Ma Qian, Liu Sijia, Doyle Siamsa M, Raggi Sara, Pařízková Barbora, Barange Deepak Kumar, Ratnakaram Hemamshu, Wilkinson Edward G, Crespo Garcia Isidro, Bygdell Joakim, Wingsle Gunnar, Boer Dirk Roeland, Strader Lucia C, Almqvist Fredrik, Novák Ondřej, Robert Stéphanie
Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, Umeå SE-901 83, Sweden.
Laboratory of Growth Regulators, Faculty of Science of Palacký University & Institute of Experimental Botany of the Czech Academy of Sciences, Olomouc CZ-783 71, Czech Republic.
Proc Natl Acad Sci U S A. 2025 Jul 29;122(30):e2407224122. doi: 10.1073/pnas.2407224122. Epub 2025 Jul 21.
Apical hook development is an ideal model for studying differential growth in plants and is controlled by complex phytohormonal crosstalk, with auxin being the major player. Here, we identified a bioactive small molecule that decelerates apical hook opening in . Our genetic studies suggest that this molecule enhances or maintains the auxin maximum found in the inner hook side and requires certain auxin signaling components to modulate apical hook opening. Using biochemical approaches, we then revealed the WD40 repeat scaffold protein RECEPTOR FOR ACTIVATED C KINASE 1A (RACK1A) as a direct target of this compound. We present data in support of RACK1A playing a positive role in apical hook opening by activating specific auxin signaling mechanisms and negatively regulating the differential auxin response gradient across the hook, thereby adjusting differential cell growth, an essential process for organ structure and function in plants.
顶端弯钩发育是研究植物差异生长的理想模型，它受复杂的植物激素相互作用调控，其中生长素起主要作用。在此，我们鉴定出一种生物活性小分子，它能减缓[具体植物名称]的顶端弯钩张开。我们的遗传学研究表明，该分子增强或维持了在内侧弯钩一侧发现的生长素最大值，并且需要某些生长素信号传导组分来调节顶端弯钩张开。随后，我们利用生化方法揭示了WD40重复支架蛋白激活的C激酶1A受体（RACK1A）是该化合物的直接靶点。我们提供的数据支持RACK1A通过激活特定的生长素信号传导机制在顶端弯钩张开中发挥积极作用，并负向调节弯钩两侧生长素差异响应梯度，从而调节差异细胞生长，这是植物器官结构和功能的一个重要过程。
