scholarly journals The VELVET Complex in the Gray Mold Fungus Botrytis cinerea: Impact of BcLAE1 on Differentiation, Secondary Metabolism, and Virulence

2015 ◽  
Vol 28 (6) ◽  
pp. 659-674 ◽  
Author(s):  
Julia Schumacher ◽  
Adeline Simon ◽  
Kim C. Cohrs ◽  
Stefanie Traeger ◽  
Antoine Porquier ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Natural Variation ◽  
Target Genes ◽  
Gray Mold ◽  
Carbohydrate Active Enzymes ◽  
Genome Wide ◽  
Mold Fungus ◽  
Velvet Complex ◽  
Genome Wide Expression ◽  
Insight Into

Botrytis cinerea, the gray mold fungus, is an important plant pathogen. Field populations are characterized by variability with regard to morphology, the mode of reproduction (conidiation or sclerotia formation), the spectrum of secondary metabolites (SM), and virulence. Natural variation in bcvel1 encoding the ortholog of Aspergillus nidulans VeA, a member of the VELVET complex, was previously shown to affect light-dependent differentiation, the formation of oxalic acid (OA), and virulence. To gain broader insight into the B. cinerea VELVET complex, an ortholog of A. nidulans LaeA, BcLAE1, a putative interaction partner of BcVEL1, was studied. BcVEL1 but not its truncated versions interacts with BcLAE1 and BcVEL2 (VelB ortholog). In accordance with the expected common as well as specific functions of BcVEL1 and BcLAE1, the deletions of both genes result in similar though not identical phenotypes. Both mutants lost the ability to produce OA, to colonize the host tissue, and to form sclerotia. However, mutants differ with regard to aerial hyphae and conidia formation. Genome-wide expression analyses revealed that BcVEL1 and BcLAE1 have common and distinct target genes. Some of the genes that are underexpressed in both mutants, e.g., those encoding SM-related enzymes, proteases, and carbohydrate-active enzymes, may account for their reduced virulence.

scholarly journals Analysis of the Molecular Dialogue Between Gray Mold (Botrytis cinerea) and Grapevine (Vitis vinifera) Reveals a Clear Shift in Defense Mechanisms During Berry Ripening

2015 ◽  
Vol 28 (11) ◽  
pp. 1167-1180 ◽  
Author(s):  
Jani Kelloniemi ◽  
Sophie Trouvelot ◽  
Marie-Claire Héloir ◽  
Adeline Simon ◽  
Bérengère Dalmais ◽  
...  
Keyword(s):  
Cell Wall ◽  
Botrytis Cinerea ◽  
Defense Mechanisms ◽  
Plant Cell Wall ◽  
Quantitative Polymerase Chain Reaction ◽  
Gray Mold ◽  
Ros Generation ◽  
Genome Wide ◽  
Mold Fungus ◽  
Berry Ripening

Mature grapevine berries at the harvesting stage (MB) are very susceptible to the gray mold fungus Botrytis cinerea, while veraison berries (VB) are not. We conducted simultaneous microscopic and transcriptomic analyses of the pathogen and the host to investigate the infection process developed by B. cinerea on MB versus VB, and the plant defense mechanisms deployed to stop the fungus spreading. On the pathogen side, our genome-wide transcriptomic data revealed that B. cinerea genes upregulated during infection of MB are enriched in functional categories related to necrotrophy, such as degradation of the plant cell wall, proteolysis, membrane transport, reactive oxygen species (ROS) generation, and detoxification. Quantitative-polymerase chain reaction on a set of representative genes related to virulence and microscopic observations further demonstrated that the infection is also initiated on VB but is stopped at the penetration stage. On the plant side, genome-wide transcriptomic analysis and metabolic data revealed a defense pathway switch during berry ripening. In response to B. cinerea inoculation, VB activated a burst of ROS, the salicylate-dependent defense pathway, the synthesis of the resveratrol phytoalexin, and cell-wall strengthening. On the contrary, in infected MB, the jasmonate-dependent pathway was activated, which did not stop the fungal necrotrophic process.

scholarly journals Cyclophilin BcCyp2 Regulates Infection-Related Development to Facilitate Virulence of the Gray Mold Fungus Botrytis cinerea

2021 ◽  
Vol 22 (4) ◽  
pp. 1694
Author(s):  
Jiao Sun ◽  
Chen-Hao Sun ◽  
Hao-Wu Chang ◽  
Song Yang ◽  
Yue Liu ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Gray Mold ◽  
Gene Encoding ◽  
Histone 3 ◽  
Mold Fungus ◽  
Related Development ◽  
Hyphal Morphology ◽  
Cellular Components

