Making Good Citizens: Policy Approaches to Increasing Civic Participation

In this dissertation, I explore the impact of several public policies on civic participation. Using a unique combination of school administrative and public–use voter files and methods for causal inference, I evaluate the impact of three new, as of yet unexplored, policies: one informational, one institutional, and one skill–based. Chapter 2 examines the causal effect of No Child Left Behind’s performance-based accountability school failure signals on turnout in school board elections and on individuals’ use of exit. I find that failure signals mobilize citizens both at the ballot box and by encouraging them to vote with their feet. However, these increases in voice and exit come primarily from citizens who already active—thus exacerbating inequalities in both forms of participation. Chapter 3 examines the causal effect of preregistration—an electoral reform that allows young citizens to enroll in the electoral system before turning 18, while also providing them with various in-school supports. Using data from the Current Population Survey and Florida Voter Files and multiple methods for causal inference, I (with my coauthor listed below) show that preregistration mobilizes and does so for a diverse set of citizens. Finally, Chapter 4 examines the impact of psychosocial or so called non-cognitive skills on voter turnout. Using information from the Fast Track intervention, I show that early– childhood investments in psychosocial skills have large, long-run spillovers on civic participation. These gains are widely distributed, being especially large for those least likely to participate. These chapters provide clear insights that reach across disciplinary boundaries and speak to current policy debates. In placing specific attention not only on whether these programs mobilize, but also on who they mobilize, I provide scholars and practitioners with new ways of thinking about how to address stubbornly low and unequal rates of citizen engagement.

Mechanisms of Cdc42 Polarization in Yeast

Polarization is important for the function and morphology of many different cell types. The keys regulators of polarity in eukaryotes are the Rho-family GTPases. In the budding yeast Saccharomyces cerevisiae, which must polarize in order to bud and to mate, the master regulator is the highly conserved Rho GTPase, Cdc42. During polarity establishment, active Cdc42 accumulates at a site on the plasma membrane characterizing the “front” of the cell where the bud will emerge. The orientation of polarization is guided by upstream cues that dictate the site of Cdc42 clustering. However, in the absence of upstream cues, yeast can still polarize in a random direction during symmetry breaking. Symmetry breaking suggests cells possess an autocatalytic polarization mechanism that can amplify stochastic fluctuations of polarity proteins through a positive feedback mechanism.

Two different positive feedback mechanisms have been proposed to polarize Cdc42 in budding yeast. One model posits that Cdc42 activation must be localized to a site at the plasma membrane. Another model posits that Cdc42 delivery must be localized to a particular site at the plasma membrane. Although both mechanisms could work in parallel to polarize Cdc42, it is unclear which mechanism is critical to polarity establishment. We directly tested the predictions of the two positive feedback models using genetics and live microscopy. We found that localized Cdc42 activation is necessary for polarity establishment.

While this explains how active Cdc42 localizes to a particular site at the plasma membrane, it does not address how Cdc42 concentrates at that site. Several different mechanisms have been proposed to concentrate Cdc42. The GDI can extract Cdc42 from membranes and selective mobilize GDP-Cdc42 in the cytoplasm. It was proposed that selectively mobilizing GDP-Cdc42 in combination with local activation could locally concentrate total Cdc42 at the polarity site. Although the GDI is important for rapid Cdc42 accumulation at the polarity site, it is not essential to Cdc42 concentration. It was proposed that delivery of Cdc42 by actin-mediated vesicle can act as a backup pathway to concentrate Cdc42. However, we found no evidence for an actin-dependent concentrating pathway. Live microscopy experiments reveal that prenylated proteins are not restricted to membranes, and can enter the cytoplasm. We found that the GDI-independent concentrating pathway still requires Cdc42 to exchange between the plasma membrane and the cytoplasm, which is supported by computational modeling. In the absence of the GDI, we found that Cdc42 GAP became essential for polarization. We propose that the GAP limits GTP-Cdc42 leak into the cytoplasm, which would be prohibitive to Cdc42 polarization.