UC Berkeley

Plant organs initiate from meristems and grow into diverse forms. Initiation is followed by a morphological phase where organ shape is elaborated, and finally tissues differentiate into their mature state. This process involves a variety of mechanisms, including complex gene regulatory networks, intricate patterning of plant hormones, and dynamic tissue growth. Hoja loca is a maize mutant that has defects in initiating and forming leaves and other lateral organs. I aim to use the Hoja loca mutation to investigate processes involved in transitioning tissue from undifferentiated meristem to lateral organs. Its unique phenotype suggests that it can greatly aid the understanding of plant organogenesis due to the specificity of mutant defects to organ initiation.

In this dissertation, I investigate the effects of the Hoja loca mutation on shoot organogenesis in Zea mays. In Chapter 1, I describe the mutant phenotype. In Chapter 2, I identify the mutant locus. I use RNA-seq differential gene expression to look at global changes and identify genes that are likely to mediate the Hoja loca defect. In Chapter 3, I investigate the localization of genes and metabolites that are important in organogenesis, namely the patterning of auxin. Together, these results suggest that Hoja loca causes an auxin-insensitivity in part of the auxin signaling response, likely at the site of organ initiation. This change is signaling leads to the misexpression of a beta glucosidase capable of activating cytokinin glucoside conjugates, and potentially the degradation of flavonols. The balance of cytokinin and auxin is a critical regulator of tissue differentiation, and flavonols affect auxin transport. Disrupting the localization of either of these compounds in the shoot could plausibly lead to the mutant phenotypes of skipped leaf initiation and altered leaf morphology.