Cyclophilin (Cyp) and Ca2+/calcineurin proteins are cellular components related to fungal morphogenesis and virulence; however, their roles in mediating the pathogenesis of Botrytis cinerea, the causative agent of gray mold on over 1000 plant species, remain largely unexplored. Here, we show that disruption of cyclophilin gene BcCYP2 did not impair the pathogen mycelial growth, osmotic and oxidative stress adaptation as well as cell wall integrity, but delayed conidial germination and germling development, altered conidial and sclerotial morphology, reduced infection cushion (IC) formation, sclerotial production and virulence. Exogenous cyclic adenosine monophosphate (cAMP) rescued the deficiency of IC formation of the ∆Bccyp2 mutants, and exogenous cyclosporine A (CsA), an inhibitor targeting cyclophilins, altered hyphal morphology and prevented host-cell penetration in the BcCYP2 harboring strains. Moreover, calcineurin-dependent (CND) genes are differentially expressed in strains losing BcCYP2 in the presence of CsA, suggesting that BcCyp2 functions in the upstream of cAMP- and Ca2+/calcineurin-dependent signaling pathways. Interestingly, during IC formation, expression of BcCYP2 is downregulated in a mutant losing BcJAR1, a gene encoding histone 3 lysine 4 (H3K4) demethylase that regulates fungal development and pathogenesis, in B. cinerea, implying that BcCyp2 functions under the control of BcJar1. Collectively, our findings provide new insights into cyclophilins mediating the pathogenesis of B. cinerea and potential targets for drug intervention for fungal diseases.

Promotion of Tomato Growth by the Volatiles Produced by the Hypovirulent Strain QT5-19 of the Plant Gray Mold Fungus Botrytis cinerea

2021 ◽  
pp. 126731
Author(s):  
Md Kamaruzzaman ◽  
Ze Wang ◽  
Mingde Wu ◽  
Long Yang ◽  
Yongchao Han ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Gray Mold ◽  
Mold Fungus ◽  
Hypovirulent Strain ◽  
Tomato Growth

scholarly journals The BMP1 Gene Is Essential for Pathogenicity in the Gray Mold Fungus Botrytis cinerea

2000 ◽  
Vol 13 (7) ◽  
pp. 724-732 ◽  
Author(s):  
Li Zheng ◽  
Mathew Campbell ◽  
Jennifer Murphy ◽  
Stephen Lam ◽  
Jin-Rong Xu
Keyword(s):  
Growth Rate ◽  
Map Kinase ◽  
Botrytis Cinerea ◽  
Magnaporthe Grisea ◽  
Pathogenic Fungi ◽  
Gray Mold ◽  
Necrotrophic Pathogen ◽  
Kinase Gene ◽  
Plant Infection ◽  
Mold Fungus

In Magnaporthe grisea, a well-conserved mitogen-activated protein (MAP) kinase gene, PMK1, is essential for fungal pathogenesis. In this study, we tested whether the same MAP kinase is essential for plant infection in the gray mold fungus Botrytis cinerea, a necrotrophic pathogen that employs infection mechanisms different from those of M. grisea. We used a polymerase chain reaction-based approach to isolate MAP kinase homologues from B. cinerea. The Botrytis MAP kinase required for pathogenesis (BMP) MAP kinase gene is highly homologous to the M. grisea PMK1. BMP1 is a single-copy gene. bmp1 gene replacement mutants produced normal conidia and mycelia but were reduced in growth rate on nutrient-rich medium. bmp1 mutants were nonpathogenic on carnation flowers and tomato leaves. Re-introduction of the wild-type BMP1 allele into the bmp1 mutant restored both normal growth rate and pathogenicity. Further studies indicated that conidia from bmp1 mutants germinated on plant surfaces but failed to penetrate and macerate plant tissues. bmp1 mutants also appeared to be defective in infecting through wounds. These results indicated that BMP1 is essential for plant infection in B. cinerea, and this MAP kinase pathway may be widely conserved in pathogenic fungi for regulating infection processes.

scholarly journals Identification of Pathogenesis-Associated Genes by T-DNA–Mediated Insertional Mutagenesis in Botrytis cinerea: A Type 2A Phosphoprotein Phosphatase and an SPT3 Transcription Factor Have Significant Impact on Virulence

2012 ◽  
Vol 25 (4) ◽  
pp. 481-495 ◽  
Author(s):  
S. Giesbert ◽  
J. Schumacher ◽  
V. Kupas ◽  
J. Espino ◽  
N. Segmüller ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Protein Phosphatase ◽  
Insertional Mutagenesis ◽  
Single Copy ◽  
Gene Replacement ◽  
Gray Mold ◽  
Dna Integration ◽  
Bean Plants ◽  
Mold Fungus ◽  
Border Sequence

