Investigating jasmonic acid reciprocal regulation of the circadian clock in Arabidopsis thaliana

Author/Creator

Author/Creator ORCID

Date

2020-01-20

Department

Biological Sciences

Program

Biological Sciences

Citation of Original Publication

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Distribution Rights granted to UMBC by the author.
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Abstract

Recent studies have established that jasmonic acid (JA)-mediated plant defense is regulated by the circadian clock. However, the reciprocation of this regulation is unclear. The Lu lab has set precedence by revealing that dosages of methyl-jasmonate, a JA agonist, affects clock activity depending on the JA receptor COI1. The question thus becomes; what part of the JA pathway, after JA perception, affects the circadian clock? JAZ proteins are co-receptors of JA that bind COI1 to negatively regulate JA signaling. MYC2 is a transcription factor acting downstream of JAZ-COI1 to positively regulate JA signaling. Loss-of-function mutations of MYC2 and JAZ genes confer altered JA sensitivity. The overall goal of this theses is to use clock-regulated luciferase reporters to assess which step in the JA signaling pathway is involved in clock regulation. Towards this goal, we have two specific aims. Aim 1: Create luciferase reporter constructs as tools for assessing clock activity. Aim 2: Elucidate which stage(s) of the JA pathway participate in a reciprocal signal to the circadian clock. We have successfully created three new reporter constructs. One of these constructs showed solid rhythmicity in both transient assays with tobacco and in stable Arabidopsis transgenic plants. Thus, this construct can be used as an excellent additional tool to investigate clock regulation by the JA pathway. In addition, JA pathway mutants, jin1-7 (a MYC2 mutants) and jaz10-1 were crossed to plants expressing known clock reporters, the luciferase driven by the CCA1 or by the GRP7 promoter. Future experiments will be carried out to test if these mutants expressing clock reporter show altered clock activity in the presence of JA.