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 Final Project Report for the Public

Like humans, plants have a highly effective immune system that keeps them healthy despite being constantly exposed to potential disease-causing microorganisms in their environment. This immune system is deployed in multiple layers that are called into action successively. But when all measures to keep the pathogen out fail, plants resort to one last strategy in which the very first cell that gets invaded commits suicide, sacrificing one or two cells at the site of infection to save the rest of the individual. Called the hypersensitive response (HR), this sacrificial cell death is triggered by so-called disease resistance proteins (R proteins). These proteins function as intracellular sensors to detect the presence of pathogens based on recognition of the molecules they produce or of their biochemical activities.  Detection then triggers an HR, but exactly how this happens remains an enigma. Various approaches used over the past two decades have turned up only a few players that relay R gene detection of pathogens into an HR response. This project was undertaken to expand our knowledge of HR using maize (corn) as an example.

 A unique feature of the project was that we exploited the natural variation between different maize varieties to uncover components of the HR response.   We used a novel genetic strategy relying on HR initiated not by a pathogen but by a mutant R gene (called Rp1-D21) that spontaneously triggers HR; in other words a type of plant autoimmunity.  The response caused by Rp1-D21 is very much exaggerated and much more easily measured compared to normal HR (which is barely visible to the naked eye) and its severity changes depending on what maize variety the gene is in, being enhanced to lethal levels in some and suppressed almost completely in others.  These different levels of HR caused by Rp1-D21 are due to the presence of different genes or versions of genes that affect the HR in the different varieties. Genes that affect any easily-measured trait can be ‘mapped’ in a fairly straightforward manner and that is what we did in this project:  We mapped genes that affect this aberrant immune response on the assumption that they would also affect the normal immune response (which is much harder to measure).

Since, in this approach we use an exaggerated, mutant version of our trait of interest as a ‘reporter’ for the trait, this strategy has been named Mutant-Assisted Gene Identification and Characterization, or MAGIC for short. Using this strategy we were able to efficiently assess dozens of varieties of maize for versions of genes that either boosted or dampened the HR response.

Rp1-D21 is an aberrant form of the maize Rp1 disease resistance gene, which normally confers HR-based immunity to the common rust disease caused by a fungal pathogen. The diverse germplasm was derived from two public sources, the maize diversity panel and the NAM association mapping panel, the development and genetic characterization (genotyping) of which was made possible by funds from NSF previously to other groups.

The two major initial goals for this project were:

1) A comprehensive screen for genes that contribute naturally-occurring variation in the hypersensitive defense response,

2) Proof-of-concept for the MAGIC approach.

Both of these goals were largely achieved. Our study demonstrated that MAGIC is a very effective approach in exploring the genetic basis of a complex trait using natural variation. It provided the first system-wide analysis of natural variation that modulates the HR response in plants, and identified the location of 44 genes that play a role in controlling the HR response.

We have now taken this work further.  In two cases we have identified the specific genes associated with modulating HR.  One of these genes is involved in lignin production, an important component of the cell wall, the other in protein degradation.   We have shown that some of the genes that control HR also control disease resistance and a type of low level, constant defense response naturally found in some plants that makes them more disease resistant but also stunts their growth.

This project provided training for 17 postdoctoral scholars, 7 graduate students, and more than 30 undergraduate and high school students in the science of genetics and genomics. Half of these trainees were women. In our outreach efforts we collaborated with the North Carolina Museum of Natural Sciences ( in a number of activities. We co-developed, financially supported and participated in two classes and a teacher workshop that have already reached more than 1000 students and 50 teachers and have been incorporated into the standard offerings of the museum. We organized plant genetics demonstrations at several local elementary and middle schools, gave several presentations on plant genetics to the public. Six publications have already resulted from this work, and several others are in review for publication or are in preparation.