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Jun 15
InterConnections: Get to Know Member Matt Neubauer

The April 2020 Editor’s pick for MPMI is “Arabidopsis EDR1 Protein Kinase Regulates the Association of EDS1 and PAD4 to Inhibit Cell Death”. First author Matt Neubauer shared a summary of how the project came about, and a little about the trials and tribulations that eventually led to publication of his graduate work while in the lab of Roger Innes at Indiana University. Matt has now gone on to a postdoctoral position at North Carolina State University. Matt recently presented the first What's New in MPMI! virtual seminar. You can watch his seminar here​

Submitted by Matt Neubauer:

After many years, it is great to have our work on the role of EDR1 in the regulation of PAD4 and EDS1 published in MPMI. This project was initially intended to be a short investigation, however, it evolved greatly over time. The winding story of this project highlights how accidental discoveries and observations can enable important scientific discoveries.

I originally became interested in plant biology and biotechnology as a high school student, which motivated me to pursue a degree in biology. After finishing my BS in biology at Loyola University Chicago, I joined the Genome, Cell, and Developmental Biology PhD program at Indiana University. I became a member of Roger Innes’s lab in early 2014 and began working on a few projects focused on investigating the role of EDR1 in regulating plant defenses. In my second year, I took up the project that we ultimately published in MPMI.

The project began when a postdoc in our lab, Irene Serrano, discovered that the edr1-1 mutants she was working with actually carried a second mutation, located in the PAD4 gene (pad4-13). PAD4 is a well-known regulator of plant disease resistance, so we worried that some of our previous experiments using edr1-1 plants may have been influenced by the presence of this mutation. Irene sought to determine what effect pad4-13 has on edr1-1 plants, and whether it had been present in any of our previous seed stocks. Her results indicated that pad4-13 results in a gain-of-function, enhancing plant resistance and cell death. Interestingly, it did not affect the primary edr1 phenotype, enhanced resistance to powdery mildew.

At this point, we felt we had a duty to report these results to the scientific community, particularly those who had studied edr1-1 mutants. We determined that our original edr1-1 stocks did not contain pad4-13, however, we wanted to inform others about this mutation and alert them to the possibility that it was present in their lines. Due to the nature of this discovery, we felt this work would best be suited for a lower impact journal. However, we had a few interesting ideas that we wanted to test which we felt might enhance our work.

One of my objectives when I became involved in the project was to investigate how the pad4-13 mutation enhances PAD4 signaling. This was a long process, with many dead ends. Ultimately, we were unable to demonstrate how pad4-13 enhances PAD4 activity. It did not alter PAD4 accumulation or localization, formation of the PAD4/EDS1 complex, or block an important modification site. We concluded that pad4-13 likely affects an unknown PAD4 signaling mechanism.

Despite these setbacks, we had another idea we wanted to pursue whether EDR1 directly regulates PAD4. This hypothesis was based upon the observation that pad4-13 enhances some, but not all, edr1 phenotypes; as well as previously published data showing that loss of PAD4 suppresses edr1 phenotypes. These observations indicate that EDR1 and PAD4 may function in a common pathway. Since the interaction between PAD4 and its partner EDS1 is important for downstream defense signaling, I tested whether expression of EDR1 affects the formation of the EDS1/PAD4 complex. We were excited to find that, indeed, expression of EDR1 inhibited the formation of the complex. This discovery prompted us to further investigate the interaction between EDR1 and EDS1/PAD4, a slow process that occurred over many years.

We were initially disappointed and worried when we found the pad4-13 mutation in our edr1-1 stocks. In fact, we thought it was appropriate that pad4-13, which had proved so difficult to understand, was the thirteenth PAD4 allele to be discovered. Despite being an unlucky discovery, pad4-13 led us to important insights into the function of EDR1. Our decision to pursue the hypothesis that EDR1 directly interacts with PAD4 and EDS1 was a fortunate one which led to a new discovery about plant defense signaling.

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