The morphogenesis checkpoint in the budding yeast Saccharomyces cerevisiae monitors bud emergence. If environmental perturbations delay budding, the cells arrest in G2 until they are able to form a bud. The morphogenesis checkpoint is mediated by Swe1p, the budding yeast homolog of Wee1, which phosphorylates and inhibits Cdc28p, the CDK that drives cell division. In unstressed cells, Swe1p is degraded, a process that is dependent on the kinase Hsl1p. Hsl1p localizes to the septins, which form a collar-like structure at the bud neck. Hsl1p binds to Hsl7p, an adapter protein that recruits Swe1p to the neck. When budding is perturbed, Hsl1p is inactive, thus allowing Swe1p to accumulate and inhibit Cdc28p. Bud formation activates Hsl1p, enabling it to recruit negative regulators of Swe1p to the bud neck, where Swe1p is marked for degradation. Interestingly, our lab has shown that Hsl1p is regulated by cell shape. Here, we reexamine a model that suggests Hsl1p is regulated by an autoinhibitory domain and discover that the model cannot be supported by our data. In addition, we present evidence suggesting that Hsl1p is regulated by an upstream kinase, Elm1p, that phosphorylates Hsl1p within the activation loop. Finally, we identify functional and regulatory regions within Hsl1p. We identify regions that participate in septin binding and Hsl7p binding. But our most interesting discovery is a regulatory region that makes Hsl1p responsive to bud emergence.