IDENTIFICATION AND CHARACTERIZATION OF TRANSCRIPTION FACTORS INVOLVED IN THE REGULATON OF JASMONATE SIGNALING

Abstract

Jasmonate (JA) is a plant-specific, oxylipin signaling molecule. JA hormone signaling is required for defense against both biotic and abiotic stressors, male-fertility, and other growth and developmental processes. Activation of JA signaling occurs rapidly upon hormone sensing. In the absence of hormone, DNA-binding transcription factors are inhibited by members of the JASMONATE ZIM DOMAIN (JAZ) family of repressors. This keeps transcription from JA-responsive promoters turned off and resources are directed away from defense and toward growth. In the presence of hormone, JA facilitates interaction between JAZs and the F-box protein CORONATINE INSENSITIVE1 (COI1). This results in the ubiquitination and subsequent degradation of JAZs, an action that alleviates repression by JAZs and allows for the activation of JA-responsive gene transcription. This body of work focuses on the identification and characterization of three new proteins and their roles within the JA signaling pathway, and also includes a review article published in Frontiers in Plant Science in 2012. The first protein, NOVEL INTERACTOR OF JAZ (NINJA), was identified in a yeast-two-hybrid screen for JAZ1-interacting proteins and functions as a co-repressor involved in JA signaling (chapter 2). TIFY8, is related to JAZs, sharing homology with JAZ family members through its conserved TIFY motif. We hypothesized that the protein may function as a dominant repressor of JA signaling, but my work here will show that this is likely not true. TIFY8 may instead have a role in regulating meristem function in early development (chapter 3). The next chapter (chapter 4) is a review article that details how protein-protein interaction studies have aided in the identification and characterization of several important transcription factors involved in JA signaling in recent years. Lastly, I present my work with the basic helix-loop-helix (bHLH) protein, MYC5, showing that overexpression of the protein in the male-sterile JA signaling mutant, coi1, restores fertility and a subset of other JA responses (chapter 5). Together, this work helps to move the field forward both by contributing to our understanding of the mechanism of JAZ repression as well as by characterizing the function of MYC5, a key regulator of JA-mediated male fertility.