Fungi Resident in Chickpea Debris and their Suppression of Growth and Reproduction of Didymella rabiei under Laboratory Conditions

نویسندگان

  • F. M. Dugan
  • S. L. Lupien
  • M. Hernandez-Bello
  • T. L. Peever
  • W. Chen
چکیده

Fungi colonizing senescent chickpea (Cicer arietinum) stems and postharvest debris from Pullman, WA, were enumerated and identified with the objective of finding species potentially useful for biological control of Didymella rabiei (conidial state 1⁄4 Ascochyta rabiei), causal agent of Ascochyta blight. In addition to D. rabiei, primary colonizers were, in order of decreasing abundance, Alternaria tenuissima, Al. infectoria, Ulocladium consortiale, Epicoccum purpurascens, U. atrum and Fusarium pseudograminearum. Present at lower frequencies were Al. malorum, Cladosporium herbarum, Aureobasidium pullulans, Clonostachys rosea and miscellaneous anamorphic ascomycetes. On agar media and autoclaved chickpea stems, Au. pullulans consistently grew faster than As. rabiei, and excluded As. rabiei from the substrate. When stems received prior inoculation with Au. pullulans or Cl. rosea, followed by inoculation with compatible mating types of D. rabiei, formation of pseudothecia and pycnidia of D. rabiei was suppressed. Results suggest that Au. pullulans and Cl. rosea can inhibit As. rabiei and its sexual stage, D. rabiei, on chickpea debris. Clonostachys rosea formed appressoria on, then invaded, hyphae of D. rabiei. Small-scale field experiments using Au. pullulans and Cl. rosea have been initiated. Introduction The adoption of reduced tillage practices to control soil erosion in US Pacific Northwest (PNW) cropping systems has created conditions that are ideal for the survival and reproduction of Ascochyta rabiei (Pass.) Lab., the causal agent of Ascochyta blight of chickpea (Cicer arietinum L.). The sexual stage, Didymella rabiei (Kovachevski) Arx, develops during the winter on chickpea debris, and ascospores infect newly emerging chickpeas the following season (Kaiser, 1992). One of the best control measures for Ascochyta blight is the deep ploughing of infected plant residues (Kaiser and Hannan, 1987); however, this practice is incompatible with soil conservation practices. The increasing amount of plant debris left on the soil surface is thought to have led to a large increase in inoculum for Ascochyta blight epidemics and to the increased severity of blight epidemics observed in the PNW the past few years. Given the importance of soil erosion control and the inevitable move towards reduced tillage in PNW agriculture, control of Ascochyta blight will increasingly depend on suppressing the sexual stage of the pathogen. The primary type of inoculum for Ascochyta blight epidemics in the PNW is thought to be ascospores (Trapero-Casas and Kaiser, 1992a,b; Trapero-Casas et al., 1996). This is based both on low rates of seed infection of PNW seed lots, and anecdotal observations of disease pattern and timing in the field (T. L. Peever, W. Chen and W. J. Kaiser, unpublished data) as well as on indirect evidence from mating type ratios and multilocus gametic disequilibrium tests with genetic markers which indicate a recombined population structure (Peever et al., 2004). Ascospores land on chickpea plants, infect directly and form lesions, which produce pycnidia. Secondary spread of Ascochyta blight within chickpea fields during the growing season is dependent upon rainfall events, which disperse conidia to uninfected plants and create appropriate environmental conditions for infection (Trapero-Casas and Kaiser, 1992a,b). The sexual stage is formed on chickpea debris colonized by the fungus the previous season and requires approximately 2 months at cool temperatures (5–10 C) to mature and produce ascospores. Ascospores are released under specific environmental conditions, are wind-borne, and can infect chickpea plants several hundred metres or more from the source, while conidia are splash-dispersed only short distances (Kaiser, 1992; Trapero-Casas et al., 1996). Long-distance movement of ascospores is the www.blackwell-synergy.com J. Phytopathology 153, 431–439 (2005) 2005 Blackwell Verlag, Berlin

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تاریخ انتشار 2005