. oryzae and P. fuscovaginae interact with their host in a similar way. This may explain why both sheath rot pathogens cause very similar symptoms despite their different nature.

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Auxin, abscisic acid and jasmonate are the central players in rice sheath rot caused by Sarocladium oryzae and Pseudomonas fuscovaginae

10.21203/rs.3.rs-44971/v2 ◽

2020 ◽

Author(s):

Kaat Peeters ◽

Maarten Ameye ◽

Kristof Demeestere ◽

Kris Audenaert ◽

Monica Hofte

Keyword(s):

Abscisic Acid ◽

Host Response ◽

Wild Type ◽

Yield Parameters ◽

Mutant Strains ◽

Rice Disease ◽

Membrane Bound ◽

Helvolic Acid ◽

Sheath Rot

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Genetic and Phenotypic Analyses of therdx Locus of Rhodobacter sphaeroides2.4.1

Journal of Bacteriology ◽

10.1128/jb.182.12.3475-3481.2000 ◽

2000 ◽

Vol 182 (12) ◽

pp. 3475-3481 ◽

Cited By ~ 15

Author(s):

Jung Hyeob Roh ◽

Samuel Kaplan

Keyword(s):

Gene Expression ◽

Rhodobacter Sphaeroides ◽

Redox Protein ◽

Deletion Mutations ◽

Metal Transporter ◽

New Class ◽

Mutant Strains ◽

Membrane Bound ◽

Photosynthesis Gene

ABSTRACT Previously, we reported that rdxB, encoding a likely membrane-bound two [4Fe-4S]-containing center, is involved in the aerobic regulation of photosystem gene expression in Rhodobacter sphaeroides 2.4.1. To further investigate the role ofrdxB as well as other genes of the rdxBHISoperon on photosystem gene expression, we constructed a series of nonpolar, in-frame deletion mutations in each of the rdxgenes. Using both puc and puf operonlacZ fusions to monitor photosystem gene expression, under aerobic conditions, in each of the mutant strains revealed significant increased photosynthesis gene expression. In the case of mutations in either rdxH, rdxI, or rdxS, the aerobic induction of photosystem gene expression is believed to be indirect by virtue of a posttranscriptional effect oncbb 3 cytochrome oxidase structure and integrity. For RdxB, we suggest that this redox protein has a more direct effect on photosystem gene expression by virtue of its interaction with the cbb 3 oxidase. An associated phenotype, involving the enhanced conversion of the carotenoid spheroidene to spheroidenone, is also observed in the RdxB, -H, -I, and -S mutant strains. This phenotype is also suggested to be the result of the role of the rdxBHIS locus incbb 3 oxidase activity and/or structure. RdxI is suggested to be a new class of metal transporter of the CPx-type ATPases.

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CCSP modulates airway dysfunction and host responses in an Ova-challenged mouse model

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2001.281.5.l1303 ◽

2001 ◽

Vol 281 (5) ◽

pp. L1303-L1311 ◽

Cited By ~ 38

Author(s):

Shan-Ze Wang ◽

Cynthia L. Rosenberger ◽

Teresa M. Espindola ◽

Edward G. Barrett ◽

Yohannes Tesfaigzi ◽

...

Keyword(s):

Airway Epithelium ◽

Host Response ◽

Secretory Protein ◽

Allergic Airway Disease ◽

Clara Cell ◽

Myeloperoxidase Activity ◽

Wild Type ◽

Airway Reactivity ◽

Mucus Production

Clara cell secretory protein (CCSP) is synthesized by nonciliated bronchiolar cells in the lung and modulates lung inflammation to infection. To determine the role of CCSP in the host response to allergic airway disease, CCSP-deficient [(−/−)] mice were immunized twice with ovalbumin (Ova) and challenged by Ova (2 or 5 mg/m3) aerosol. After 2, 3, and 5 days of Ova aerosol challenge (6 h/day), airway reactivity was increased in CCSP(−/−) mice compared with wild-type [CCSP(+/+)] mice. Neutrophils were markedly increased in the bronchoalveolar lavage fluid of CCSP(−/−) Ova mice, coinciding with increased myeloperoxidase activity and macrophage inflammatory protein-2 levels. Lung histopathology and inflammation were increased in CCSP(−/−) compared with wild-type mice after Ova challenge. Mucus production, as assessed by histological staining, was increased in the airway epithelium of CCSP(−/−) Ova mice compared with that in CCSP(+/+) Ova mice. These data suggest a role for CCSP in airway reactivity and the host response to allergic airway inflammation and provide further evidence for the role of the airway epithelium in regulating airway responses in allergic disease.

