AI Article Synopsis

  • Plant pattern recognition receptors (PRRs) detect microbial threats and trigger the immune response, but the connection between immune activation and cell death is complex and not fully understood.
  • The study focuses on a specific protein, Ps109281, secreted by the pathogen Phytophthora sojae, which can enhance infection while also being recognized by plant receptors to induce immune responses without causing cell death.
  • The lack of cell death induction in Ps109281 is linked to a specific change in its protein sequence, suggesting that different areas of the protein interact with receptors to produce varied immune outcomes, revealing insights into how pathogen effectors evolve different functions.

Article Abstract

Plant pattern recognition receptors (PRRs) are sentinels at the cell surface sensing microbial invasion and activating innate immune responses. During infection, certain microbial apoplastic effectors can be recognized by plant PRRs, culminating in immune responses accompanied by cell death. However, the intricated relationships between the activation of immune responses and cell death are unclear. Here, we studied the glycoside hydrolase family 12 (GH12) protein, Ps109281, secreted by Phytophthora sojae into the plant apoplast during infection. Ps109281 exhibits xyloglucanase activity, and promotes P. sojae infection in a manner dependent on the enzyme activity. Ps109281 is recognized by the membrane-localized receptor-like protein RXEG1 and triggers immune responses in various plant species. Unlike other characterized GH12 members, Ps109281 fails to trigger cell death in plants. The loss of cell death induction activity is closely linked to a sequence polymorphism at the N-terminus. This sequence polymorphism does not affect the in planta interaction of Ps109281 with the recognition receptor RXEG1, indicating that cell death and immune response activation are determined using different regions of the GH12 proteins. Such GH12 protein also exists in other Phytophthora and fungal pathogens. Taken together, these results unravel the evolution of effector sequences underpinning different immune outputs.

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Source
http://dx.doi.org/10.1111/jipb.13337DOI Listing

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