A hallmark of biological life is the cell’s apparent ability to orient itself purposefully in space. This property is referred to as cell polarity. Cell polarity is enabled by specific polarity proteins that are asymmetrically distributed on the cell surface. These polarity proteins interact within conserved modules to form biochemical feedback circuits and as result, the asymmetries they form tend to be self-stabilizing. While the constituent parts of these circuits are known in many cell contexts, how they generate self-stabilizing asymmetries remains only partially understood. In the first chapter of this dissertation, I review the current literature on cell polarity. I discuss three examples of core polarity modules that stabilize asymmetries through various feedback loops. These core modules are utilized across cellular contexts to polarize cells in response to multiple different inputs and produce different asymmetries by interacting with different effector proteins. I show that these core circuits can be abstracted in mass conserved activator substrate (MCAS) models and review the insights we have gained from studying theoretical models. Finally, I discuss the role of protein clustering in core polarity circuits and show how it enables the establishment, maintenance, and elaboration of cell polarities. In the second chapter of this dissertation, I take a theoretical approach to show how protein oligomerization can modulate the potential for and dynamics of cell polarization. I show that size-dependent binding avidity and mobility of membrane-bound oligomers endow polarity circuits with several key properties. Dynamic oligomerization and size-dependent membrane binding avidity confers local positive feedback on the accumulation of oligomer subunits, which while insufficient by itself, sharply reduces the amount of additional feedback required for spontaneous emergence and stable maintenance of polarized states. Size-dependent oligomer mobility makes symmetry-breaking and stable polarity more robust with respect to variation in subunit diffusivities and cell sizes, and slows the approach to a final stable spatial distribution, allowing cells to “remember” polarity boundaries imposed by transient external cues. Given its prevalence and widespread involvement in cell polarity, I speculate that self-oligomerization may have provided an accessible path to evolving simple polarity circuits. In the third chapter, I apply this mathematical model to PAR protein polarity in the C.elegans zygote. Specifically, I consider the role of PAR-3 oligomerization in stabilizing PAR asymmetries. Using fast single molecule imaging, I show that PAR-3 oligomers are larger on the anterior membrane, and measure oligomer size-dependent membrane dissociation. This combination results in PAR-3 more stably associating with the anterior membrane than the posterior. I further show that asymmetries in the distributions of PAR-3 oligomers are dynamically maintained and that the recruitment of new PAR-3 monomers to the cell membrane exhibits an anterior bias. Using a combination of mathematical modeling and experiments, I provide evidence that the combination of feedback on monomer recruitment, dynamic oligomerization, and avidity effects enables PAR-3 asymmetries to self-stabilize, and that these processes are in turn regulated by interactions with other PAR proteins on the anterior membrane. Finally, I show that the positions of PAR-3 domain boundaries are not encoded by a reaction diffusion system, and propose instead that oligomer size-dependent decreases in PAR-3 mobility effectively preserve arbitrary domain boundaries for the duration of polarity maintenance. Together, these results reveal a novel mechanism for stabilizing PAR-3 asymmetries in the C.elegans zygote. In the final chapter, I discuss the implications of this work and future directions in this field. I discuss the potential to apply my modeling work to other polarity systems, the possible sources of feedback on PAR-3 membrane binding, and the potential and pitfalls of constructing mathematical models of PAR polarity. Finally, I outline a potential future project to understand how PAR-3 asymmetries shape PAR-6/PKC-3 distributions.