Occurrence of head rot disease caused by Fusarium verticillioides on Chinese flowering cabbage (Brassica rapa L subsp. parachinensis) in China

Fusarium verticillioides infects maize ears, causing ear rot disease and contamination of grain with fumonisin mycotoxins. This contamination can be reduced by the presence of bioactive compounds in kernels that are able to inhibit fumonisin biosynthesis. To identify such compounds, we used kernels from a maize genotype with moderate susceptibility to F. verticillioides, harvested at the milk-dough stage (i.e., when fumonisin production initiates in planta), and applied a bioguided fractionation approach. Chlorogenic acid was the most abundant compound in the purified active fraction and its contribution to fumonisin inhibitory activity was up to 70%. Moreover, using a set of maize genotypes with different levels of susceptibility, chlorogenic acid was shown to be significantly higher in immature kernels of the moderately susceptible group. Altogether, our data indicate that chlorogenic acid may considerably contribute to either maize resistance to Fusarium ear rot, fumonisin accumulation, or both. We further investigated the mechanisms involved in the inhibition of fumonisin production by chlorogenic acid and one of its hydrolyzed products, caffeic acid, by following their metabolic fate in supplemented F. verticillioides broths. Our data indicate that F. verticillioides was able to biotransform these phenolic compounds and that the resulting products can contribute to their inhibitory activity.

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Biology of Maize Kernel Infection by Fusarium verticillioides

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-1-0006 ◽

2010 ◽

Vol 23 (1) ◽

pp. 6-16 ◽

Cited By ~ 69

Author(s):

Keith E. Duncan ◽

Richard J. Howard

Keyword(s):

Fungal Pathogen ◽

Fluorescent Protein ◽

Fusarium Verticillioides ◽

Passive Movement ◽

Host Cells ◽

Conidial Suspension ◽

Symptom Development ◽

Kernel Infection ◽

Rot Disease ◽

First Time

Fusarium kernel rot disease starburst symptomatology was characterized fully for the first time. Two maize lines were hand pollinated and inoculated, using a fluorescent protein-expressing transformant of the fungal pathogen Fusarium verticillioides, by introduction of a conidial suspension through the silk channel of intact ears. Microscopy was used to identify the infection court and document initial stages of kernel colonization and subsequent manifestation of macroscopic symptoms. The fungus entered kernels of susceptible line AD38 via an open stylar canal and spread extracellularly and over the kernel through the nucellus region, sporadically entering pericarp and filling the long thick-walled mesocarp cells. Hyphae spread within pericarp from cell to cell via pits, colonizing files of host cells by growing both up and down the kernel in a radial pattern that preceded macroscopic symptom development. The starburst symptom developed subsequently, and mirrored colonization exactly, when there was extensive dissolution of the thick walls of pericarp cells. Line HT1 exhibited a closed stylar canal phenotype and was not susceptible—except when the pericarp surface was breached mechanically. We hypothesize the passive movement of conidia along the surface of silks, perhaps via capillarity, as a possible mechanism for pathogen access to the infection court.

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First Report of Root Rot on Rhodiola sachalinensis Caused by Fusarium verticillioides (Gibberella fujikuroi) in China

Plant Disease ◽

10.1094/pdis-08-10-0582 ◽

2011 ◽

Vol 95 (2) ◽

pp. 222-222

Author(s):

J. F. Liu ◽

Y. Q. Cheng

Keyword(s):

