Plants are sessile organisms and therefore are limited in their ability to gather resources. Therefore, they have evolved several mechanisms that aid them in their quest to gather light, water and nutrients. One such mechanism is phototropism, a plants ability to bend towards or away from a light source. This mechanism is mediated by the blue light photoreceptor phototropin (phot). Arabidopsis thaliana contains two phototropins, phot1 which is the primary photoreceptor under low intensity light and phot2, which acts redundantly with phot1 under high intensity light. The perception of blue light by the phototropins (phot1 and phot2) initiates signaling events that lead to a lateral redistribution of the plant hormone auxin; which ultimately results in differential growth and the bending response. In addition to phototropism, these proteins mediate several other growth and developmental responses such as leaf movement, chloroplast movement, and stomatal opening. A second protein which is critical to the phototropic response and interacts with phot1 is NONPHOTOTROPIC HYPOCOTYL3 (NPH3). In addition to phototropism, NPH3 has a role in phot1-mediated leaf movement. NPH3 has been shown to act as a substrate adapter in an E3 ubiquitin ligase complex with the protein CULLIN3 (CUL3). This CRL3NPH3 complex is responsible for ubiquitinating the phot1 photoreceptor in a blue light fashion. This ubiquitination has been shown to be necessary for the bending response, but it's role in receptor ubiquitination is still not fully understood. To better understand this component of phot1-mediated phototropism, we characterized an allelic series of NPH3 mutants to further understand the role of this substrate adapter in this mechanism. Additionally, we characterized several mutant plant lines containing a mutant phot1 protein in which critical ubiquitination sites were mutated in an effort to render the protein unable to be ubiquitinated to further understand phot1 ubiquitination.