As the world energy consumption increases, the necessity for clean energy proves vital and urgent as catastrophic effects of global climate change are imminent. The sun delivers more energy to Earth in just over an hour than we have consumed over the course of last year, making solar technology a most promising candidate for a sustainable future. Currently, state-of-the-art silicon-based solar technologies dominate the market owed to their maturity in processing knowledge, performance reliability, and lifetime. Despite lower costs in recent years, the levelized cost of electricity of silicon-based solar PV technologies is still much greater than conventional fossil fuel sources, providing large incentive to find more cost-effective alternative solar PV technologies. Solution-processed solar technologies are appealing as a low-cost alternative, among which, hybrid perovskites have recently risen as a high performance solution-processed PV technology achieving laboratory scale efficiencies >23%, which are rapidly approaching those of conventional Si-based PV (~26%). However, owed to the solution-processed nature of perovskites, there are many associated defects and grain boundary regions that can adversely affect performances and lifetimes. In this dissertation, I will focus on addressing defect and grain boundary engineering, taking advantage of the wet chemical environment of perovskite thin film processing to manipulate crystallization dynamics and modulate defect and grain boundary properties.

In Chapter 4, the guanidinium molecule was first discovered for use in hybrid perovskites. It was found that inclusion of guanidinium can provide extraordinary enhancements in photoluminescent properties of the thin film and enhanced open-circuit voltage of the devices. Based on further experimental analyses and results, we believe that the guanidinium ion serves to suppress formation of defects via lattice strain relaxation and also may serve as a passivant at grain boundaries, giving rise to these impressive improvements. This work opened the door to future works throughout my Ph.D. to control crystallization and defect properties.

To further investigate the nature of controlling crystal growth and associated defect natures, a Lewis acid-base adduct approach was developed and is discussed in Chapter 5. The strength of interactios between the Lewis acid perovskite precursors and Lewis base additives were shown to greatly influence nucleation and growth dynamics. The Lewis base urea was found to provide great enhancement in crystal growth, producing larger sized grains and enhanced photoluminescent properties, alongside a greater performance and stability of the device.

Lastly, in Chapter 6, the intrinsic stability of the perovskite thin film is addressed by utilizing the compositional and dimensional tenability of hybrid perovskite materials, utilizing a hybrid 3- and 2-dimensionality of the perovskite structure to lead to even further enhanced performances and long-term lifetimes. It was found that the 2-D perovskite forms around grains (at grain boundaries) to facilitate the production of high quality 3-D grains and serve as passivating layers to grain boundaries. These works provide important future directions for hybrid perovskite PV research to realize commercial technologies with competitive efficiencies, long lifetimes, and low costs. Conclusions and future outlooks of these works are discussed in Chapter 7.

The mechanisms linking inducible transcription factor (ITF) activity with neuronal connectivity and receptive field properties are of great interest, but poorly understood. Of note, the immediate early gene transcription factor (IEG-TF), neuronal PAS domain 4 (NPAS4), is an ITF that is expressed exclusively in response to neuronal activity or depolarization. In the mouse visual cortex, NPAS4 is expressed at high levels during the critical period, a time during development in which neural plasticity is increased. To study NPAS4 in the visual cortex, we have elected to use in vivo calcium imaging. However, it is not known if GCaMP expression affects neuronal development or the induction of NPAS4. By utilizing in utero electroporation, we aimed to introduce GCaMP into the pyramidal neurons of the mouse visual cortex and analyze the function of the cells that were electroporated. We first found that the cells electroporated with GCaMP in early development are neurons. In addition, expression of GCaMP does not impact basal or stimulus-dependent induction of NPAS4 in the visual cortex of mice. Thus, GCaMP can be used to study the impact of NPAS4 expression on neurons in vivo without disrupting endogenous NPAS4 induction.

Endemic to sub-Saharan African, African trypanosomes are devastating protozoan pathogens that present a significant medical and economic burden. Transmitted by the bite of an infected tsetse fly, Trypanosoma brucei causes Human African Trypanosomiasis (HAT) and a related diseased called Nagana in animals. In both its tsetse fly and mammalian hosts, T. brucei closely interacts with host tissue environments. Parasites must traverse a number of tissue barriers and enact specific developmental changes to complete their transmission cycle. How T. brucei senses and responds to signals from its extracellular environment, however, is not well-understood. When tsetse fly midgut stage T. brucei is cultivated on a surface in vitro, they coordinate their movements to engage in a group behavior termed social motility (SoMo), an ability that requires sensing both surfaces and other cells then engaging signal transduction cascades to respond. Thus, investigating the mechanisms that control social motility may elucidate T. brucei signaling systems that are important for their transmission through their hosts in vivo. In vitro studies have demonstrated the importance of cAMP signaling in the regulation of social motility.

This dissertation describes the use of molecular and systems-level analyses to investigate the regulation of social motility and signaling systems in T. brucei. Through labeling of tsetse fly tissues in conjunction with infection of fluorescently labeled T. brucei, we show that phosphodiesterase B1 (PDEB1) knockout parasites, which are unable to engage in SoMo, are blocked in a specific step in their fly transmission cycle, demonstrating the requirement for T. brucei cAMP signaling in vivo. To identify novel regulators of social motility that may or may not act in the cAMP pathway, two different RNA sequencing experiments were performed, leading to the identification of three novel candidate genes as potential social motility regulators. Additionally, we show that when engaged in SoMo, T. brucei exhibits positive chemotaxis toward a neighboring E. coli colony. Further characterization of T. brucei signaling systems will provide greater insight into how these deadly pathogens navigate through their hosts, potentially leading to new treatments and transmission-blocking agents.