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.
| Identifer | oai:union.ndltd.org:LSU/oai:etd.lsu.edu:etd-05172016-085953 |
| Date | 09 June 2016 |
| Creators | Pattaravayo, Ratchanee |
| Contributors | Labonte, Don R., Clark, Christopher A., Villordon, Arthur O., Smith, Tara, Cook, Robert |
| Publisher | LSU |
| Source Sets | Louisiana State University |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lsu.edu/docs/available/etd-05172016-085953/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached herein a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to LSU or its agents the non-exclusive license to archive and make accessible, under the conditions specified below and in appropriate University policies, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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