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Tip growth is a highly polarized growth process essential for plant growth and reproduction. However, its molecular mechanism and evolutional significance still remain elusive. Here, we show that plant-specific armadillo-repeat containing kinesin, MpARK1, drives long-range organelle transport and microtubule convergence in tip growing rhizoids in a basal land plant Marchantia polymorpha. MpARK1 is required for anterograde transport of the nucleus and plastids to maintain their position during persistent tip growth. Furthermore, MpARK1 participates in microtubule focusing on the apex to stabilize growth direction. MpARK1-dependent rhizoid growth is essential for plant anchorage and soil holding capacity. Thus, ARK might be co-opted to serve as a long-range transporter and intracellular organizer in the primitive rooting structure (rhizoid) for the adaptation to terrestrial environments. Our findings suggest that ARK was comparable to animal anterograde kinesin, challenging the traditional view that actomyosin-based cytoplasmic streaming is a dominant transport mode in plant kingdom.

Inflammation is implicated in the onset and progression of various diseases, including cerebral pathologies. Here we report that DJ-1, which plays a role within cells as an antioxidant protein, functions as a damage-associated molecular pattern (DAMP), and triggers inflammation if released from dead cells into the extracellular space. We first found that recombinant DJ-1 protein induces the production of various inflammatory cytokines in bone marrow-derived macrophages (BMMs). We further identified a unique peptide sequence in the αG and αH helices of DJ-1 that activates Toll-like receptor 2 (TLR2) and TLR4. In the ischemic brain, DJ-1 is released into the extracellular space from necrotic neurons within 24 hours after stroke onset and makes direct contact with the surfaces of infiltrating myeloid cells. Administration of an antibody against DJ-1 suppresses the expression of inflammatory cytokines in infiltrating immune cells and attenuates ischemic neuronal damage. Our results demonstrate a previously unknown function of DJ-1 as a DAMP and suggest that extracellular DJ-1 could be a therapeutic target to prevent inflammation in tissue injuries and neurodegenerative diseases.Significance statementDJ-1 has been thoroughly investigated as a cytoprotective antioxidant protein in neurons. However, here we demonstrate that extracellularly released DJ-1 triggers neurotoxic inflammation after ischemic stroke. Intracellular DJ-1 increases in response to oxidative stress in ischemic neurons, but if ischemic stresses result in necrotic cell death, DJ-1 is released extracellularly. Released DJ-1 interacts with TLR2 and TLR4 on the surface of infiltrating myeloid cells and triggers post-ischemic inflammation, leading to the exacerbated pathologies of ischemic stroke. Thus, extracellular DJ-1 is a previously unknown inflammatogenic DAMP, and may be a putative target for therapeutic intervention to prevent progression of inflammatory and neurodegenerative diseases.