The Zavaliev Lab at Kennesaw State University explores how the plant immune system reprograms cellular homeostasis and tissue organization during pathogen infection. We use molecular, cellular, and genomic approaches to uncover the mechanisms that activate and coordinate immune responses across cell types and tissues, and determine their impact on plant growth, development, and disease resistance.
Embedded Files
OUR RESEARCH
Plants are constantly challenged by pathogens and environmental stresses. Without specialized immune cells and cell mobility, plants are uniquely capable of sensing danger and launching their defences from each and every cell and communicating these signals to neighboring cells and distant tissues. Understanding how cellular processes are reprogrammed upon immune activation, and how these changes ultimately determine plant growth, development, and survival, is a central focus of our research. One of the most important immune pathways in plants is Systemic Acquired Resistance (SAR), a long-lasting immune state that protects plants against a broad spectrum of pathogens and environmental stresses. At the heart of SAR lies the NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1) protein, the master regulator of salicylic acid-mediated immunity, which initiates extensive transcriptional reprogramming in tresponse to pathogen attack. However, SAR involves much more than changes in gene expression. Becasue it is a systemic plant resposne, SAR also leads to major changes in cellular homeostasis enabling to adjust the growth and developmental processes with demands of the immune system. We are particularly interested in understanding how cells establish this enhanced survival state and how these protective responses are coordinated across the entire plant.
Biotrophic bacterial pathogens provide powerful systems for studying these questions because their intricate interactions with host cells allow us to examine immune processes in living cells that exhibit a wide spectrum of responses to infection. Our laboratory uses bacterial pathogens that cause significant losses in agricultural crops and influence crop productivity and resilience, including Xanthomonas vasicola (Xvh) and multiple Pseudomonas syringae pathovars, including P. syringae pv. syringae (Pss), pv. maculicola (Psm), and pv. tomato (Pst). We have established both crop and model plant pathosystems using these pathogens: Xvh and Pss in sorghum, and Psm and Pst in Arabidopsis thaliana. By combining these complementary systems, we are able to investigate both conserved mechanisms of plant immunity and crop-specific immune adaptations. To establish infection, most bacterial pathogens utilize type III secretion systems to inject effector proteins into host cells. These effectors suppress immune signaling and reprogram host cellular processes to promote pathogen growth and colonization. In resistant plants, recognition of these effectors by specific immune receptors activates effector-triggered immunity (ETI), a potent defense response that restricts pathogen spread and often culminates in localized programmed cell death at the site of infection. In susceptible plants, however, effectors evade recognition, allowing pathogens to suppress both local and systemic immune responses and ultimately cause disease. By examining how bacterial effectors interact with host cellular machinery at molecular and subcellular levels, we aim to identify key regulatory nodes that control the coordination of immunity, cellular homeostasis, and survival. These studies provide valuable insights into how plants balance defense activation with the maintenance of normal cellular functions. By integrating molecular biology, cell biology, plant pathology, genetics, and advanced imaging approaches, our laboratory seeks to uncover the fundamental principles governing plant immunity. Ultimately, we aim to translate these discoveries into strategies for engineering disease-resistant bioenergy and agricultural crops with enhanced resilience, sustainability, and productivity.
CURRENT PROJECTS
1. Plasmodesmata and Intercellular Immune Signaling
Plant cells are interconnected by plasmodesmata (PD), nanoscale membrane-lined channels that facilitate the movement of signals, metabolites, proteins, and RNA between neighboring cells. These structures form the physical network through which tissues coordinate their physiological and immune responses. We investigate how plasmodesmata regulate the spread of immune signals and contribute to the coordination of defense responses across the plant.
To understand plant immunity beyond the level of individual cells, it is essential to examine how tissues are organized and how cells communicate with one another. Because plasmodesmata provide direct cytoplasmic connections between cells, they are ideally positioned to mediate the integration of local and systemic responses to environmental and pathogenic challenges. We are particularly interested in defining the roles of plasmodesmata in normal physiology, immune coordination and, tissue homeostasis. Using inducible, tissue-specific approaches to manipulate plasmodesmatal connectivity, we determine how restricting cell-to-cell communication affects local immune responses and the establishment of Systemic Acquired Resistance (SAR).
Our findings indicate that plant immunity is not purely cell-autonomous; rather, effective tissue and organ defense requires extensive cell-cell connectivity. By combining plasmodesmata biology with studies of NPR1-mediated immune signaling, we are exploring how immune signals move throughout the plant and how distinct cells within a tissue synchronize their responses during infection. Ultimately, this work seeks to establish a framework for understanding the hierarchy of immune and homeostatic regulation across cellular, tissue, and organismal scales, revealing how localized cellular responses are integrated into robust systemic immunity.
2. Stress-Induced Protein Assemblies
Plants continuously encounter environmental and biotic stresses that disrupt cellular homeostasis. In response, cells rapidly reorganize their internal architecture through the formation of dynamic protein assemblies, including stress granules, processing bodies, and other biomolecular condensates. These structures temporarily compartmentalize proteins and RNAs, allowing cells to prioritize survival, reprogram gene expression, and coordinate stress responses. Our research investigates how stress-induced protein assemblies contribute to plant immunity and systemic defense. We are particularly interested in understanding how pathogen infection, salicylic acid signaling, and activation of Systemic Acquired Resistance (SAR) influence the formation and function of these assemblies.
We are particularly interested in understanding how cells establish this enhanced survival state and how these protective responses are coordinated across the entire plant. While transcriptional reprogramming is a major component of immune activation, emerging evidence suggests that post-transcriptional regulation mediated by protein-RNA condensates plays a critical role in determining the timing, magnitude, and duration of defense responses. Using advanced imaging, molecular genetics, and cell biological approaches, we examine the composition, dynamics, and function of stress-induced assemblies in living plant cells. We seek to identify the molecular mechanisms that govern their formation and disassembly, determine how they interact with immune signaling pathways such as NPR1-dependent signaling, and establish how they influence cellular survival during stress. Ultimately, our goal is to understand how plants use dynamic intracellular organization to coordinate stress adaptation across cellular and tissue scales. By uncovering the principles that regulate stress-induced protein assemblies, we aim to reveal new mechanisms that enhance resilience against pathogens and environmental challenges.
3. Balancing Immunity with Growth and Development
Plants face a fundamental challenge: resources allocated to defense are unavailable for growth and development. As a result, immune activation often comes at the cost of reduced growth, altered development, and decreased productivity. Understanding how plants balance these competing demands is essential for developing crops that are both resilient and high yielding. A major focus of this project is to define how growth and developmental processes are altered in cells exposed to sustained immune signaling. While plant immunity has traditionally been viewed as a property of every cell, an important unanswered question is whether all cells in a tissue and all tissues are equally immune competent. We are intrigued by the possibility that plants achieve functional specialization during defense, whereby a subset of cells in a tissue acquires enhanced immune functions, allowing other cells to maintain growth, development, and essential physiological activities. Such a division of labor could provide an efficient strategy for balancing survival with productivity during periods of stress. Using single-cell transcriptomic and multi-omic approaches, we seek to identify these specialized immune cell populations and the cellular circuits.
We are particularly interested in uncovering the molecular mechanisms that coordinate communication between immune-active and growth-supporting cells, and in understanding how these interactions shape plant growth and development during stress.
Page updated
Google Sites
Report abuse