Details

Autor(en) / Beteiligte

• Zhao, Fu
• Zhi, Taihui
• Hu, Renjian
• Fan, Rong
• Long, Youhua
• Tian, Fenghua
• Zhao, Zhibo

Titel

The OmpR-like Transcription Factor as a Negative Regulator of hrpR/S in Pseudomonas syringae pv. actinidiae

Ist Teil von

• International journal of molecular sciences, 2022-10, Vol.23 (20), p.12306

Ort / Verlag

Basel: MDPI AG

Erscheinungsjahr

2022

Link zum Volltext

Quelle

EZB Free E-Journals

Beschreibungen/Notizen

• Bacterial canker of kiwifruit is a devastating disease caused by Pseudomonas syringae pv. actinidiae (Psa). The type III secretion system (T3SS), which translocates effectors into plant cells to subvert plant immunity and promote extracellular bacterial growth, is required for Psa virulence. Despite that the “HrpR/S-HrpL” cascade that sophisticatedly regulates the expression of T3SS and effectors has been well documented, the transcriptional regulators of hrpR/S remain to be determined. In this study, the OmpR-like transcription factor, previously identified by DNA pull-down assay, was found to be involved in the regulation of hrpR/S genes, and its regulatory mechanisms and other functions in Psa were explored through techniques including gene knockout and overexpression, ChIP-seq, and RNA-seq. The OmpR-like transcription factor had binding sites in the promoter region of the hrpR/S, and the transcriptional level of the hrpR/S increased after the deletion of OmpR-like and decreased upon its overexpression in an OmpR-like deletion background. Additionally, OmpR-like overexpression reduced the strain’s capacity to form biofilms and lipopolysaccharides, led to its slow growth in King’s B medium, and reduced its swimming ability, although there was no significant effect on its pathogenicity against kiwifruit hosts. Our results indicated that OmpR-like directly and negatively regulates the transcription of hrpR/S and may be involved in the regulation of multiple biological processes in Psa. Our results provide a basis for further understanding the transcriptional regulation mechanism of hrpR/S in Psa.