The secreted lipase FGL1 is sufficient to restore the initial infection step to the apathogenic Fusarium graminearum MAP kinase disruption mutant Δgpmk1

2012 ◽  
Vol 134 (1) ◽  
pp. 23-37 ◽  
Author(s):  
Siegfried Salomon ◽  
Attila Gácser ◽  
Sebastian Frerichmann ◽  
Cathrin Kröger ◽  
Wilhelm Schäfer ◽  
...  
Keyword(s):  
Map Kinase ◽  
Fusarium Graminearum ◽  
Initial Infection ◽  
Disruption Mutant ◽  
Secreted Lipase

scholarly journals Resistance in Winter Wheat Lines to Initial Infection and Spread Within Spikes by Deoxynivalenol and Nivalenol Chemotypes of Fusarium graminearum

Plant Disease ◽  
2011 ◽  
Vol 95 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Peter Horevaj ◽  
Liane R. Gale ◽  
Eugene A. Milus
Keyword(s):  
United States ◽  
Winter Wheat ◽  
Fusarium Graminearum ◽  
The United States ◽  
Blight Resistance ◽  
Head Blight ◽  
Initial Infection ◽  
Additional Information ◽  
Progress Curve ◽  
Wheat Lines

Head blight of wheat in the United States is caused primarily by the deoxynivalenol (DON)-producing chemotype of Fusarium graminearum. However, the discovery of the nivalenol (NIV) chemotype of F. graminearum in Louisiana and Arkansas necessitates having resistance in wheat to both chemotypes. The objectives of this research were to quantify resistance of selected winter wheat lines to initial infection and pathogen spread within spikes, to determine whether wheat lines selected for resistance to the DON chemotype also have resistance to the NIV chemotype, and to improve the methods for quantifying resistance to initial infection. A susceptible check (Coker 9835) and 15 winter wheat lines, which are adapted to the southeastern United States and possess diverse sources of head blight resistance, were evaluated for head blight resistance in a series of greenhouse and growth-chamber experiments. Significant levels of resistance to both initial infection and spread within a spike were found among the lines, and lines with resistance to isolates of the DON chemotype had even higher levels of resistance to isolates of the NIV chemotype. Quantifying resistance to initial infection was improved by standardizing the inoculum and environmental conditions. Additional information related to resistance to spread within a spike was obtained by calculating the area under the disease progress curve from 7 to 21 days after inoculation.

scholarly journals Two oat genotypes with different field resistance to Fusarium head blight respond similarly to the infection at spikelet level

2020 ◽  
Author(s):  
Juho Hautsalo ◽  
Satu Latvala ◽  
Outi Manninen ◽  
Minna Haapalainen ◽  
Asko Hannukkala ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Fusarium Head Blight ◽  
Fusarium Graminearum ◽  
High Resistance ◽  
Field Resistance ◽  
Cultivar Resistance ◽  
Fresh Weight ◽  
Head Blight ◽  
Initial Infection ◽  
Resistance Sources

Abstract Cultivar resistance is essential for the management of Fusarium head blight (FHB) disease in oat production. However, the breeders lack methods suitable for phenotyping disease resistance and resistance sources. In this paper we compared two oat genotypes, a rejected variety BOR31 and a landrace VIR7766, with four different traits that could reflect resistance to FHB in a greenhouse environment. Spray and point inoculations were used to inoculate Fusarium graminearum into flowering oat plants. When spray-inoculated, VIR7766 was significantly more resistant against the initial infection than BOR31, measured by the number of Fusarium-infected kernels and by DON accumulation. In the point-inoculated oats, the loss of fresh weight in the inoculated spikelet correlated well with the increasing F. graminearum biomass in the spikelet, measured six days after inoculation. However, no difference in the growth of the fungus was observed between the tested oat genotypes by point inoculation. We speculate that once the infection is established, the ability of the oat plant to resist the spread of the infection within a spikelet is low in the genotypes studied, although oat, in general, due to its panicle structure, is considered to have a high resistance against Fusarium infection.

scholarly journals A secreted lipase of Fusarium graminearum is a virulence factor required for infection of cereals

2005 ◽  
Vol 42 (3) ◽  
pp. 364-375 ◽  
Author(s):  
Christian A. Voigt ◽  
Wilhelm Schäfer ◽  
Siegfried Salomon
Keyword(s):  
Fusarium Graminearum ◽  
Virulence Factor ◽  
Secreted Lipase

scholarly journals Characterization of Three Fusarium graminearum Effectors and Their Roles During Fusarium Head Blight

2020 ◽  
Vol 11 ◽  
Author(s):  
Guixia Hao ◽  
Susan McCormick ◽  
Thomas Usgaard ◽  
Helene Tiley ◽  
Martha M. Vaughan
Keyword(s):  
Fusarium Head Blight ◽  
Fusarium Graminearum ◽  
Early Stage ◽  
Expression Profiles ◽  
Plant Immunity ◽  
Resistant Variety ◽  
Deletion Mutants ◽  
Head Blight ◽  
Initial Infection ◽  
Significant Difference

