ARMOR

In plants and animals, the plasma membrane (PM) is a fundamental boundary between the cell and its environment. The PM acts as a critical interface to mediate interactions with mutualistic and pathogenic fungi, facilitating processes such as microbial adhesion, signalling and immune modulation to maintain homeostasis or trigger adaptive host responses. The PM is a dynamic structure composed mainly of a lipid bilayer interspersed with proteins and sugars, with lipids, particularly sterols, playing a crucial role in maintaining membrane fluidity and cellular integrity. Inside cells, autophagy can be activated to mediate the degradation of intracellular components through the sequential and regulated action of over 30 autophagy-related proteins (ATGs). Initially believed to function solely in the autophagy process, ATGs are now recognized for their role in regulating cell membrane dynamics. Recent studies, including one from our laboratory, have identified autophagy proteins ATG5, ATG8, and ATG16L1 as critical contributors to PM repair following damage caused by pathogenic microorganisms during host cell invasion. Whereas these findings suggest that ATGs play a central role in the PM-associated stress response to limit pathogen invasion, they question about (i) the involvement of such ATGs response in the establishment of beneficial microorganisms and (ii) the existence of specific ATGs responses to pathogen or beneficial micro-organisms.

In line with WP2 of the HARMI project, focusing on microbiota-host interactions, this project aims to explore, in both plant and animal cells, the evolutionary conserved molecular mechanisms by which ATGs influence PM dynamics induced in host cells during biotic interactions. We propose to (i) characterize the recruitment of ATGs at PM in plant and animal cells induced by interactions with mutualistic or pathogenic fungi, and (ii) evaluate ATG-mediated functional changes in the PM in response to microbial contact, with a focus on PM spatial organization, lipid composition, and stress resistance. By sharing tools and approaches already developed by both partner laboratories, in fungal/animal (P1) and fungal/plant (P2) interactions, this project will identify common or specific mechanisms of microorganism-host cell interactions. By examining the critical step of microbial penetration across various host-fungal interaction models, we aim to identify the key mechanisms underlying the distinct cellular strategies activated in each type of interaction (mutualistic or pathogenic).