Finding. Arabidopsis subclass I actin depolymerizing factors (ADF1 through ADF4) help Colletotrichum higginsianum by fragmenting actin filaments and keeping PENETRATION 2 (PEN2)-associated mitochondria off the fungal entry site. Losing ADF4, or silencing the subclass, restores that mitochondrial pile-up and blocks penetration and secondary hyphae.
Why this paper matters
Plant immunity has a spatial problem. The first successful cell is the one the fungus enters, and several PEN genes solve that problem by delivering organelles and metabolites to the attempted hole. PEN2 is already known as a myrosinase that rides a membrane compartment. This paper's mitochondrial sentence is that the compartment shows up with mitochondria, and that a host actin regulator decides whether they are allowed to stay.
Ohashi, Aoki, Inada and colleagues call subclass I ADFs susceptibility factors: genes the plant would be better off without during this infection. That is a sharper claim than 'actin is involved in immunity.' It says a conserved filament-severing protein is running interference against the plant's own organelle recruitment.
What they actually measured
Arabidopsis encodes 11 ADFs. Subclass I (ADF1 to ADF4) is the broadly expressed set. An adf4 knockout and an ADF1-4 RNA-interference line both resist Colletotrichum higginsianum. Cytology says the fungus fails at two sequential jobs: getting in, and then making secondary hyphae once it is in. Those failures travel with a visible defect: infection no longer fragments actin filaments the way it does in wild-type cells.
PEN2 is not a side note. The extra resistance of adf4 and ADF1-4Ri depends on it. The mechanistic sketch is therefore ordered: subclass I ADFs fragment actin during infection, fragmented actin suppresses PEN2-associated mitochondrial accumulation at entry sites, and without those mitochondria (or the PEN2 that rides with them) the fungus proceeds.
The authors are careful in the last sentence. They raise the possibility that Colletotrichum exploits host ADF-dependent actin regulation. They do not show a fungal protein that binds ADF.
How to read the score
This is a high-70s plant-microbe paper with a concrete mitochondrial localization claim and a genetic dependency (PEN2). Confidence is medium because the abstract is stronger on resistance and actin cytology than on what the mitochondria are doing once they arrive. It is not a bioenergetics paper. The organelle is a placed object in an immune synapse.
What to do with it
If you track mitochondrial positioning in immunity (plant or animal), this is the week's entry-site example. Pair it with other PEN-organelle stories before you generalize to mammalian phagocytosis. Do not write 'mitochondria kill Colletotrichum.' Write 'PEN2-associated mitochondria are part of the penetration block that ADFs appear to dismantle.'