Jennifer D. Lewis Special Seminar Friday, Feb. 10

February 06, 2012


 

  • WHEN: Friday, Feb. 10, noon to 1 pm
  • WHERE: Barker 101, UC Berkeley
  • WHO: Jennifer Lewis, new faculty at PMB
ABSTRACT
The plant pathogen Pseudomonas syringae causes disease in a large number of different plant species using the type III secretion system to secrete and translocate effector proteins into the plant. Many of these effector proteins are believed to function primarily in the suppression of host defense signaling. However recognition of these effector proteins by resistance (R) proteins induces a defense response. The YopJ / HopZ family of effector proteins is a common and widely distributed effector family found in both animal and plant pathogenic bacteria. The P. syringae HopZ family includes three major allele types (one ancestral and two brought in by horizontal gene transfer) whose diversification was driven by the host defense response. We previously demonstrated that virulence and avirulence phenotypes in Arabidopsis are strongly allele-specific and that the ZAR1 resistance protein recognizes HopZ1a in Arabidopsis. I will describe a novel, high-throughput interactor screen using next-generation sequencing technology to elucidate the host targets of all the HopZ alleles and the ZAR1 resistance complex. I will also describe how genetic screens are identifying additional players in innate immunity. This work addresses how differences in host target specificity within one family of type III effector proteins contributes to the host specificity of this important pathogen.