Our Research at UMAydis@IPMB
Embedded Files
To combat fungal pathogens
To combat fungal pathogens
Corn Smut fungi Ustilago maydis
The dimorphic biotroph U. maydis, causing large tumors on maize, initially grows as haploid yeast-like cells outside the host. Triggered by plant environmental cues, U. maydis integrates signals and transitions to a parasitic filamentous stage with a complex and irreversible developmental process. This involves the formation of infective structures for penetration, tumorigenesis, and eventual sporogenesis, and requires precise regulation.
A key aspect of U. maydis's ability to colonize plant cells is its reliance on a diverse array of secreted effector proteins, major contributors to the interplay of plant immunity and pathogen virulence. Their precise expression is coordinated to ensure accurate production, timing, and distribution, enabling interactions with specific host cell targets, influencing plant cellular activities, suppressing immunity, and facilitating disease progression.
Rust fungi, notorious biotrophic pathogens affecting agriculture and forestry, pose challenges in isolation and cultivation due to their dependence on living host cells. U. maydis, sharing key characteristics with rust fungi, can be cultured and genetically manipulated in the laboratory. This makes U. maydis a valuable model species for studying broader aspects of biotrophic interactions and diseases caused by pathogenic fungi, exploring molecular mechanisms behind fungal dimorphism, and contributing to our understanding of fungal biology.
Cell-surface Effectors at Work
Ustilago maydis, like other filamentous pathogenic fungi, relies on host environmental cues to switch between developmental stages and complete its life cycle. The central unexplored area in fungal pathogenesis lies in understanding how fungal cells perceive external signals and integrate them to regulate developmental transitions and effector waves. At the critical interface of U. maydis-maize interactions, fungal cell walls act as the initial point of contact, with cell surface-localized proteins potentially playing a crucial role in perceiving environmental signals, providing hyphal protection, and avoiding recognition. These proteins may activate downstream signaling components, regulating subsets of effector proteins and inducing morphological changes for fungal adaptation in ever-changing plant environments. Understanding fungal sensing and adaptation mechanisms will offer valuable insights to develop strategies to impede fungal filamentous transition, holding promise for ultimately preventing fungal diseases.
Extracellular-localized Effectors at Work
The extracellular space serves as the initial battleground where plants confront fungal pathogens. It is protected by a sophisticated defense system comprising cell-surface receptors, hydrolytic enzymes, and toxic secondary metabolites. These components trigger plant innate immunity, forming a robust barrier against microbial intrusion. However, despite the effectiveness of this defense system, the precise mechanisms by which pathogens like U. maydis breach this barrier to colonize plant cells remain enigmatic. Unraveling the molecular intricacies of effectors localized at the forefront of this interaction will unveil the strategies employed by U. maydis to circumvent plant defenses. Additionally, this research aims to elucidate the host plant’s defense mechanisms, providing valuable insights into the dynamics of apoplast immunity.
Our Focus: Effectors
Given the crucial role of effectors in disease progression, delving into their biochemical functions is vital for understanding fungal virulence mechanisms. Analyzing effectors comprehensively will provide insights into fungal virulence and plant defense mechanisms, advancing our understanding of plant-pathogenic basidiomycete interactions, and potentially guiding crop disease management strategies.
Our research interest
To uncover the invasion strategies of U. maydis and prevent the onset of initial infection, we focus on studying effectors located at the interaction interface of maize-U. maydis, aiming to reveal the following mechanisms:
Sensing and adaptation mechanisms
Effector regulatory mechanisms
The mechanisms by which fungal cells deactivate apoplastic immunity
Corn smut disease
U. maydis sporidial cells
U. maydis colonizes maize leaves
U. maydis-infected maize seedlings
Page updated
Google Sites
Report abuse