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First Report of Fusarium temperatum Causing Fusarium Ear Rot on Maize in Northern China

September 2014 , Volume 98 , Number  9
Pages  1,273.1 - 1,273.1

H. Zhang, W. Luo, Y. Pan, J. Xu, J. S. Xu, W. Q. Chen, and J. Feng, State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China. Funding provided by National Natural Science Foundation (No. 31201477)



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Accepted for publication 16 April 2014.

In China, several diseases of maize (Zea mays L.) including ear rot are caused by Fusarium spp., leading to significant yield losses and potential risk of mycotoxin contamination (2,3). In 2013, a survey was conducted to determine the population composition of Fusarium species on maize ears in Jilin Province. Symptomatic maize ears with pink or white mold were collected and surface disinfested with 70% ethanol and 10% sodium hypochlorite, followed by three rinses with sterile distilled water and placed onto potato dextrose agar (PDA). After 3 days of incubation at 25°C in the dark, newly grown-out mycelia were transferred onto fresh medium and purified by the single-spore isolation method (4). Fusarium spp. were identified by morphological characteristics (2) and sequence analysis of translation elongation factor-1α (TEF) gene (1). A large number of Fusarium spp. were found including F. graminearum species complex and F. verticillioides. In addition, a new species, F. temperatum, recently described in Belgium (2), was also identified. F. temperatum was originally described as F. subglutinans, but a robust polyphasic approach proved it to be a new biological species closely related to F. subglutinans (2). Previous studies had reported ~15% of Fusarium maize ear rot in Jilin was F. subglutinans. In this study, we found both F. subglutinans s. str. and F. temperatum in the proportion of 16.3% and 9.2%, respectively. Similar to previous studies (2), colonies of our strains on PDA were initially white cottony mycelium that become pinkish white. Conidiophores formed abundantly on SNA that were erect, branched, and terminated in 1 to 3 phialides. Microconidia were abundant, hyaline, 0 to 2 septa, obovoid to oval, and not produced in chains. Chlamydospores were absent. Typically macroconidia were falcate, 3 to 5 septate (mostly 4 septate), hyaline with a curved and blunt apical cell and a distinct foot-shaped basal cell. In order to validate this result, partial translation elongation factor (TEF-1α, 629 bp) gene sequences of isolates were generated (GenBank Accession No. KJ137018) (1). BLASTn analysis revealed 100% sequence identity to F. temperatum (HM067690). A pathogenicity test was performed on maize cv. Zhengdan958. Four days after silk emergence, 2 ml conidial suspension (105 macroconidia/ml) of each isolate was injected into each of 10 maize ears through silk channel. Control plants were inoculated with sterile distilled water. Twenty days after inoculation, typical Fusarium ear rot symptoms (reddish-white mold) was observed on inoculated ears and no symptoms were observed on water controls. Koch's postulates were fulfilled by re-isolating the same fungus from the infected seeds. Although F. temperatum was reported to attack maize kernels in southern China where the annual average temperatures are moderately high (3), to our knowledge, this is the first report of F. temperatum causing Fusarium ear rot in northern China, where the winter is long and very cold, the annual average temperature is 4 to 5°C, and the lowest temperature is lower than –35°C. This indicated that F. temperatum was widely distributed in different ecological regions in China. Furthermore, the northeast spring corn region that includes Jinlin is the most important corn belt, with corn production of this region accounting for 42% of the total corn production in China. Therefore, we should pay more attention to the new species in this region and consider them in the development of maize cultivars with broad-based resistance to the pathogens.

References: (1) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004. (2) J. Scauflaire et al. Mycologia 103:586, 2011. (3) J. H. Wang et al. J. Phytopathol. 162:147, 2014. (4) L. Yang et al. Phytopathology 98:719, 2008.



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