Fvchli deficiency impairs ABA-mediated stomatal closure and enhances susceptibility to Xanthomonas fragariae in strawberry.
Luo J, Jin J, Ma Y, Jiang Y, Zhu F
Crispr
Strawberry angular leaf spot — caused by the bacterium this study targets — is one of the most damaging diseases for strawberry growers, and understanding how plants naturally lock their 'doors' against it could lead to varieties that fight back without fungicides.
Plants have tiny pores on their leaves called stomata that open and close to breathe — and also to keep out bacterial invaders. Researchers found that a gene in strawberries, previously thought to only help make chlorophyll, is actually critical for slamming those pores shut when bacteria show up. Strawberry plants with this gene disabled left their stomata wide open, letting bacteria waltz right in and cause far more disease than in normal plants.
Key Findings
Strawberry mutants with 70% gene editing efficiency reduced stomatal closure from 32% to only 16% aperture after ABA treatment, compared to wild-type plants that closed from 32% to 2.3%
Disease lesion area and incidence positively correlated with CRISPR editing efficiency — more gene disruption meant more disease
Scanning electron microscopy confirmed mutant plants had significantly wider stomatal openings at 5 and 12 hours post-infection, enabling extensive bacterial colonization
chevron_right Technical Summary
A gene involved in chlorophyll production (Fvchli) turns out to also control how well strawberry plants defend themselves against a serious bacterial disease. When this gene is disabled using CRISPR, strawberry plants can't close their stomata fast enough to block invading bacteria, making them far more susceptible to infection.
Abstract Preview
The magnesium chelatase subunit CHLI is well-characterized in chlorophyll biosynthesis, but its role in plant immunity remains unclear. In this study, we generated chimeric Fvchli mutant strawberri...
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