scholarly journals Mating System in the Brown Rot Pathogens Monilinia fructicola, M. laxa, and M. fructigena

2018 ◽  
Vol 108 (11) ◽  
pp. 1315-1325 ◽  
Author(s):  
Domenico Abate ◽  
Rita M. De Miccolis Angelini ◽  
Caterina Rotolo ◽  
Stefania Pollastro ◽  
Francesco Faretra
Keyword(s):  
Mating System ◽  
Population Biology ◽  
Constitutive Expression ◽  
Brown Rot ◽  
Antisense Transcription ◽  
Inter Simple Sequence Repeat ◽  
Monilinia Fructicola ◽  
Specific Pcr ◽  
Rot Disease ◽  
Flanking Regions

Monilinia fructicola, M. laxa, and M. fructigena are the most important pathogens responsible for brown rot disease of stone and pome fruits. Information on their mating system and sexual behavior is scant. A mating-type-specific PCR-based assay was developed and applied to 155 Monilinia isolates from 10 countries and 10 different host plants. We showed that single isolates carry only one of two opposite idiomorphs at the MAT1 locus consistent with a heterothallic mating system for all three species. MAT1-1 and MAT1-2 mating types were detected in similar proportions in samples of isolates of each species and hence there do not appear to be genetic obstacles to the occurrence of sexual reproduction in their populations. Inter simple sequence repeat markers suggested that asexual reproduction is prevalent, but that sexual recombination occurs in M. fructicola populations in Italy. The genetic architectures of the MAT1 loci of the three pathogens were analyzed. MAT1-1 and MAT1-2 idiomorphs are flanked upstream and downstream by the APN2 and SLA2 genes and resemble those of Botrytis cinerea and other heterothallic fungi in the family Sclerotiniaceae. Each idiomorph contains a specific couple of genes, MAT1-1-1 (with alpha-box domain) and MAT1-1-5 in MAT1-1, and MAT1-2-1 (with HMG-box domain) and MAT1-2-10 in MAT1-2. Small gene fragments (dMAT1-1-1 and dMAT1-2-1) from the opposite idiomorph were detected close to their flanking regions. Constitutive expression of the four MAT1 genes during vegetative growth was ascertained by transcriptomic analysis (RNA-Seq). Antisense transcription of the MAT1-1-1 and MAT1-2-1 genes and intergenic transcribed regions of the MAT1 locus were detected. These results represent new insights into the mating systems of these three economically-important pathogens which could contribute to improve the knowledge on their population biology.

scholarly journals Overexpression of a Redox-Regulated Cutinase Gene, MfCUT1, Increases Virulence of the Brown Rot Pathogen Monilinia fructicola on Prunus spp.

2010 ◽  
Vol 23 (2) ◽  
pp. 176-186 ◽  
Author(s):  
Miin-Huey Lee ◽  
Chiu-Min Chiu ◽  
Tatiana Roubtsova ◽  
Chien-Ming Chou ◽  
Richard M. Bostock
Keyword(s):  
Gene Expression ◽  
Redox Regulation ◽  
Brown Rot ◽  
Gus Expression ◽  
Apple Fruit ◽  
Gus Activity ◽  
Monilinia Fructicola ◽  
Gus Reporter ◽  
Flanking Regions ◽  
Prunus Spp

A 4.5-kb genomic DNA containing a Monilinia fructicola cutinase gene, MfCUT1, and its flanking regions were isolated and characterized. Sequence analysis revealed that the genomic MfCUT1 carries a 63-bp intron and a promoter region with several transcription factor binding sites that may confer redox regulation of MfCUT1 expression. Redox regulation is indicated by the effect of antioxidants, shown previously to inhibit MfCUT1 gene expression in cutin-induced cultures, and in the present study, where H2O2 enhanced MfCUT1 gene expression. A β-glucuronidase (GUS) reporter gene (gusA) was fused to MfCUT1 under the control of the MfCUT1 promoter, and this construct was then used to generate an MfCUT1-GUS strain by Agrobacterium spp.-mediated transformation. The appearance of GUS activity in response to cutin and suppression of GUS activity by glucose in cutinase-inducing medium verified that the MfCUT1-GUS fusion protein was expressed correctly under the control of the MfCUT1 promoter. MfCUT1-GUS expression was detected following inoculation of peach and apple fruit, peach flower petals, and onion epidermis, and during brown rot symptom development on nectarine fruit at a relatively late stage of infection (24 h postinoculation). However, semiquantitative reverse-transcriptase polymerase chain reaction provided sensitive detection of MfCUT1 expression within 5 h of inoculation in both almond and peach petals. MfCUT1-GUS transformants expressed MfCUT1 transcripts at twice the level as the wild type and caused more severe symptoms on Prunus flower petals, consistent with MfCUT1 contributing to the virulence of M. fructicola.

