Title: Identifying immune regulators via dominant negative resistance proteins 

Presenter: Prof. Morten Petersen

University: Department of Biology, University of Copenhagen

Time: 10:00-11:15, July 13, 2012

Venue: Room A203, Institute of Microbiology, Chinese Academy of Sciences

Abstract:

There are numerous examples of mutants with autoimmunity-related phenotypes. These so-called “lesion-mimics” are, in many cases, caused by mutations in genes hypothesized to be negative regulators of the HR. Other examples include point mutations in R proteins. The lethal, recessive accelerated cell death 11 (acd11) mutant of Arabidopsis is characterized by constitutive activation of immune responses and PCD in the absence of pathogen attack. ACD11 encodes a putative sphingosine transfer protein, but its specific biochemical function remains unknown. acd11 mutants develop normally until the 2-4 leaf stage, and the genetic requirements for acd11 cell death are similar to those for the HR triggered by one class of R protein immune receptor.

Using a screen for genetic suppressors of death in acd11 (lazarus mutants), we discovered that acd11 is suppressed by a dominant negative mutation in the P-loop motif in a resistance (R) protein, LAZ5. We therefore proposed that the R receptor is triggered by the absence of ACD11, implying that ACD11 (or a complex containing ACD11) may be a guarded pathogen effector target. Site-directed DN mutant alleles can be made for other R genes and we have exploited this and discovered that other lesion mimic mutants can be suppressed by specific R-DN alleles and identified R proteins that function below pattern recognition receptors.