ArticleScience advances2024
A pathogen effector co-opts a host RabGAP protein to remodel pathogen interface and subvert defense-related secretion.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A broad-host-range Rhizobium rhizogenes strain enables transient expression across diverse crop species.PLoS biology · 2026Article
- Oomycete plant pathogens: biology, pathogenesis and emerging control strategies.Nature reviews. Microbiology · 2026Review
- The transformative power of structural predictions with AI in plant science.The Plant journal : for cell and molecular biology · 2026Review
- Membrane contact sites between chloroplasts and the pathogen interface underpin plant focal immune responses.The Plant cell · 2025Article
- The Magnaporthe oryzae effector Pwl2 alters HIPP43 localization to suppress host immunity.The Plant cell · 2025Article
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Authors and funding
13 authors.
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Abstract
Pathogens have evolved sophisticated mechanisms to manipulate host cell membrane dynamics, a crucial adaptation to survive in hostile environments shaped by innate immune responses. Plant-derived membrane interfaces, engulfing invasive hyphal projections of fungal and oomycete pathogens, are prominent junctures dictating infection outcomes. Understanding how pathogens transform these host-pathogen interfaces to their advantage remains a key biological question. Here, we identified a conserved effector, secreted by plant pathogenic oomycetes, that co-opts a host Rab GTPase-activating protein (RabGAP), TOPGAP, to remodel the host-pathogen interface. The effector, PiE354, hijacks TOPGAP as a susceptibility factor to usurp its GAP activity on Rab8a, a key Rab GTPase crucial for defense-related secretion. By hijacking TOPGAP, PiE354 purges Rab8a from the plasma membrane, diverting Rab8a-mediated immune trafficking away from the pathogen interface. This mechanism signifies an uncanny evolutionary adaptation of a pathogen effector in co-opting a host regulatory component to subvert defense-related secretion, thereby providing unprecedented mechanistic insights into the reprogramming of host membrane dynamics by pathogens.
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