A Bacterial Virulence Protein Suppresses Host Innate Immunity to Cause Plant Disease

Transcription

1 A Bacterial Virulence Protein Suppresses Host Innate Immunity to Cause Plant Disease Nomura, K., Debroy, S., Lee, Y.H., Pumplin, N., Jones, J., and He, S.Y. (2006). Science 313, Presented by: Bob Berkey

2 Background Plants have evolved immune system to defend against microbial organisms that attempt to inject virulence proteins to suppress immunity Mammalian pathogens can regulate cytoskeleton, membrane composition, vesicle trafficking, and host immunity Not much is known about molecular mechanisms of bacterial effector proteins in plants Believed effector proteins suppress the host immune responses

3 Pseudomonas syringae Gram negative plant pathogenic bacterium Over 40 pathovars of P. syringae that can infect a variety of plant species including economically important ones like tomato Examined strains all use Type III secretion system for pathogenesis Associated hrp/hrc genes Exchangeable effector locus Conserved effector locus

4 Paper Overview Looking for the molecular targets of bacterial virulence proteins important in disease development, specifically Pst DC3000 HopM1, conserved P. syringae virulence protein, targets the immunity associated protein AtMIN7 in Arabidopsis Mediates this through proteasome degradation Results show strategy of pathogens that exploit proteasome to overrun immunity and cause disease symptoms

5 Previous Work & Information Partial deletion of conserved effector locus in CEL mutant reduction of bacterial population and elimination of disease symptoms (tomato and Arabidopsis) Deletion is functionally redundant effector genes hopm1 and avre HopM1: 712 amino acid protein translocated into cell during infection by type III system porf43: plasmid expressing HopM1 and cognate chaperone ShcM

6 HopM1 Transgenic Expression Recovers Virulence of CEL Mutant & Important Regions for Virulence Function of HopM1 Figure 1

7 Pink arrows indicate the dominant negative effect of HopM and HopM on ΔCEL mutant. Blue arrows indicate the ability of fulllength HopM1 or HopM to completely or partially complement the ΔCEL mutant Figure S1

8 The Dominant Negative Effect & Y2H Screens Figure 2 Figure S2B

9 Figure S4B Destabilization of AtMIN Protein(s) Necessary for promotion of P. syringae Pathogenesis by HopM1 Figure 3

10 BFA Can Supplement for HopM1 and Restore Virulence ARF GEF proteins: key pats of vesicle trafficking system BFA: well known inhibitor of vesicle trafficking Figure 3C

11 AtMIN7 Required for Cell Wall Associated Defense Callose deposition: cellular marker of cell wall defense Figure 4

12 Conclusions HopM1 is necessary for the destabilization of AtMIN7, a host ARF GEF family protein active in host immune response, through the proteasome Recent findings show a P. syringae effector protein AvrPtoB has intrinsic E3 ligase activity and that vesicle trafficking and extra cellular secretion are important in immune response HopM1 does not show sequence homology to AvrPtoB or common motifs for components of ubiquitination/proteasome system HopM1 probably functions as an adaptor protein that targets AtMIN7 to degradation pathway

13 P. Syringae Actions Eliminated component of vesicle trafficking pathway in order to suppress cell wall associated host defense Salmonella enerica Modulation of trafficking is a common goal of human and plant pathogens Figure S6

14 Possible Future Directions GFP fluorescent tag studies of HopM1 Only looked at Pst DC3000, do other P. syringae strains work in a similar manner in regards to AtMIN proteins particularly AtMIN7? Mechanisms of AtMIN7 targeting for degradation, and what protein(s) is HopM1 functioning as adaptor with? Similar function results seen in Arabidopsis from other bacterial pathogens? Other molecular targets of HopM1 since BFA treatment showed more complete virulence recovery than AtMIN7 KO?