A low temperature-sensitive regulator that enhances virulence in the kiwifruit canker pathogen Pseudomonas syringae pv. actinidiae
Pseudomonas syringae pv. actinidiae (Psa) is responsible for causing kiwifruit canker disease, which severely impacts on the global kiwifruit industry, leading to substantial economic losses. Cooler environmental temperatures (below 20?) are known to favor the outbreak of this bacterial disease in the field. However, the specific mechanisms that enable Psa to adapt and thrive in such conditions have remained elusive. In this study, we discovered that the gene RS16350, encoding a heat shock protein, positively regulates pathogenicity in kiwifruit leaves at low temperature (16?), but not at room temperature (28?). Delving into the mechanics, we found that RS16350 directly interacts with HrpL, an RpoN-dependent RNA polymerase sigma factor that serves as a master regulator of the type III secretion system (T3SS) in Psa. This RS16350-HrpL interaction enhances HrpL's binding affinity to hrp-box, which in turn elevates the expression of downstream T3SS genes, thereby boosting virulence. Consequently, we have designated RS16350 as TspR (temperature sensitive and pathogenic regulator). Our findings shed light on how a kiwi pathogen enhances its virulence in response to low temperatures, paving the way for the development of innovative strategies to combat kiwifruit canker disease. Overall design: To investigate the impact of low temperatures on kiwifruit canker disease, we conducted transcriptomic profiling in T3SS-inducing medium (minimal medium, MM) at low temperature (16?) and room temperature (28?) to mimic field conditions conducive to the disease. The wild type Psa_M228 strain was cultured in MM at 28? for 2 hours and then transferred to 16? for 5 more hours, while the control group was cultured at 28? for a total of 7 hours.