Pseudomonas syringae pv. actinidiae (Psa) causes destructive kiwifruit bacterial canker by invading vascular tissues across multiple plant organs. However, the cellular mechanism underlying its systemic transmission and cell-to-cell movement within these specialized vascular conduits remains unclear. In this study, a Psa-GFP strain and various microscopic techniques were used to investigate the interaction between kiwifruit and Psa. Our results reveal that Psa strategically exploits host vascular conduits for systemic movement, with the xylem vessel being the predominant avenue. In the phloem, Psa exhibits adaptive alteration in bacterial shape to traverse sieve pores, facilitating its systemic spread along sieve tubes and inducing phloem necrosis. Within the xylem, Psa breaches pit membranes to migrate between adjacent vessels. Furthermore, phloem fibers act as an initial barrier at the early stages of infection, delaying Psa's entry into vascular tissues during its journey to the xylem. Additionally, at the junctions of stem–stem or stem-leaf, branch trace or leaf trace mediates the bacterial organ-to-organ translocation, thus facilitating the systemic progression of disease. In conclusion, our findings shed light on the cellular mechanism employed by Psa to exploit the woody plant's vascular network for infection, thereby enhancing a better understanding of the biology of this poorly defined bacterium. These insights carry implications for the pathogenesis of Psa and other vascular pathogens, offering theoretical guidance for effective control strategies.

Ambient temperature affects the occurrence and prevalence of plant disease. Most bacterial diseases are damaging at high temperatures. However, kiwifruit bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa) has been found to be prevalent at relatively cool temperatures, and it is unclear how ambient temperature affects the development of kiwifruit bacterial canker. In this study, basal resistance to Psa was suppressed in kiwifruit at cool growth temperature (16 ℃) compared with at normal temperature (24 ℃). In addition, RNA sequence analysis and ethylene content assessment indicated that ethylene modulated kiwifruit resistance to Psa at normal growth temperature and that cool temperature inhibited ethylene accumulation and Psa-induced activation of the ethylene signaling pathway in kiwifruit. Virus-mediated silencing of the kiwifruit ethylene signaling gene AcEIN2 suppressed kiwifruit resistance to Psa at normal growth temperature. Exogenous application of ethylene inhibitor 1-methylcyclopropene eliminated the difference in kiwifruit resistance to Psa at 16 and 24 ℃. Exogenous application of ethylene analogues ethephon induced resistance to Psa in kiwifruit. In conclusion, cool temperatures impair basal resistance to Psa by reducing the activation of ethylene biosynthesis and signaling in kiwifruit. The results provide clues for new strategies to control plant diseases in a context of global environmental change.