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Elucidation of the process by which pathogenic bacteria force open stomata to invade — Paving the way for creating resistant crops using genome editing

2026.03.18

Stomata, which exist on the surface of plant leaves, are important organs responsible for gas exchange necessary for photosynthesis, but they also serve as entry points for bacteria. Plants prevent bacterial invasion by closing their stomata, but pathogenic bacteria are known to reopen closed stomata. However, the details of this mechanism were unclear.

A research group led by Associate Professor Akira Mine from the Graduate School of Agriculture at Kyoto University discovered through experiments with Arabidopsis that pathogenic bacteria reopen stomata by exploiting the plants gene regulatory mechanisms. Plant stomata close in response to abscisic acid, a type of hormone, Arabidopsis possesses the CYP707A1 gene that encodes an enzyme for abscisic acid degradation. The research group found that coronatine, a toxin produced by pathogenic bacteria, reopens closed stomata by enhancing the expression of this gene. Furthermore, they demonstrated that the CYP707A1 gene helps Arabidopsis rapidly open stomata in response to morning light, showing that pathogenic bacteria exploit the expression control mechanism of this gene that promotes gas exchange to open stomata. They also found that some species in the Brassicaceae family exhibits resistance to bacteria instead of having this gene expression control, revealing an evolutionary trade-off between "the ability to rapidly open stomata" and "resistance to pathogens."

It is estimated that annual crop losses due to pathogens are equivalent to the food required for more than 500 million people. This achievement demonstrates the possibility of creating crops with resistance to pathogenic bacteria using breeding and genome editing.

(Article: Masanori Nakajo)

The expression control mechanism of the CYP707A1 gene in Arabidopsis is advantageous for rapidly opening stomata for gas exchange, but disadvantageous in terms of resistance to pathogenic bacteria that exploit this mechanism. Some closely related species show resistance by not having this gene expression control.

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