When a rice leaf is torn or bitten, the plant doesn’t just sit still. It launches a series of rapid molecular alarms. Within minutes, chemical signals rush through its tissues to close wounds, fend off infection, and begin repair. But responding to damage is a balancing act. Too strong a defence can slow growth, while focusing on healing too early can leave the plant vulnerable.
A recent study at NCBS now explains how rice manages this trade-off through a single molecular coordinator. The research team found a transcription factor called OsWRKY53 acts as a switch that helps the plant move seamlessly from defence to growth after wounding. The team had previously shown that two small signalling molecules - plant elicitor peptides (PEPs) and phytosulfokine (PSK) - play opposing roles in this process. PEPs trigger an immediate immune response, while PSK promotes growth and tissue repair once the danger has passed. What remained unknown was how the plant coordinates the transition between these two modes.
“This study identifies OsWRKY53 as the missing link between them,” says Dr Chitthavalli Y. Harshith, the lead author of the study. “We found that OsWRKY53 levels surge within minutes of wounding or exposure to wound-derived peptides like OsPep2. This protein binds to DNA and activates genes that drive defence responses while keeping growth-related genes in check,” he added.
Over time, as the need for defence wanes, OsWRKY53 reduces its activity, allowing PSK-mediated growth signals to take over. Plants engineered to lack OsWRKY53 showed a breakdown in this coordination - their defence genes failed to activate properly, and growth genes turned on too early, leaving them less equipped to handle injury.
To understand how OsWRKY53 works at the molecular level, the team combined gene expression profiling, chromatin immunoprecipitation sequencing (ChIP-seq), and genome editing using CRISPR. They discovered that OsWRKY53 binds to the promoters of hundreds of genes, changing its DNA-binding sites depending on how long the plant had been exposed to wound signals. This property allows it to continuously adjust the plant’s gene expression as the response begins. The protein itself becomes more stable when phosphorylated - chemically modified by enzymes activated during wounding - suggesting that the plant fine-tunes OsWRKY53’s activity through post-translational control.
OsWRKY53 does not merely turn genes on or off. It seems to orchestrate a dialogue between defence and growth pathways. The study found that OsWRKY53 enhances the expression of genes triggered by PEP signalling while suppressing those activated by PSK, effectively delaying growth responses until the threat has subsided. This dual role places it at the heart of a regulatory loop that ensures rice responds to wounds with both precision and restraint.
“Beyond revealing a new layer of control in plant stress biology, the work highlights how a single transcription factor can mediate crosstalk between seemingly opposing processes. By mapping how OsWRKY53 integrates defence and repair pathways, we provide a framework for understanding how monocot plants - like rice - recover from damage. These findings may eventually help us design crops that recover faster after pest attacks or physical injury, maintaining yield even under stress,” says Dr PV Shivaprasad, the principal investigator of the study.
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