Plant pathogens are challenges to crop production. In particular, fungal pathogens cause destructive diseases that threaten global food, feed and fiber production and jeopardize diversity of plant species. Studies that expand fundamental knowledge on how plants fend off microbial infection is expected to help design better disease control strategies. Multifaceted molecular, biochemical and genomic approaches will be deployed to understand how plants regulation activation of defense against pathogens. Plants activate a battery of defense mechanisms including the synthesis of diverse antimicrobial agents and other immune responses to deter infection or restrict the extent of damage after infection. How plants activate or suppress these mechanisms will be studied. Knowledge on the temporal and spatial regulation of such changes are important to understand the mechanisms of disease resistance. The untimely activation of some of these immune responses in the absence of pathogens is not beneficial to the plant. Consequently a tight control of on timing and spatial activation is critical. The molecular and biochemical mechanisms underlying such defense gene activation, reprogramming, and how these occurs in the context of eukaryotic DNA that is packed with chromatin will be determined. The cellular communication that link pathogen sensing to the activation of defense in the plant cell will be analyzed. Discoveries from this project will expand basic knowledge, and pave the way to develop disease resistant plants. Finally, this project will train undergraduate, graduate students and post-doctoral scientists in plant molecular biology.
Plant immune gene transcription is a major component of plant immunity with rapid and massive transcriptional programming occurring in response to pathogens. Changes in equilibrium of histone modifications mediated by histone modifying enzymes (HMEs) are critical players orchestrating these cellular responses. However, the mechanisms underlying transcription reprogramming in response to infection in the context of chromatin are not understood. This project is to dissect the signal transduction pathway connecting pathogen sensing to histone modifications, and the consequent dynamics in chromatin accessibility and transcription. The regulatory impacts of shifts in equilibrium of histone lysine methylations (HLMs) will be studied using histone methyl transferases and demethylases with antagonistic biochemical and functions. Molecular mechanisms and factors regulating events preceding reversible histone modifications and the subsequent changes in gene expression will be elucidated. Factors that regulate activation and recruitment of HMEs to target loci in response to infection to trigger shifts in HLMs and immune gene transcription will be studied. Transcription factors and nucleosome assembly proteins that are functional partners of HMEs in gene regulation will be analyzed. Aim1 focuses on regulation of HMEs by protein kinases, linking early events in immune responses to changes in chromatin state and gene expression. Aim2 is to characterize the functions of HME interacting transcription factors (TFs) and nucleosome assembly proteins. Aim3 is to determine genome wide gene expression profiles underlying shifts in equilibrium of HLM and decipher its biological impact. Discoveries from this project will improve basic knowledge and pave the way for epi-genome modifications of traits. Finally, this project will train undergraduate, graduate students and post-doctoral scientists.
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.
