UC Berkeley

Bacteria must be able to respond to a multitude of unanticipated environmental insults in order to survive and ensure the production of subsequent generations. Appropriate responses are dictated via the coordination of intricate signal transduction pathways that transmit circumstantial information into a physical cellular output. Many of these processes integrate into regulation of the cell cycle to control growth and development with environmental status. Here, I start by summarizing the current literature pertaining to cell cycle regulation of the model alpha-proteobacterium Caulobacter crescentus. I discuss how the Caulobacter cell cycle is governed by a complex network of two-component signal transduction proteins; adaptor-mediated, regulated proteolysis of critical cell cycle-regulators; and the interplay of these proteins with an assortment of second messenger molecules, all of which involve both canonical and non-canonical interactions of which Caulobacter has played an integral role towards their understanding. This summary is followed by my own research into the regulation and interaction of a selection of these signal transduction proteins, and how these processes may affect Caulobacter’s physiology. Namely, I define a non-canonical, second messenger-mediated interaction by two response regulator proteins. In the last section, I elucidate the role of an essential tyrosine phosphatase homolog as being required for maintaining wild-type levels of lipid A, a molecule comprising the outer leaflet of the outer membrane of Gram-negative bacteria. Lipid A is generally thought to be an essential structure stabilizing the lipid bilayer of the outer membrane. Through suppressor analysis, I discover mutations that allow Caulobacter to survive in the absence of this tyrosine phosphatase homolog, and extend these results to known players in lipid A biosynthesis, generating strains devoid of lipid A and demonstrating the conditionally-essential nature of lipid A in Caulobacter.