scholarly journals Identification and Characterization of Benzimidazole Resistance in Monilinia fructicola from Stone Fruit Orchards in California

2003 ◽  
Vol 69 (12) ◽  
pp. 7145-7152 ◽  
Author(s):  
Zhonghua Ma ◽  
Michael A. Yoshimura ◽  
Themis J. Michailides
Keyword(s):  
Dna Sequences ◽  
Point Mutations ◽  
Brown Rot ◽  
Stone Fruit ◽  
Monilinia Fructicola ◽  
Tubulin Gene ◽  
Benzimidazole Fungicides ◽  
Specific Pcr ◽  
Allele Specific ◽  
Fruit Orchards

ABSTRACT Low and high levels of resistance to the benzimidazole fungicides benomyl and thiophanate-methyl were observed in field isolates of Monilinia fructicola, which is the causative agent of brown rot of stone fruit. Isolates that had low levels of resistance (hereafter referred to as LR isolates) and high levels of resistance (hereafter referred to as HR isolates) were also cold and heat sensitive, respectively. Results from microsatellite DNA fingerprints showed that genetic identities among the populations of sensitive (S), LR, and HR isolates were very high (>0.96). Analysis of DNA sequences of theβ -tubulin gene showed that the LR isolates had a point mutation at codon 6, causing a replacement of the amino acid histidine by tyrosine. Codon 198, which encodes a glutamic acid in S and LR isolates, was converted to a codon for alanine in HR isolates. Based on these point mutations in the β-tubulin gene, allele-specific PCR assays were developed for rapid detection of benzimidazole-resistant isolates of M. fructicola from stone fruit.

Cloning and differential expression of a plum single repeat-MYB, PdMYB3, in compatible and incompatible interactions during fungal infection

2013 ◽  
Vol 93 (4) ◽  
pp. 599-605 ◽  
Author(s):  
Ashraf El-kereamy ◽  
Subramanian Jayasankar
Keyword(s):  
Fungal Infection ◽  
Differential Expression ◽  
Potential Role ◽  
Brown Rot ◽  
Myb Transcription Factor ◽  
Economic Damage ◽  
Monilinia Fructicola ◽  
Resistant Varieties ◽  
Rot Disease ◽  
Incompatible Interactions

El-kereamy, A. and Jayasankar, S. 2013. Cloning and differential expression of a plum single repeat-MYB, PdMYB3, in compatible and incompatible interactions during fungal infection. Can. J. Plant Sci. 93: 599–605. Enhancing resistance to pathogen attack through conventional breeding is a major challenge, especially in perennial species. Monilinia fructicola fungal infection causes brown rot disease, resulting in economic damage of stone fruits at flowering, pre- and post-harvest stages. The molecular mechanism of resistance to this disease is still not known. In the present study, we cloned and analyzed the expression of a novel MYB transcription factor from European plums (PdMYB3) induced in response to M. fructicola fungal infection. The identified PdMYB3 is a single repeat-MYB protein that contains a conserved SHAQKYF motif. Monilinia fructicola infection induces the expression of PdMYB3 in fruits of four cultivars within 24 h; however, it is differentially expressed in the susceptible and resistant varieties. By comparing four different cultivars we found that PdMYB3 is induced in much higher levels in the susceptible cultivars than the resistant ones. In addition the PdMYB3 expression is higher in the early stages of fruit development prior to pit hardening, suggesting a potential role for PdMYB3 during this stage. Promoter analysis revealed the presence of some hormone cis-elements suggesting a possible role for PdMYB3 gene in transmitting a signal from the hormonal pathways to downstream components during host-pathogen interactions.

scholarly journals Draft Genome Resources for the Phytopathogenic Fungi Monilinia fructicola, M. fructigena, M. polystroma, and M. laxa, the Causal Agents of Brown Rot

