Systemic acquired resistance is an immune response in plants that confers long-lasting resistance against a broad spectrum of pathogens. It is controlled by NPR1 and SNI1, which serve as the "on" and "off" switches for expression of proteins with antimicrobial activities, respectively. Pathogen infection also triggers an increase in DNA recombination to generate new traits for better adaptation to the selective pressure. The investigators of this project identified several additional proteins affecting both antimicrobial gene expression and DNA recombination and showed that they physically interact with SNI1. Through this project, these investigators will apply molecular genetic and genomic approaches to study the SNI1 protein complex and elucidate how this complex regulates both gene transcription and DNA recombination during plant immune responses. This project pushes the boundaries between studies of plant defense-related gene expression and chromosome structure and function in all higher organisms. For example, one of the proteins of interest is BRCA2, which is associated with familial breast cancer in humans. But the molecular function of BRCA2 is not well known. Studies of BRCA2 function in plant defense may shed new light on how this protein functions in general. The success of this project will also have a significant impact on agriculture in controlling crop disease and benefit the efforts to project the environment. The broader impacts of this project also include excellent training opportunities for postdocs, graduate and undergraduate students in molecular genetics and genomics. It will allow the principle investigator of the project to continue serving as a mentor in a program for minority undergraduate summer research and a panelist in the University Women in Science and Engineering program.

Project Report

Through this NSF sponsored project, we made two major breakthroughs in our understanding of the immune mechanisms in plants. (1) DNA damage is normally detrimental to living organisms. Our study shows that it can also serve as a signal to promote immune responses in plants. We found that the plant immune hormone salicylic acid (SA) can trigger DNA damage in the absence of a genotoxic agent. Through genetic approaches, we showed that DNA damage sensor proteins are required for effective immune responses. We propose that activation of DNA damage responses is an intrinsic component of the plant immune responses. (2) In plants, death of infected cell is a common immune strategy. However, even through years of research, it is still a mystery how recognition of a pathogen signal can lead to plant cell death because the genes required for cell death in animals are not found in plants. Through genetic and genomic studies we discovered that in response to pathogen challenge, the key cell cycle regulators are perturbed. Overactivation of these proteins results in cell death and disease resistance. Immunity, DNA damage repair, and cell cycle regulations are fundamental biological processes presence in all organisms. Our study revealed the underlying connections between them. Understanding these processes will benefit agriculture and lead to development of safer and more effective ways of controlling crop disease.

Agency
National Science Foundation (NSF)
Institute
Division of Integrative Organismal Systems (IOS)
Application #
0744602
Program Officer
Michael L. Mishkind
Project Start
Project End
Budget Start
2008-03-01
Budget End
2013-02-28
Support Year
Fiscal Year
2007
Total Cost
$680,000
Indirect Cost
Name
Duke University
Department
Type
DUNS #
City
Durham
State
NC
Country
United States
Zip Code
27705