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Pneumococcal Surface Protein C Contributes to Sepsis Caused by Streptococcus pneumoniae in Mice

Infection and Immunity ◽

10.1128/iai.72.5.3077-3080.2004 ◽

2004 ◽

Vol 72 (5) ◽

pp. 3077-3080 ◽

Cited By ~ 47

Author(s):

Francesco Iannelli ◽

Damiana Chiavolini ◽

Susanna Ricci ◽

Marco Rinaldo Oggioni ◽

Gianni Pozzi

Keyword(s):

Streptococcus Pneumoniae ◽

Protein C ◽

Lethal Dose ◽

Surface Protein ◽

Infection Model ◽

Wild Type ◽

Mutant Strains ◽

Type 3

ABSTRACT The role of pneumococcal surface protein C (PspC; also called SpsA, CbpA, and Hic) in sepsis by Streptococcus pneumoniae was investigated in a murine infection model. The pspC gene was deleted in strains D39 (type 2) and A66 (type 3), and the mutants were tested by being injected intravenously into mice. The animals infected with the mutant strains showed a significant increase in survival, with the 50% lethal dose up to 250-fold higher than that for the wild type. Our findings indicate that PspC affords a decisive contribution to sepsis development.

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Expression of Mycobacterium smegmatisPyrazinamidase in Mycobacterium tuberculosis Confers Hypersensitivity to Pyrazinamide and Related Amides

Journal of Bacteriology ◽

10.1128/jb.182.19.5479-5485.2000 ◽

2000 ◽

Vol 182 (19) ◽

pp. 5479-5485 ◽

Cited By ~ 34

Author(s):

Helena I. M. Boshoff ◽

Valerie Mizrahi

Keyword(s):

Mycobacterium Tuberculosis ◽

Mycobacterium Smegmatis ◽

Intracellular Localization ◽

Wild Type ◽

Gene Encoding ◽

Allelic Exchange ◽

Mutant Strains ◽

Established Role ◽

Amidase Gene

ABSTRACT A pyrazinamidase (PZase)-deficient pncA mutant ofMycobacterium tuberculosis, constructed by allelic exchange, was used to investigate the effects of heterologous amidase gene expression on the susceptibility of this organism to pyrazinamide (PZA) and related amides. The mutant was highly resistant to PZA (MIC, >2,000 μg/ml), in accordance with the well-established role ofpncA in the PZA susceptibility of M. tuberculosis (A. Scorpio and Y. Zhang, Nat. Med. 2:662–667, 1996). Integration of the pzaA gene encoding the major PZase/nicotinamidase from Mycobacterium smegmatis (H. I. M. Boshoff and V. Mizrahi, J. Bacteriol. 180:5809–5814, 1998) or the M. tuberculosis pncA gene into the pncAmutant complemented its PZase/nicotinamidase defect. In bothpzaA- and pncA-complemented mutant strains, the PZase activity was detected exclusively in the cytoplasm, suggesting an intracellular localization for PzaA and PncA. ThepzaA-complemented strain was hypersensitive to PZA (MIC, ≤10 μg/ml) and nicotinamide (MIC, ≥20 μg/ml) and was also sensitive to benzamide (MIC, 20 μg/ml), unlike the wild-type andpncA-complemented mutant strains, which were highly resistant to this amide (MIC, >500 μg/ml). This finding was consistent with the observation that benzamide is hydrolyzed by PzaA but not by PncA. Overexpression of PzaA also conferred sensitivity to PZA, nicotinamide, and benzamide on M. smegmatis (MIC, 150 μg/ml in all cases) and rendered Escherichia colihypersensitive for growth at low pH.

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Role of CpALS4790 and CpALS0660 in Candida parapsilosis Virulence: Evidence from a Murine Model of Vaginal Candidiasis

Journal of Fungi ◽

10.3390/jof6020086 ◽

2020 ◽

Vol 6 (2) ◽

pp. 86

Author(s):

Marina Zoppo ◽

Fabrizio Fiorentini ◽

Cosmeri Rizzato ◽

Mariagrazia Di Luca ◽

Antonella Lupetti ◽

...

Keyword(s):

Cell Wall ◽

Murine Model ◽

Type Strain ◽

Wild Type Strain ◽

Candida Parapsilosis ◽

Vaginal Candidiasis ◽

Phenotypic Characterization ◽

Wild Type ◽

Mutant Strains

The Candida parapsilosis genome encodes for five agglutinin-like sequence (Als) cell-wall glycoproteins involved in adhesion to biotic and abiotic surfaces. The work presented here is aimed at analyzing the role of the two still uncharacterized ALS genes in C. parapsilosis, CpALS4790 and CpALS0660, by the generation and characterization of CpALS4790 and CpALS066 single mutant strains. Phenotypic characterization showed that both mutant strains behaved as the parental wild type strain regarding growth rate in liquid/solid media supplemented with cell-wall perturbing agents, and in the ability to produce pseudohyphae. Interestingly, the ability of the CpALS0660 null mutant to adhere to human buccal epithelial cells (HBECs) was not altered when compared with the wild-type strain, whereas deletion of CpALS4790 led to a significant loss of the adhesion capability. RT-qPCR analysis performed on the mutant strains in co-incubation with HBECs did not highlight significant changes in the expression levels of others ALS genes. In vivo experiments in a murine model of vaginal candidiasis indicated a significant reduction in CFUs recovered from BALB/C mice infected with each mutant strain in comparison to those infected with the wild type strain, confirming the involvement of CpAls4790 and CpAls5600 proteins in C. parapsilosis vaginal candidiasis in mice.

