This program is an ongoing project within the James R. Alfano laboratory at the University of Nebraska- Lincoln. Tom Elmo Clemente will serve as the PI on this project due to the passing of Dr. Alfano on November 21, 2019.

Improving soybean resistance to biotic stress is a strategy to protect yield. To accomplish biotic resistance requires an understanding of the mechanism underlying the resistance trait. Additionally, insight into how microbial pathogens successfully breach the plant’s innate immunity to pests, will aid in our ability to design genetic resistance strategies. Given pathogens have co-evolved with their host plants they circumvent the weak links of the plant’s immune system that if disabled will result in disease. This proposal seeks to exploit our current understanding underlying disease resistance strategies gleaned from model organisms and translate these findings to soybean [Glycine max (L.) Merr] with the goal of enhancing resistance to biotic stress. The bacterial pathogen Pseudomonas syringae pv. glycinea causes the economically significant bacterial blight disease of soybean. One of the primary pathogenic strategies that P. syringae uses is the injection of specific proteins referred to as type III effector proteins into plant cells to suppress the plant’s resistance response. The elucidation of the targets of these effector proteins within soybean is valuable information that can be used to subsequently design genetic approaches to circumvent disease. It is known that mechanisms of plant disease resistance are often commonly shared across various plant/pest interactions. Hence, gaining insight on resistance mechanism(s) underlying soybean/P. syringae interaction will inform the project on how to proceed in designing resistance towards other pathogens including oomycete and fungal plant pathogens. The collective information gathered can subsequently be utilized to help guide genetic strategies to enhance soybean resistance to plant pests

1- Continue to evaluate soybean events expressing GRP7 RNA-binding protein to monitor for enhanced resistance towards oomycete pathogens.
2- Develop genetic approaches to modulate cellular microtubule network, as a means to improve soybean resistance to pests.
3- Determine if the soybean blue light receptor protein, Phototropin 2, is associated with plant disease resistance in a similar mechanism observed in Arabidopsis.
4- Continue to identify soybean cellular targets of type III effectors injected upon infection by the pathogen P. syringae pv. glycinea, evaluate the importance of these targets to soybean immunity, and explore the extent that these targets can be manipulated to produce soybean plants with improve resistance to biotic stress.

1-Continue to evaluate soybean events expressing GRP7 RNA-binding protein to monitor for enhanced resistance towards oomycete pathogens.
2- Develop genetic approaches to modulate cellular microtubule network, as a means to improve soybean resistance to pests.
3- Determine if the soybean blue light receptor protein, Phototropin 2, is associated with plant disease resistance in a similar mechanism observed in Arabidopsis.
4-Continue to identify soybean cellular targets of type III effectors injected upon infection by the pathogen P. syringae pv. glycinea, evaluate the importance of these targets to soybean immunity, and explore the extent that these targets can be manipulated to produce soybean plants with improved resistance to biotic stress.

Continued support of this program will increase our knowledge on the genetic underpinnings that govern soybean's response to pathogen attack. This in turn, will aid in our ability to enhance soybean resistance and protect yield under disease pressure environments.
• This program will identify cellular components that are targeted by pathogens as a means to circumvent the plant's response to disease pressure
• The identified targets will subsequently be re-engineered into soybean through the tools of biotechnology, and the resultant transgenic events monitored for enhanced disease resistance phenotype