Plant diseases caused by diverse pathogens severely reduce crop yields and threaten global food security. Enhancing plant innate immunity against various pathogens is one of the most effective ways to defend plants against infection and prevent epidemics in crops. Understanding plant innate immunity at the molecular level is the key to enable and accelerate breeding and production of plants with enhanced disease resistance. The past three decades have seen a tremendous increase of knowledge on plant innate immunity systems at the molecular and cellular levels. Plants utilize induced responses in addition to existing physical barriers to deter pathogen invasion. It is known that calcium acts as a signal and messenger to mediate such an induction of immune responses. Specific features of calcium ion in the cell, such as its level, shape, amplitude, and frequency, in response to environment may carry stimulus information and induce distinct responses. How the signal of calcium is generated in response to pathogen and how it translates into responses are not understood. The project will investigate the function of several proteins that are important to generate calcium signals in a model plant-pathogen interaction system. The investigation will reveal how calcium signal and signaling contribute to plant innate immune response. Additionally, this project will train graduate students, postdoc fellows and undergraduate students and prepare them to become next-generation scientists in basic science and agriculture sectors. It will also provide public education on crop disease resistance, agriculture and climate change.

Recent studies have revealed a regulatory role of evolutionarily conserved BON proteins in disease resistance of both Arabidopsis and rice. The Arabidopsis BON1 is found to work closely with auto-inhibitory calcium ATPases ACA10/8 and a calcium dependent protein kinase CPK3 to modulate calcium signature and signaling in Arabidopsis. Preliminary study also implicates calcium transport proteins including ACA10/8, CCX4 and GLR2 as CPK3 target in a feedback regulation of calcium signaling. This study aims to identify calcium signal generating molecules and their regulation by BON1 and CPK3 in plant immunity. Four specific aims are to: 1) determine the impact of ACA10/8, CCX4 and GLR2 on defense responses and calcium signature, 2) investigate the regulatory role of BON1 on ACA10/8, 3) investigate the potential regulation of ACA10/8 by CPK3 in defense response, and 4) identify components acting in parallel with CPK3 in dampening defense responses. This study will reveal new regulatory mechanisms in plant immunity. Novel information will be obtained on characteristics of calcium signatures in response to bacterial pathogens, calcium transport molecules for generating calcium signature, as well as regulatory mechanisms of calcium signature and its decoding in defense responses.

This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.

Agency
National Science Foundation (NSF)
Institute
Division of Integrative Organismal Systems (IOS)
Application #
1946174
Program Officer
Michael Mishkind
Project Start
Project End
Budget Start
2020-03-15
Budget End
2023-02-28
Support Year
Fiscal Year
2019
Total Cost
$925,000
Indirect Cost
Name
Cornell University
Department
Type
DUNS #
City
Ithaca
State
NY
Country
United States
Zip Code
14850