The stability of transcription factor PfSPL1 participates in the response to phytoplasma stress in Paulownia fortunei

The current understanding of the pathogenesis of phytoplasma is still very limited and challenging. Here, ceRNA regulatory network and degradome sequencing identified a PfmiR156f-PfSPL regulatory module in Paulownia fortunei infected by phytoplasma, and RLM-5 ' RACE and dual luciferase analyses verified the relationship. The PfmiR156 cleavage site was located at 1104 nt and 1177 nt of PfSPL1 and PfSPL10, respectively. MG132 and epoxomicin, two 26S proteasome inhibitors, significantly increased the accumulation of PfSPL1. PfSPL1 was also the attack target of phytoplasma effectors (Pawb 3/9/16/37/51) after the phytoplasma invaded Paulownia. Moreover, molecular docking implied that the effectors may interact with the conserved SBP domain of the target protein PfSPL1. Basically, these results indicated that the stability of PfSPL1 was regulated by PfmiR156 cleavage activity and/or the 26S proteasome pathway at the post-translation level. The PfSPL1, which is a transcription factor, was also the one of the targets of multiple effectors attacking Paulownia. This study provides a good scope to understand the paulownia phytoplasma infecting mechanism.

Automated summary

A PfmiR156f-PfSPL regulatory module was identified in Paulownia fortunei infected by phytoplasma through ceRNA regulatory network and degradome sequencing, and its relationship was verified. The stability of PfSPL1 was found to be regulated by PfmiR156 cleavage activity and/or the 26S proteasome pathway at the post-translation level. PfSPL1, a transcription factor, was targeted by multiple effectors attacking Paulownia. This study provides insights into the mechanism of phytoplasma infection in Paulownia.