2018 ◽  
Vol 108 (10) ◽  
pp. 1141-1142 ◽  
Author(s):  
Yazmín Rivera ◽  
Kurt Zeller ◽  
Subodh Srivastava ◽  
Jeremy Sutherland ◽  
Marco Galvez ◽  
...  
Keyword(s):  
Draft Genome ◽  
Brown Rot ◽  
Phytopathogenic Fungi ◽  
Monilinia Fructicola ◽  
Pome Fruits ◽  
Rot Disease ◽  
Genome Assemblies

Fungi in the genus Monilinia cause brown rot disease of stone and pome fruits. Here, we report the draft genome assemblies of four important phytopathogenic species: M. fructicola, M. fructigena, M. polystroma, and M. laxa. The draft genome assemblies were 39 Mb (M. fructigena), 42 Mb (M. laxa), 43 Mb (M. fructicola), and 45 Mb (M. polystroma) with as few as 550 contigs (M. laxa). These are the first draft genome resources publicly available for M. laxa, M. fructigena, and M. polystroma.

scholarly journals Characterization of Monilinia fructicola Strains Resistant to Both Propiconazole and Boscalid

Plant Disease ◽  
2013 ◽  
Vol 97 (5) ◽  
pp. 645-651 ◽  
Author(s):  
F. Chen ◽  
X. Liu ◽  
S. Chen ◽  
E. Schnabel ◽  
G. Schnabel
Keyword(s):  
Succinate Dehydrogenase ◽  
Disease Incidence ◽  
Mobile Element ◽  
Brown Rot ◽  
Monilinia Fructicola ◽  
Quinone Outside Inhibitor ◽  
Dehydrogenase Enzyme ◽  
Rot Disease ◽  
Succinate Dehydrogenase Inhibitor ◽  
Spartanburg County

In 2011 and 2012, significant brown rot disease caused by Monilinia fructicola was observed in a peach orchard in Spartanburg County, SC, despite preharvest fungicide applications of demethylation inhibitor (DMI), quinone outside inhibitor (QoI), and succinate dehydrogenase inhibitor (SDHI) fungicides. All 22 isolates obtained in 2011 from this orchard were sensitive to the QoI fungicide, azoxystrobin, and the methyl benzimidazole carbamate (MBC) fungicide, thiophanate-methyl. Five were resistant to the DMI fungicide, propiconazole, and were selected, together with five propiconazole-sensitive isolates, for further investigations. One of the 10 isolates was resistant to propiconazole but sensitive to the SDHI fungicide, boscalid (EC50 = 0.42 μg/ml), 3 were resistant to propiconazole with intermediate sensitivity to boscalid (EC50 0.72 to 2.1 μg/ml); 2 were sensitive to propiconazole with intermediate sensitivity to boscalid; 3 were sensitive to propiconazole but resistant to boscalid (EC50 ≥ 2.1 μg/ml); and 1 (isolate MD22) was resistant to both propiconazole and boscalid. Disease incidence on detached fruit treated with formulated propiconazole or boscalid was significantly higher for MD22 compared to a sensitive control isolate. Continued monitoring of fungicide resistance in the same orchard in 2012 revealed an increase of isolates resistant to propiconazole from 22.7% in 2011 to 34.7%, and an increase of isolates resistant to both propiconazole and boscalid from 4.5% in 2011 to 18.4%. Propiconazole resistance was always associated with the presence of the ‘Mona’ mobile element located upstream of the sterol 14α-demethylase (MfCYP51) gene. To investigate whether mutations in the subunits of the succinate dehydrogenase enzyme were involved in boscalid resistance, significant portions of the M. fructicola SdhA, SdhB, SdhC, and SdhD genes were cloned and analyzed for 2 sensitive, 2 boscalid-resistant, and 6 dual-resistant isolates. Although sequence variation was found among the isolates, no single change correlated with resistance. Interestingly, analysis of isolates collected from orchards in 2001 and 2002, prior to the registration of boscalid, revealed a range of sensitivities to boscalid (EC50 0.03 to 3.46 μg/ml) including boscalid-resistant isolates. The presence of boscalid-resistant isolates in the baseline population was unexpected and requires further investigation.

Sign in / Sign up

Export Citation Format

Share Document