Signaling Components of Adventitious Root Development

Abstract

Plant development is highly plastic, allowing plants to continually alter and adjust their body plan in response to a changing environment by integrating complex endogenous and exogenous signals for the precise timing of organ growth and patterning. This thesis aims to understand aspects of signaling that are essential for plant development. This thesis consists of two parts. First, this work addresses signaling components of adventitious root regeneration. Adventitious roots form from non-root tissue after wounding, exemplifying de novo organ regeneration. Wounding stress initiates signaling that permits formation a new meristem in specific cell types. While the phytohormones auxin and cytokinin are critical in this process, the mechanisms that confer the ability of cells to respond to these cues remain poorly understood. This work investigates a proposed pathway that controls adventitious root development in response to wounding, specifically the PHYTOSULFOKINE peptide signaling pathway. Investigation of this pathway with genetic and molecular approaches reveal the PSK peptide pathway is a negative regulator of adventitious root development in response to wounding. The completion of this investigation provides evidence of a signaling pathway that, together with other pathways, modulates the ability of specific cells to regenerate new roots. The second part of this thesis work addresses mechanisms of auxin signaling at the transcriptional level. Auxin is a critical phytohormone for many growth and developmental processes. A large family of transcription factors has evolved to modulate transcription of auxin related genes referred to as the AUXIN RESPONSE FACTORs (ARFs). Interestingly, this family has diversified into activators and repressors. The activator ARFs participate in the canonical auxin signaling pathway, however much less is known about repressor ARFs. This work examines a repressor ARF, ARF9 for its DNA binding profile and employs forward genetics to identify regulators of its accumulation. Completion of this work reveals new insight into how Class-B ARFs contribute to auxin-related transcriptional regulation.