In nature, plants constantly face the threat of pathogen invasion. However, their immune systems are always confronted with a fundamental challenge: they must rapidly and effectively eliminate intruders while avoiding self-harm caused by excessive immune responses. Once defense reactions spiral out of control, they not only trigger cellular damage and lead to excessive energy consumption, but also severely inhibit plant growth and development. Therefore, the ability of plants to promptly suppress excessive immune responses and maintain immune homeostasis after successfully defending against pathogen invasion represents a core capability for their survival and environmental adaptation. Yet, for a long time, the molecular mechanisms by which plants achieve this exquisite homeostasis remains largely unknown.
Recently, the team of Prof. Chen Xuewei from the New Cornerstone Science Laboratory, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China at Sichuan Agricultural University published a research article titled “A phospho-switch centered on OsAHL23 orchestrates immune homeostasis in rice” online in the internationally renowned academic journal Science Bulletin . This study reveals a regulatory circuit composed of the kinase OsMPK5, the phosphatase PP2A-A, and the transcription factor OsAHL23. By precisely controlling the phosphorylation status of serine 321 (S321) on the OsAHL23 protein as a “molecular switch”, this circuit dynamically balances immune responses and growth and development in rice.
The study revealed that the transcription factor OsAHL23 negatively regulates immune responses but positively promotes growth and development. Using gene editing technology to knock out this gene significantly enhanced rice resistance to rice blast disease, but resulted in reduced yield. Conversely, rice overexpressing this gene showed increased yield but exhibited higher susceptibility to disease. Mechanistic studies demonstrated that OsAHL23 activates the expression of the immune negative regulator OsNTL6 , which in turn suppresses the expression of defense genes OsWRKY45 and OsPR1b , thereby weakening the disease resistance of rice.
Further research revealed that the activity of the OsAHL23 transcription factor is precisely regulated by phosphorylation modifications. When the rice blast fungus ( Magnaporthe oryzae ) infects the plant, the phosphatase PP2A-A accumulates and dephosphorylates S321 of OsAHL23, attenuating the transcriptional activity of OsAHL23 and thereby relieving immune suppression. After effectively resisting the pathogen infection, PP2A-A levels decline, and the kinase OsMPK5 phosphorylates the S321 residue of OsAHL23, restoring the suppression of immune responses and thus re-establishing immune homeostasis.
Interestingly, this regulatory module is likely conserved in other plants such like maize and tomato, suggesting that this mechanism may represent an evolutionarily conserved strategy for immune homeostasis regulation in the plant kingdom. This study not only elucidates the molecular mechanism by which rice cleverly coordinates immunity and growth through a single phosphorylation site of a transcription factor, but also opens new avenues for crop genetic improvement. In the future, by precisely editing this phosphorylation switch, it is expected to cultivate new crop varieties with both disease resistance and high-yield.
Science Bulletin