セミナー情報

In both plants and animals, the recognition of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) activates innate immune signaling, which further launches a cascade of defense responses including rapid cytoplasmic rearrangements. The actin cytoskeleton has been suggested as a central component for innate immune signaling and associated cellular responses.
However, the molecular mechanisms that underpin actin remodeling and the precise functions of these rearrangements during innate immune signaling remain to be fully elucidated. Combining high spatiotemporal imaging and powerful tools for quantitative analysis of actin architecture and dynamics, we are able to test the rapid response of cytoskeletal remodeling to MAMP perception in plant epidermal cells. We demonstrate that the abundance of actin filaments increases within minutes in response to several distinct MAMP signaling pathways and that regulation of filament dynamics is a convergence point for basal defense machinery. Actin remodeling is necessary for cell wall fortification as well as transcriptional reprogramming through MAPK and CDPK signaling pathways. Our quantitative analyses of actin dynamics and genetic studies suggest that MAMP-stimulated actin remodeling results from the inhibition of several key actin-binding proteins by cytoplasmic innate immune signals. In addition, we uncovered both parallel and convergent pathways for actin remodeling. Actin Depolymerizing Factor4 (ADF4) functions downstream of a signaling pathway elicited by the perception of a specific bacterial MAMP (elf26), whereas the ubiquitous barbed-end regulator, capping protein (CP), is identified as a universal target for multiple innate immune signaling events. Moreover, we demonstrate that the inhibition of CP by the signaling lipid, phosphatidic acid, plays an essential role for actin remodeling in response to MAMP signaling. Collectively, our data provide deeper and broader understanding of the mechanisms underlying actin remodeling during plant innate immunity.