Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/22/2005
Publication Date: 1/1/2006
Citation: Lewandowski, S.M., Bushnell, W.R., Evans, C.K. 2006. Mycelial colonies and lesions in barley florets of field-grown barley inoculated with Fusarium graminearum. Phytopathology. 96:567-581.
Interpretive Summary: Fusarium Head Blight (FHB) is one of the most devastating diseases of wheat and barley in the eastern and mid-western parts of the U.S. Epidemics in the 1990s were especially severe and continue to produce significant damage to these crops. The fungus that causes FHB (Fusarium graminearum) produces spores on crop residues of corn, wheat, and barley. In mid summer these spores are carried in wind currents to newly emerged heads of wheat or barley where they infect individual florets on the heads. The research reported here was undertaken to learn what pathways the fungus follows to enter these barley florets under field conditions. Spores were shown to germinate on the outer floret surfaces and to produce sparse fungal networks that extend to the mouth at the floret apex and to the crevice between the overlapping petal-like structures (lemma and palea) that enclose the floret. Once inside the floret, the fungus quickly penetrates the highly susceptible interior surfaces, causing yellow and brown lesions. The results highlight the importance of initial fungus growth on the outer floret surfaces in disease development. The information will be useful to scientists for developing fungicidal control methods for FHB and for understanding how genetic resistance to FHB in barley reduces disease development.
Technical Abstract: To learn how the head blight pathogen, Fusarium graminearum, enters barley florets, field-grown plants were sprayed with macroconidial inoculum and then mist-irrigated daily in morning and evening. On selected days, 1-8 days after inoculation (DAI), 80-190 florets per day were harvested, dissected, and examined for presence and location of fungal colonies. At 1-12 DAI, 57-100 florets were likewise examined for lesions. Patterns of colonization indicated 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 about 8 days after heads emerged. Most florets had 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 were always associated with lesions in the palea. The results show the importance of initial mycelial colonization of floret outer surfaces, pathways of entry via lemma/palea crevices or floret mouth, and spread of lesions within the floret at interfaces between lemma, palea, and caryopsis.