Date of Award

Winter 2007

Project Type


Program or Major


Degree Name

Master of Science


The symbiosis of Euprymna scolopes and Vibrio fischeri depends on the ability of the bacterium to colonize the squid and produce light. GacA is an activator of symbiosis phenotypes including luminescence though it is not understood how GacA functions. My hypothesis, based on other bacterial models, is that GacA activates expression of CsrBs, functional RNAs, which sequester and repress a translational repressor, CsrA. I approached this question with mutagenesis and complementation techniques. We found mutation of CsrA or addition of a CsrB in trans could complement the GacA mutant for symbiosis and luminescence phenotypes. The inability of other luminescence regulators including a constitutively expressed lux operon to complement GacADelta indicated that luminescence was regulated post-transcriptionally. A putative CsrA binding site found in the sequence of the lux mRNA increased light production when deleted. These data demonstrate that GacA regulates luminescence post-transcriptionally via CsrB/CsrA antagonism, supporting my hypothesis.