Pseudomonas syringae Type III Secretion Protein HrpP Manipulates Plant Immunity To Promote Infection

Area of Science:

• Plant Pathology
• Microbial Pathogenesis
• Molecular Plant-Microbe Interactions

Background:

• Pseudomonas syringae utilizes the type III secretion system (T3SS) to inject effector proteins into host plant cells, a critical step in pathogenesis.
• While many P. syringae effectors are characterized, the roles of T3SS apparatus proteins, such as HrpP, in plant interactions remain largely unexplored.

Purpose of the Study:

• To investigate the function of the P. syringae pv. tomato DC3000 T3SS protein HrpP in plant immunity and bacterial infection.
• To elucidate the molecular mechanisms by which HrpP interacts with plant components and influences host responses.

Main Methods:

• Generation and analysis of HrpP-transgenic Arabidopsis lines.
• Assessment of pattern-triggered immunity (PTI) responses and disease susceptibility.
• Transcriptome analysis to identify HrpP-modulated signaling pathways.
• Yeast two-hybrid and bimolecular fluorescence complementation assays to study protein-protein interactions.
• Analysis of HrpP truncations for interaction and functional studies.

Main Results:

• HrpP induces host cell death, suppresses PTI, and restores effector translocation in hrpP mutants.
• HrpP-transgenic plants show reduced PTI and increased susceptibility to P. syringae pv. tomato DC3000.
• HrpP activates salicylic acid (SA) signaling and suppresses jasmonic acid (JA) signaling, leading to altered SA accumulation and JA biosynthesis.
• HrpP directly interacts with mitogen-activated protein kinase kinase 2 (MKK2) in plant cells.
• The N-terminal truncation HrpP1-119 retains MKK2 interaction and PTI suppression, while HrpP1-101 causes cell death but not MKK2 interaction.

Conclusions:

• The T3SS protein HrpP plays a dual role in facilitating P. syringae infection by promoting effector translocation and manipulating plant immunity.
• HrpP interacts with MKK2, modulating plant defense signaling pathways (SA and JA) to benefit bacterial pathogenesis.
• This study highlights a key T3SS component involved in the intricate regulation of plant immunity during bacterial infection.