Identification of fungi that cause tip rot of carrot and determine effect of storage temperature and cultivar on tip rot development
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- Master's theses (IPV) 
Carrot is one of the important vegetables in Norway, and after harvesting it stored in cold storage for up to 7 months. During such long storage time, there is great yield and quality losses due to various diseases, and one of the most severe problem is tip rot of carrots. Tip rot starts as discoloration and necrosis from the tip (base) of the taproot and goes upwards in the edible part of the root. The symptom appears during and after cold storage but may be seen already at harvesting. In this study, we hypothesized that fungi have a role in tip rot disease development. To identify the primary causal agents of tip rot in Norway, we took samples from four fixed fields from Rogaland, Trøndelag, Innlandet, Viken and six commercial cold storages, in Rogaland, Trøndelag, Innlandet and Viken. Selection of fields and cold storages and sampling were caried out in close collaboration with advisors in Norsk Landbruksrådgiving (NLR). Based on morphological (symptoms appearance, isolation, and microscopy) and molecular approaches like (DNA sequencing and metabarcoding), the most frequently appearing pathogens were selected for further studies. The pathogenicity of the candidate pathogens was tested on four carrot cultivars, Dailyance, Brillyance, Namdal and Romance. In addition, the effect of temperature on the latent period of tip rot was determined by incubating inoculated carrots with candidate pathogens at 0+1°C, 3±1°C and 6±1°C. Several fungi were found on carrots with tip rot symptom, but the most abundant were Mycocentrospora acerina, Cylindrocarpon spp., Fusarium spp. and Dictyostelium spp. Those were used for pathogenicity test. The latent period was significantly different among storage temperature for all candidates (P < 0.05), and the latent period become shorter with an increase in temperature. There was variation in disease development between pathogens i.e. the development of M. acerina was faster than Cylindrocarpon spp., and Fusarium spp., while the lowest disease development was for Dictyostelium spp. Disease severity (lesion size) expressed as Area under disease progress (AUDPC) was significantly different among storage temperature for all candidates and between the pathogens i.e. M. acerina had the highest severity (AUDPC) while Dictyostelium spp., had the lowest ones. All the tested pathogens showed both the wet and dry type tip rot. The tested pathogens showed a slightly difference symptoms (discoloration) on carrot tissue when observed on the outside surface of the carrot and inside after splitting the carrot. The most typical symptom of M. acerina was brown to black discoloration starts from the tip of taproot, and the infection goes inside the carrots (xylem tissue) of the carrot with wet type black discoloration. On advanced infection, chlamydospores formed on the surface of the carrot tissue and gave the characteristic black symptom of liquorice rot. The symptom for Cylindrocarpon spp. was brown or dark brown to black infection starts from the tip of taproot, and the infection inside the carrot was as drying the whole area (core with surrounded flesh) and getting brown to black. The symptom of Fusarium spp. was light brown, brown and sometimes pink, while the infection inside the carrot was as dry, and brown core goes deep in the cylindrical core of the carrot tissue. Fusarium infection is mostly dry type, but it could be wet too. The symptom of Dictyostelium spp. was light brown, brown to dark brown, and the infection inside the carrot was as dry ii and brown core goes deep in the core. In conclusion, tip rot of carrots is a disease complex of stored carrots caused by different fungi with possible interaction with other microorganisms and physiology of the carrot taproot. Tip rot of carrot is caused by biotic agents. Tip rot causal agent identification based on symptom on the tip of the carrot is difficult, so one has to split the carrot and see how deep the symptom goes in the taproot. Even the splitting and symptom was not sufficient to correctly identify the causal agent, so one has to confirm the pathogen structure as spores, chlamydospores and hyphal structure under a microscope or conduct DNA based identification.