Fusarium graminearum causes Fusarium head blight (FHB) on wheat, barley, and other grains. During infection, F. graminearum produces deoxynivalenol (DON), which contaminates grain and functions as a virulence factor to promote FHB spread throughout the wheat head. F. graminearum secretes hundreds of putative effectors, which can interfere with plant immunity to promote disease development. However, the function of most of these putative effectors remains unknown. In this study, we investigated the expression profiles of 23 F. graminearum effector-coding genes during the early stage of wheat head infection. Gene expression analyses revealed that three effectors, FGSG_01831, FGSG_03599, and FGSG_12160, respectively, were highly induced in both a FHB susceptible and a moderately resistant variety. We generated deletion mutants for these effector genes and performed FHB virulence assays on wheat head using point and dip inoculations to evaluate FHB spread and initial infection. No statistically significant difference in FHB spread was observed in the deletion mutants. However, deletion mutants Δ01831 displayed a significant reduction in initial infection, and thus resulted in less DON contamination. To investigate the potential mechanisms involved, these three effectors were transiently expressed in Nicotiana benthamiana leaves. N. benthamiana leaves expressing these individual effectors had significantly reduced production of reactive oxygen species induced by chitin, but not by flg22. Furthermore, FGSG_01831 and FGSG_03599 markedly suppressed Bax-induced cell death when co-expressed with Bax in N. benthamiana leaves. Our study provides new insights into the functions of these effectors and suggests they play collective or redundant roles that likely ensure the successful plant infection.

scholarly journals Map kinase MGV1: a potential shared control point of butenolide and deoxynivalenol biosynthesis In Fusarium graminearum

2011 ◽  
Vol 64 (1) ◽  
Author(s):  
Christof Rampitsch ◽  
Winnie Leung ◽  
Barbara Blackwell ◽  
Rajagopal Subramaniam
Keyword(s):  
Map Kinase ◽  
Fusarium Graminearum ◽  
Control Point ◽  
Shared Control

scholarly journals RAS2 Regulates Growth and Pathogenesis in Fusarium graminearum

2007 ◽  
Vol 20 (6) ◽  
pp. 627-636 ◽  
Author(s):  
B. H. Bluhm ◽  
X. Zhao ◽  
J. E. Flaherty ◽  
J.-R. Xu ◽  
L. D. Dunkle
Keyword(s):  
Map Kinase ◽  
Fusarium Graminearum ◽  
Intracellular Camp ◽  
Ras Gtpases ◽  
Solid Media ◽  
Mitogen Activated Protein ◽  
Morphological Defects ◽  
A Minor ◽  
Exogenous Treatment

Fusarium graminearum is a ubiquitous pathogen of cereal crops, including wheat, barley, and maize. Diseases caused by F. graminearum are of particular concern because harvested grains frequently are contaminated with harmful mycotoxins such as deoxynivalenol (DON). In this study, we explored the role of Ras GTPases in pathogenesis. The genome of F. graminearum contains two putative Ras GTPase-encoding genes. The two genes (RAS1 and RAS2) showed different patterns of expression under different conditions of nutrient availability and in various mutant backgrounds. RAS2 was dispensable for survival but, when disrupted, caused a variety of morphological defects, including slower growth on solid media, delayed spore germination, and significant reductions in virulence on wheat heads and maize silks. Intracellular cAMP levels were not affected by deletion of RAS2 and exogenous treatment of the ras2 mutant with cAMP did not affect phenotypic abnormalities, thus indicating that RAS2 plays a minor or no role in cAMP signaling. However, phosphorylation of the mitogen-activated protein (MAP) kinase Gpmk1 and expression of a secreted lipase (FGL1) required for infection were reduced significantly in the ras2 mutant. Based on these observations, we hypothesize that RAS2 regulates growth and virulence in F. graminearum by regulating the Gpmk1 MAP kinase pathway.

scholarly journals A secreted lipase encoded by LIP1 is necessary for efficient use of saturated triglyceride lipids in Fusarium graminearum

Microbiology ◽  
2005 ◽  
Vol 151 (12) ◽  
pp. 3911-3921 ◽  
Author(s):  
Jie Feng ◽  
Guosheng Liu ◽  
Gopalan Selvaraj ◽  
Geoffrey R. Hughes ◽  
Yangdou Wei
Keyword(s):  
Fusarium Graminearum ◽  
Minimal Medium ◽  
Lipolytic Activity ◽  
Saturated Fatty Acids ◽  
Candida Rugosa ◽  
Yeast Cells ◽  
Wall Material ◽  
Wild Type ◽  
Saturated Triglyceride ◽  
Secreted Lipase

A triglyceride lipase gene LIP1 was identified in the genome of Fusarium graminearum strain PH-1. The predicted protein encoded by LIP1 contains 591 amino acid residues with a putative N-terminal signal peptide and shows 57 and 40–44 % identity to a Botrytis cinerea lipase and five Candida rugosa lipases, respectively. Yeast cells overexpressing LIP1 showed lipolytic activity against a broad range of triglyceride substrates. Northern blot analyses revealed that expression of LIP1 was activated in planta during the fungal infection process. LIP1 expression was strongly induced in minimal medium supplemented with wheatgerm oil, but only weakly induced by olive oil and triolein. In contrast, supplementation with other carbon sources, including glucose, sucrose, apple pectin and wheat cell-wall material, did not induce LIP1 expression. Saturated fatty acids were the strongest inducers for LIP1 expression and this induction was suppressed proportionally by the presence of the unsaturated fatty acid. To determine the potential function of LIP1, gene replacement was conducted on strain PH-1. When compared with wild-type PH-1, ΔLIP1 mutants showed greatly reduced lipolytic activities at the early stage of incubation on minimal medium supplemented with either saturated or unsaturated lipid as the substrate, indicating that LIP1 encodes a secreted lipase for exogenous lipid hydrolysis. Moreover, the ΔLIP1 mutants exhibited growth deficiency on both liquid and solid minimal media supplemented with the saturated triglyceride tristearin as the sole carbon source, suggesting that LIP1 is required for utilization of this substance. Despite these differences, no variation in disease symptoms between the ΔLIP1 mutants and the wild-type strain was observed on susceptible cereal hosts.

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