Agrobacterium tumefaciens–mediated transformation (ATMT) was used to generate an insertional mutant library of the gray mold fungus Botrytis cinerea. From a total of 2,367 transformants, 68 mutants showing significant reduction in virulence on tomato and bean plants were analyzed in detail. As reported for other fungal ATMT libraries, integrations were mostly single copy, occurred preferentially in noncoding (regulatory) regions, and were frequently accompanied by small deletions of the target sequences and loss of parts of the border sequence. Two T-DNA integration events that were found to be linked to virulence were characterized in more detail: a catalytic subunit of a PP2A serine/threonine protein phosphatase (BcPP2Ac) and the SPT3 subunit of a Spt-Ada-Gcn5-acetyltransferase (SAGA-like) transcriptional regulator complex. Gene replacement and silencing approaches revealed that both Bcpp2Ac and SPT3 are crucial for virulence, growth, and differentiation as well as for resistance to H2O2 in B. cinerea.

scholarly journals Involvement of the Autophagy Protein Atg6 in Development and Virulence in the Gray Mold Fungus Botrytis cinerea

2021 ◽  
Vol 12 ◽  
Author(s):  
Na Liu ◽  
Shanyue Zhou ◽  
Baohua Li ◽  
Weichao Ren
Keyword(s):  
Botrytis Cinerea ◽  
Biological Function ◽  
Gray Mold ◽  
Economic Losses ◽  
Related Protein ◽  
Targeted Deletion ◽  
Cellular Processes ◽  
Mold Fungus ◽  
Evolutionarily Conserved ◽  
Sclerotial Formation

Gray mold caused by Botrytis cinerea is a devastating disease that leads to huge economic losses worldwide. Autophagy is an evolutionarily conserved process that maintains intracellular homeostasis through self-eating. In this study, we identified and characterized the biological function of the autophagy-related protein Atg6 in B. cinerea. Targeted deletion of the BcATG6 gene showed block of autophagy and several phenotypic defects in aspects of mycelial growth, conidiation, sclerotial formation and virulence. All of the phenotypic defects were restored by targeted gene complementation. Taken together, these results suggest that BcAtg6 plays important roles in the regulation of various cellular processes in B. cinerea.

Genome-wide expression profiling of A3243G MELAS patients in quest for potential disease-modifying target genes

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
S Mende ◽  
A Herr ◽  
J Schmiedel ◽  
M Deschauer ◽  
T Klopstock ◽  
...  
Keyword(s):  
Expression Profiling ◽  
Target Genes ◽  
Genome Wide ◽  
Disease Modifying ◽  
Genome Wide Expression

scholarly journals Genome-wide Mapping of the Coactivator Ada2p Yields Insight into the Functional Roles of SAGA/ADA Complex inCandida albicans

2009 ◽  
Vol 20 (9) ◽  
pp. 2389-2400 ◽  
Author(s):  
Adnane Sellam ◽  
Christopher Askew ◽  
Elias Epp ◽  
Hugo Lavoie ◽  
Malcolm Whiteway ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Resistance Genes ◽  
Target Genes ◽  
Transferase Activity ◽  
Histone Acetyl Transferase ◽  
Functional Roles ◽  
Cellular Processes ◽  
Oxidative Resistance ◽  
Genome Wide ◽  
Insight Into

The SAGA/ADA coactivator complex, which regulates numerous cellular processes by coordinating histone acetylation, is widely conserved throughout eukaryotes, and analysis of the Candida albicans genome identifies the components of this complex in the fungal pathogen. We investigated the multiple functions of SAGA/ADA in C. albicans by determining the genome-wide occupancy of Ada2p using chromatin immunoprecipitation (ChIP). Ada2p is recruited to 200 promoters upstream of genes involved in different stress-response functions and metabolic processes. Phenotypic and transcriptomic analysis of ada2 mutant showed that Ada2p is required for the responses to oxidative stress, as well as to treatments with tunicamycin and fluconazole. Ada2p recruitment to the promoters of oxidative resistance genes is mediated by the transcription factor Cap1p, and coactivator function were also established for Gal4p, which recruits Ada2p to the promoters of glycolysis and pyruvate metabolism genes. Cooccupancy of Ada2p and the drug resistance regulator Mrr1p on the promoters of core resistance genes characterizing drug resistance in clinical strains was also demonstrated. Ada2p recruitment to the promoters of these genes were shown to be completely dependent on Mrr1p. Furthermore, ADA2 deletion causes a decrease in H3K9 acetylation levels of target genes, thus illustrating its importance for histone acetyl transferase activity.

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