Erin Garcia, PhD

The focus of my lab is to understand the molecular mechanisms that govern antagonistic and cooperative interactions between Burkholderia species in the context of infectious disease.

Contact-dependent growth inhibition (CDI) systems are protein toxin delivery systems only recently appreciated to be widespread among Gram-negative bacteria. CDI occurs when bacteria use the toxic C-terminus of a polymorphic surface-exposed protein to inhibit the growth of neighboring bacteria upon cell-cell contact. The protein toxin (called BcpA in Burkholderia species) is delivered to the cytoplasm of target cells where it functions as a nuclease. Autoinhibition is prevented by production of a small immunity protein (BcpI). Toxins are variable and immunity proteins specifically bind and inactivate only their cognate toxin. CDI systems have been shown in a number of species to mediate bacteria-bacteria competition and biofilm formation.

Although work from many labs is increasing our understanding of how CDI system proteins work, many fundamental questions about their mechanism remain unknown, particularly for Burkholderia species. We use Burkholderia cepacia complex species, which cause opportunistic infections, as a model to investigate the molecular mechanisms that control CDI system fuction. Projects in the lab center on understanding how BcpA is secreted from donor/inhibitor cells, how it is imported into recipient/target bacteria, and how the genes that encode CDI sytems are regulated.