Root Rot ◽

Tap Water ◽

Fusarium Verticillioides ◽

Gibberella Fujikuroi ◽

Herbaceous Plant ◽

Conidial Suspension ◽

First Report ◽

Rhodiola Sachalinensis ◽

Root Rot Disease ◽

Rot Disease

Rhodiola sachalinensis (family Crassulaceae), a perennial herbaceous plant with adaptogenic properties, cardiopulmonary protective effects, and central nervous system activities, is widely used as a traditional Chinese medicine (3). R. sachalinensis naturally exists only above 1,500 m elevation in the mountain area of Changbai Mountain (average July temperature ≤10°C), China. Introduction and cultivation of R. sachalinensis has been carried out in several low-altitude districts of northeast China. From 2007 to 2010, severe root rot disease was observed on R. sachalinensis in Siping districts, Jilin, China. Approximately 75 to 95% of the fields were affected with root rot disease incidence ranging from 85 to 100% under conditions of high temperatures (24 to 30°C) and high humidity. As the disease progressed, brown lesions expanded on lateral and main roots, and aboveground tissues shriveled and died. Over the 4- to 5-year period from culture to harvest, root rot became more serious. Symptomatic plants were collected from Siping districts. Samples were rinsed in tap water, necrotic areas were excised and cut into 2-mm pieces, surface sterilized with 5% NaOCl for 30 s, and rinsed in four successive changes of sterile distilled water. A single fungus was isolated on potato dextrose agar (PDA). The fungus was white, then pink and cottony, with nearly round margins after 8 days (27°C). Hyphae were separate and hyaline but macroconidia were sparse and occurred in a false head. Conidiogenous cells were monophialides. Microconidia in chains were abundant and mostly nonseptate, oval to clavate, and measured 8.1 to 14.5 × 2.0 to 3.4 μm. Morphological characteristics suggested the isolate was Fusarium verticillioides (Gibberella fujikuroi), which differed from the reported root rot pathogen of R. sachalinensis, F. oxysporum by forming microconidia in chains (1). The sexual stage of F. verticillioides was not observed. The internal transcribed spacer (ITS) fragments were amplified using ITS1 and ITS4 as primers and the 351-bp sequence was deposited in GenBank (Accession No. HQ025928). The ITS sequence showed 100% nucleotide sequence identity with F. verticillioides (GenBank Accession No. AY188916.1.). For pathogenicity tests, the isolate was cultured on PDA for 8 days. Inoculations were performed on 15 healthy R. sachalinensis plants by spraying a conidial suspension (2.0 × 105 microconidia ml–1) on roots wounded with a metal needle (6 wounds cm–2) (2). Ten plants were mock inoculated with water. Plants were incubated in a growth chamber (25°C, 70 to 80% relative humidity, 300 μmol·m–2·s–1 light intensity, and a 12-h photoperiod). After 15 days, defoliation and root rot symptoms were similar to the original symptoms observed under field conditions. F. verticillioides was reisolated from the roots of infected plants. Control plants remained asymptomatic. To our knowledge, this is the first report of F. verticillioides on R. sachalinensis in China. References: (1) X. Y. Li et al. J. Northeast For. Univ. 34:12, 2003. (2) M. Ma. Syahit et al. Am. J. Appl. Sci. 6:902, 2009. (3) T. F. Yan et al. Conserv. Genet. 4:213, 2003.

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The etiology of head rot disease of broccoli

Australian Journal of Agricultural Research ◽

10.1071/ar9870735 ◽

1987 ◽

Vol 38 (4) ◽

pp. 735 ◽

Cited By ~ 6

Author(s):

DLS Wimalajeewa ◽

ND Hallam ◽

AC Hayward ◽

TV Price

Keyword(s):

Tomato Fruit ◽

Field Tests ◽

Fluorescent Pseudomonad ◽

Isolation Technique ◽

Disease Symptoms ◽

Pathogenicity Tests ◽

Rot Disease ◽

Head Rot ◽

Physiological And Biochemical Characters ◽

Physiological And Biochemical

Transmission and scanning electron microscope studies of broccoli florets affected by head rot, at various stages of disease development, strongly indicated a bacterial etiology for the disease. Nevertheless, the different species of bacteria isolated from diseased heads, using standard techniques, failed to reproduce symptoms in pathogenicity tests conducted in the glasshouse and in the field. However, a modified isolation technique, using broccoli heads showing incipient watersoaking symptoms, yielded a fluorescent pseudomonad which reproduced disease symptoms readily in glasshouse and field tests. On the basis of physiological and biochemical characters, the pathogenic bacterium was identified as a highly pectolytic pathovar of Pseudomonas marginalis. The bacterium also caused the rotting of potato, tomato and swede turnip slices, and also of intact and detached tomato fruit. However, it was not pathogenic on lettuce, parsnip or lucerne, and also failed to rot carrot slices.

