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Distribution of mycelial colonies and lesions in field-grown barley inoculated with Fusarium graminearum

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PHYTOPATHOLOGY
卷 96, 期 6, 页码 567-581

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AMER PHYTOPATHOLOGICAL SOC
DOI: 10.1094/PHYTO-96-0567

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deoxynivalenol; Gibberella zeae

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External surfaces of barley florets have thick-walled epidermal cells resistant to direct penetration by the head blight pathogen, Fusarium graminearum. Surfaces within the floral cavity have thin-walled, susceptible cells. How the fungus gains access to the floral cavity, causing head blight. has not been determined. To investigate pathways of entry. field-grown plants were sprayed with macroconidial inoculum after heads emerged from the flag leaf sheath and then were mist irrigated daily in the morning and evening. On selected days, 1 to 8 days after inoculation (DAI), 80 to 190 florets per day were harvested, dissected, and examined for presence and location of mycelial colonies. At 1 to 12 DAI, 57 to 100 florets likewise were examined for lesions. Patterns of colonization indicated that the fungus entered florets principally through crevices between the overlapping lemma and palea or through the apical floret mouth. The crevices were open for entry until approximate to 8 days after heads emerged. Most florets had mycelial colonies on the external Surface in a Sheltered pocket near the base of the ventral furrow of the palea. Mycelia spread laterally from the furrow to the crevice between lemma and palea. Anther colonization had only a minor role in invasion of florets. Hyphal penetration of stomates was not seen. Lesions usually developed first within 3 mm of the floret apex or 3 mm of the floret base. Within florets. lesions often were Contiguous between lemma and palea, palea and caryopsis, or in all three floret parts. However, lesions in the caryopsis developed later and were fewer in number than in the lemma and palea and always were associated with lesions in the palea. The results show the importance of initial mycelial colonization of floret outer surfaces, pathways of entry via lemma or palea crevices or floret mouth, and spread of lesions within the floret at interfaces between lemma, palea, and caryopsis.

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