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ISHS Acta Horticulturae 1144: III International Symposium on Postharvest Pathology: Using Science to Increase Food Availability

Role of two inoculation methods in the expression of anthracnose resistance gene in chili (Capsicum annuum L.)

Authors:   P. Suwor, P. Thummabenjapone, J. Sanitchon, S. Kumar, S. Techawongstien
Keywords:   dominant gene, inheritance, linkage, microinjection, recessive gene, spray inoculation method
DOI:   10.17660/ActaHortic.2016.1144.30
Abstract:
Anthracnose disease of chili (Capsicum annuum L.) can cause substantial pre- and postharvest qualitative and quantitative losses of fruit. Colletotrichum acutatum is the most prevalent and aggressive pathogen species causing chili anthracnose in north-east Thailand. Identification of germplasm resistant to anthracnose requires a reliable technique for C. acutatum inoculation. Two inoculation methods (microinjection and spray inoculation) were investigated with a cross between resistant (AVPP0207; PR) and susceptible (KKU-P31118; PS) parents (C. annuum) and their segregating progenies. Thirty green mature fruits of six populations (PR, PS, F1, F2, BC1PS and BC1PR) were inoculated by spray and microinjection using C. acutatum isolate Ca153 at concentrations of 107 and 5105 conidia mL-1, respectively. Lesion diameters were measured and recorded five days after inoculation (DAI) for the microinjected fruit and the percent disease severity was recorded seven DAI for the spray inoculated fruit. Frequency distribution of the disease score in F2 and backcross plants revealed that a single recessive gene controlled resistance when plants were challenged with the microinjection method. In contrast, resistance was under the control of a single dominant gene when plants were challenged with the spray method. The linkage analysis showed that both these monogenic resistance genes inherited independently at 47.45 cM distance. The results revealed and confirmed that irrespective of the two inoculation methods, inoculated fruit of anthracnose resistant sources triggered the same defense mechanism, i.e., hypersensitive reaction.

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