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First Report of Sclerotinia minor on Brassica rapa subsp. pekinensis in Central China

Plant Disease ◽

10.1094/pdis-06-13-0625-pdn ◽

2014 ◽

Vol 98 (7) ◽

pp. 992-992 ◽

Cited By ~ 3

Author(s):

A. Lyu ◽

J. Zhang ◽

L. Yang ◽

G. Q. Li

Keyword(s):

Brassica Rapa ◽

Chinese Cabbage ◽

Morphological Characteristics ◽

Leaf Tissue ◽

Central China ◽

Sclerotinia Minor ◽

First Report ◽

Leaf Tissues ◽

Rot Disease ◽

Leaf Rot

Chinese cabbage (Brassica rapa subsp. pekinensis Hanelt) is a leafy vegetable widely grown in China. In December 2012 to March 2013, a leaf rot disease was observed on the lower part of cabbage leaves in a field in Xianning, Hubei Province, China, with the incidence of 6.3% in that field. The diseased leaves showed water-soaked rot and brown symptoms at the top surface. White fluffy mycelia and small black sclerotia were produced on the lesion surface. Cabbage leaf tissues from the disease/healthy-bordering areas and the sclerotia from the lesions were separately surface-sterilized in 75% ethanol (v/v) for 30 s, followed by rinsing three times in sterilized water. The surface-sterilized tissues and sclerotia were placed on potato dextrose agar (PDA) and incubated at 22°C. Individual emerging fungal colonies from the leaf tissue pieces and the sclerotia were transferred to new 9-cm-diameter PDA plates and incubated for 15 days. A total of 40 isolates (20 from diseased tissue and 20 from sclerotia) were obtained. All the isolates grew rapidly on PDA with an average growth rate of 2.2 cm/day and produced abundant sclerotia on the colony surface (1,179 sclerotia/plate on average). None of the isolates produced conidia and any other spores in the PDA cultures. Mature sclerotia were black, irregular, spherical or elliptical, had a diameter of 0.5 to 1 mm, and easily detached from the colonies. The cultural and morphological characteristics of the isolates matched the description for Sclerotinia minor Jagger (3). Two isolates, A1 (from leaf tissue) and S2 (from a sclerotium), were further identified by analysis of the ITS region (ITS1-5.8S rDNA-ITS2) using the primer pair ITS1/ITS4. The resulting 540-bp DNA sequences (GenBank Accession Nos. KC836493 for A1 and KC836494 for S2) shared 100% identity S. minor isolate 62907 (JF279880). Pathogenicity of the isolates A1 and S2 was tested by inoculating detached cabbage leaves with mycelial agar plugs removed from the colony margin of the 3-day-old cultures. Isolates A1 and S2 were each inoculated on three leaves with three plugs per leaf. Three cabbage leaves inoculated with PDA plugs were treated as a control. The treated leaves were covered with plastic films to maintain high humidity (>90% RH) and incubated at 22°C for 72 h under the regime of 12 h light/12 h dark. Results showed that while the control leaves remained healthy, brown and water-soaked lesions appeared around the mycelial agar plugs of each isolate. Average lesion diameters were 47.5 mm for A1 and 47.8 mm for S2. Abundant small sclerotia were produced on necrotic leaf lesions after 7 days. The fungus in diseased leaf tissues was re-isolated and the morphological characteristics of the resulting fungus were the same as S. minor isolated from infected field-grown cabbages. Therefore, S. minor is the causal agent for the leaf rot disease on Chinese cabbage. S. minor has been reported to infect a few plant species in the genus Brassica, including B. rapa subsp. oleifera (3), B. oleracea var. gemmifera (3), B. napus (2), B. oleracea var. capitata (3), B. oleracea var. botrytis (3), and B. rapa (3). It was found on B. rapa subsp. pekinensis in Korea (1). To our knowledge, this is the first report of S. minor on B. rapa subsp. pekinensis in China. References: (1) W. D. Cho and H. D. Shin. Page 779 in: List of Plant Diseases in Korea, 4th ed. Korean Society of Plant Pathology, 2004. (2) S. A. Gaetán and M. Madia. Plant Dis. 92:172, 2008. (3) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997.

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