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Role of FAD-I in Fusobacterial Interspecies Interaction and Biofilm Formation

Microorganisms ◽

10.3390/microorganisms8010070 ◽

2020 ◽

Vol 8 (1) ◽

pp. 70 ◽

Cited By ~ 1

Author(s):

Bhumika Shokeen ◽

Jane Park ◽

Emily Duong ◽

Sonam Rambhia ◽

Manash Paul ◽

...

Keyword(s):

Biofilm Formation ◽

Fusobacterium Nucleatum ◽

Interspecies Interaction ◽

Wild Type ◽

Oral Epithelial Cells ◽

Small Proteins ◽

Mutant Strains ◽

Oral Epithelial ◽

Wild Type Parent

RadD, a major adhesin of oral fusobacteria, is part of a four-gene operon encoding the small lipoprotein FAD-I and two currently uncharacterized small proteins encoded by the rapA and rapB genes. Previously, we described a role for FAD-I in the induction of human B-defensin 2 (hBD2) upon contact with oral epithelial cells. Here, we investigated potential roles for fad-I, rapA, and rapB in interspecies interaction and biofilm formation. Gene inactivation mutants were generated for each of these genes in the nucleatum and polymorphum subspecies of Fusobacterium nucleatum and characterized for their adherence to partner species, biofilm formation, and operon transcription. Binding to Streptococcus gordonii was increased in all mutant strains with Δfad-I having the most significant effect. This increased adherence was directly proportional to elevated radD transcript levels and resulted in significantly different architecture and height of the biofilms formed by Δfad-I and S. gordonii compared to the wild-type parent. In conclusion, FAD-I is important for fusobacterial interspecies interaction as its lack leads to increased production of the RadD adhesin suggesting a role of FAD-I in its regulation. This regulatory effect does not require the presence of functional RadD.

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The RcsCB His-Asp Phosphorelay System Is Essential To Overcome Chlorpromazine-Induced Stress in Escherichia coli

Journal of Bacteriology ◽

10.1128/jb.184.10.2850-2853.2002 ◽

2002 ◽

Vol 184 (10) ◽

pp. 2850-2853 ◽

Cited By ~ 39

Author(s):

Annie Conter ◽

Rachel Sturny ◽

Claude Gutierrez ◽

Kaymeuang Cam

Keyword(s):

Escherichia Coli ◽

Type Strain ◽

Wild Type Strain ◽

Cell Envelope ◽

Wild Type ◽

E Coli ◽

Induced Stress ◽

Mutant Strains ◽

Molecular Nature

ABSTRACT The RcsCB His-Asp phosphorelay system regulates the expression of several genes of Escherichia coli, but the molecular nature of the inducing signal is still unknown. We show here that treatment of an exponentially growing culture of E. coli with the cationic amphipathic compound chlorpromazine (CPZ) stimulates expression of a set of genes positively regulated by the RcsCB system. This induction is abolished in rcsB or rcsC mutant strains. In addition, treatment with CPZ inhibits growth. The wild-type strain is able to recover from this inhibition and resume growth after a period of adaptation. In contrast, strains deficient in the RcsCB His-Asp phosphorelay system are hypersensitive to CPZ. These results suggest that cells must express specific RcsCB-regulated genes in order to cope with the CPZ-induced stress. This is the first report of the essential role of the RcsCB system in a stress situation. These results also strengthen the notion that alterations of the cell envelope induce a signal recognized by the RcsC sensor.

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Survival of the fittest: How the rice microbial community forces Sarocladium oryzae into pathogenicity

FEMS Microbiology Ecology ◽

10.1093/femsec/fiaa253 ◽

2020 ◽

Author(s):

K J Peeters ◽

K Audenaert ◽

M Höfte

Keyword(s):

Null Model ◽

Toxin Production ◽

Pairwise Interactions ◽

Helvolic Acid ◽

Community Forces ◽

Survival Of The Fittest ◽

Endophyte Community ◽

Rice Endophytes ◽

Sheath Rot

ABSTRACT The fungus Sarocladium oryzae (Sawada) causes rice sheath rot and produces the phytotoxins cerulenin and helvolic acid. Both toxins show antimicrobial activity but only helvolic acid production in the rice sheath correlates with virulence. S. oryzae isolates that differ in their toxin production were used to study their interaction with the rice culturable bacterial endophyte community. The diversity and community structure was defined in the edge of sheath rot lesions, followed by a null model-based co-occurrence analysis to discover pairwise interactions. Non-random pairs were co-cultured to study the nature of the interactions and the role of the toxins herein. Compared to healthy sheaths, endophyte diversity strongly increased when infected with the least virulent S. oryzae isolates producing low amounts of toxins. Virulent S. oryzae isolates did not affect diversity but caused strong shifts in species composition. The endophyte community of healthy rice plants was dominated by B. cereus. This bacterium was enriched in lesions produced by low-virulent S. oryzae isolates and caused hyphal lysis. Contrarily, helvolic acid producers eliminated this bacterium from the sheath endosphere. We conclude that S. oryzae needs to produce antibiotics to defend itself against antagonistic rice endophytes to successfully colonize and infect the rice sheath.

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