ArticleCell reports2025
JAG modulates sepal flatness by regulating cell growth direction, interacts with AS2, and is antagonized by TCP24.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Growth directions and stiffness across cell layers determine whether tissues stay smooth or buckle.Current biology : CB · 2026Article
- Correlations between surface area and volume in cell size and growth in Arabidopsis thaliana.BMC plant biology · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Flat plant organs are crucial for optimal organ functionality. Polarity establishment and growth coordination between tissues are key factors in maintaining organ flatness. Ectopic ASYMMETRIC LEAVES2 (AS2) expression in the as2-7D mutant has been shown to disrupt growth across cell layers, leading to epidermal buckling in sepals. However, the detailed molecular mechanism remains unclear. Here, we show that mutation of the JAGGED (JAG) gene suppresses buckling of the as2-7D sepal epidermis. Cellular growth analysis reveals that the jag mutant suppresses the sepal epidermal buckling phenotype by altering cellular growth directions to be more parallel with the proximal-distal direction. On the molecular level, JAG physically interacts with AS2. TEOSINTE BRANCHED 1, CYCLOIDEA, AND PCF FAMILY 24 (TCP24) antagonizes JAG in sepal morphogenesis by repressing JAG transcription and inhibiting the AS2-JAG protein interaction. Our study uncovers a complex molecular network involving AS2, JAG, and TCP24 that is critical for generating flat plant organs.
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