Early blight, caused by the fungus Alternaria solani, is a common foliar disease in potato. Quinone outside inhibitor (QoIs) fungicides have commonly been used against A. solani. To avoid or delay development of fungicide resistance it is recommended to alternate or combine fungicides with different modes of action. Therefore, we compared two different fungicide programs against early blight in field trials and studied within season changes in the pathogen population. An untreated control was compared with treatments using azoxystrobin alone and with a program involving difenoconazole followed by boscalid and pyraclostrobin combined. Isolates of A. solani were collected during the growing season and changes in the population structure was investigated. We also screened for the amino acid substitution in the cytochrome b gene and investigated changes in sensitivity to azoxystrobin. Treatment with azoxystrobin alone did not improve disease control in 2014 when the disease pressure was high. However, lower severity of the disease was observed after combined use of difenoconazole, boscalid and pyraclostrobin. The efficacy of both fungicide treatments were similar during the field trial in 2017. Two mitochondrial genotypes (GI and GII) were found among isolates, where all isolates, except two, were GII. All GII isolates had the F129 L substitution while the two GI isolates were wild type. Population structure analysis and principal component analysis (PCA) of amplified fragment length polymorphisms (AFLP) data revealed within season changes in the A. solani populations in response to fungicide application. Isolates with the F129 L substitution had reduced sensitivity to azoxystrobin in vitro and their sensitivity tended to decrease with time.
Botrytis squamosa, Botrytis aclada, and Sclerotium cepivorum are three fungal species of the family Sclerotiniaceae that are pathogenic on onion. Despite their close relatedness, these fungi cause very distinct diseases, respectively called leaf blight, neck rot, and white rot, which pose serious threats to onion cultivation. The infection biology of neck rot and white rot in particular is poorly understood. In this study, we used GFP-expressing transformants of all three fungi to visualize the early phases of infection. B. squamosa entered onion leaves by growing either through stomata or into anticlinal walls of onion epidermal cells. B. aclada, known to cause post-harvest rot and spoilage of onion bulbs, did not penetrate the leaf surface but instead formed superficial colonies which produced new conidia. S. cepivorum entered onion roots via infection cushions and appressorium-like structures. In the non-host tomato, S. cepivorum also produced appressorium-like structures and infection cushions, but upon prolonged contact with the non-host the infection structures died. With this study, we have gained understanding in the infection biology and strategy of each of these onion pathogens. Moreover, by comparing the infection mechanisms we were able to increase insight into how these closely related fungi can cause such different diseases.
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