Abstract
Conserved microbe-associated molecular patterns (MAMPs) are sensed by pattern recognition receptors (PRRs) on cells of plants and animals. MAMP perception typically triggers rearrangements to actin cytoskeletal arrays during innate immune signaling. However, the signaling cascades linking PRR activation by MAMPs to cytoskeleton remodeling are not well characterized. Here, we developed a system to dissect, at high spatial and temporal resolution, the regulation of actin dynamics during innate immune signaling in plant cells. Within minutes of MAMP perception, we detected changes to single actin filament turnover in epidermal cells treated with bacterial and fungal MAMPs. These MAMP-induced alterations phenocopied an ACTIN DEPOLYMERIZING FACTOR4 (ADF4) knockout mutant. Moreover, actin arrays in the adf4 mutant were unresponsive to a bacterial MAMP, elf26, but responded normally to the fungal MAMP, chitin. Together, our data provide strong genetic and cytological evidence for the inhibition of ADF activity regulating actin remodeling during innate immune signaling. This work is the first to directly link an ADF/cofilin to the cytoskeletal rearrangements elicited directly after pathogen perception in plant or mammalian cells.
Highlights
The innate immune system is a critical line of defense to protect the host from infection by potential pathogens; this includes both nonspecific basal and inducible responses
We demonstrated that both pathogenic bacteria and microbe-associated molecular patterns (MAMPs) peptides trigger a transient increase in actin filament abundance during the innate immune response of plant epidermal cells (Henty-Ridilla et al, 2013a)
Increased actin abundance is an important feature of plant innate immunity, as plants infiltrated with the actin polymerization inhibitor latrunculin B (LatB) are more susceptible to the growth of the bacterial phytopathogen Pseudomonas syringae pv tomato DC3000 (Henty-Ridilla et al, 2013a)
Summary
The innate immune system is a critical line of defense to protect the host from infection by potential pathogens; this includes both nonspecific basal and inducible responses. Much of our understanding of innate immune responses comes from studies of toll-like receptor (TLR) signaling pathways in mammalian cells. The resulting signal transduction cascades stimulate de novo gene transcription and regulate changes in lipid content, membrane ruffling, and endocytosis; the latter events have been correlated with changes in actin cytoskeletal dynamics during basal immune signaling (Granucci et al, 2001; Huang et al, 2001). Actin cytoskeletal remodeling in mammalian cells is a critical facet of innate immunity that functions in phagocytosis, the arrangement and endocytosis of
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