Identifier

etd-05172016-085953

Degree

Doctor of Philosophy (PhD)

Department

Plant, Enviromental and Soil Sciences

Document Type

Dissertation

Abstract

End rot development in sweetpotato is caused by several pathogens and exacerbated by unfavorable environments. A critical need exists to know what factors in the environment trigger end rot development and how to manage the crop to minimize the incidence of end rots which are the overall objectives of this study. This research was divided into three studies: 1) Effect of environmental factors on expression of end rot in sweetpotato roots. Factorial combinations consisted of flooding/non-flooding; skinned/non-skinned; cured/non-cured; recommended storage/ambient storage are environmental variables not tested previously together in a systematic way. Results showed that curing at 29oC and 85-90% RH for five days and storage at 13oC and 85-90% RH were the critical factors mitigating end rot incidence. 2) Understand the role of calcium deficiency on end rot incidence. Relationship was observed between calcium and ethephon. Ethephon induced proximal and distal end rot incidences and decayed areas in sweetpotato. End rot symptoms are akin to blossom end rot in tomato caused by calcium deficiency. Increased rates of calcium in hydroponic solution increased calcium content in storage roots and reduced incidence of end rot. Calcium deficiency had impact on end rot incidence. 3) Identify expressed genes in storage roots treated with ethephon and 1-MCP. Molecular mechanisms triggered by the onset of end rot are unknown and may provide insight into plant protective mechanisms to exploit in a breeding program. This study identified differentially expressed genes (DEGs) using the annealing control primers (ACPs). DEGs identified are involved in protective mechanisms, transcriptional regulation, and an expressed protein (unknown). All 5 genes expressed in sweetpotato with end rot were confirmed by semi-quantitative reverse transcription polymerase chain reaction (sqRT-PCR) analysis. Genes differentially responded to 3.9 mM ethephon and 1 ppm 1-MCP. 1-MCP induced higher expression of TH2 and ATG8 than ethephon treated storage roots and minimized end rot incidence. This study furthered our knowledge of the role environment plays in inciting end rot development and how to minimize the incidence of end rots. Also, new genes were found that putatively lessen end rot and may have value as markers in breeding programs.

Date

2016

Document Availability at the Time of Submission

Release the entire work immediately for access worldwide.

Committee Chair

Labonte, Don R.

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