Herrmann Arvid, Sepuru Krishna Mohan, Endo Hitoshi, Nakagawa Ayami, Kusano Shuhei, Bai Pengfei, Ziadi Asraa, Kato Hiroe, Sato Ayato, Liu Jun, Shan Libo, Kimura Seisuke, Itami Kenichiro, Uchida Naoyuki, Hagihara Shinya, Torii Keiko U
Howard Hughes Medical Institute, The University of Texas at Austin, Austin, TX 78712 USA.
Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712 USA.
bioRxiv. 2024 Jul 30:2024.07.29.605519. doi: 10.1101/2024.07.29.605519.
Cells sense and integrate multiple signals to coordinate development and defence. A receptor-kinase signaling pathway for plant stomatal development shares components with the immunity pathway. The mechanism ensuring their signal specificities remains unclear. Using chemical genetics, here we report the identification of a small molecule, kC9, that triggers excessive stomatal differentiation by inhibiting the canonical ERECTA receptor-kinase pathway. kC9 binds to and inhibits the downstream MAP kinase MPK6, perturbing its substrate interaction. Strikingly, activation of immune signaling by a bacterial flagellin peptide nullified kC9's effects on stomatal development. This cross-activation of stomatal development by immune signaling depends on the immune receptor FLS2 and occurs even in the absence of kC9 if the ERECTA-family receptor population becomes suboptimal. Furthermore, proliferating stomatal-lineage cells are vulnerable to the immune signal penetration. Our findings suggest that the signal specificity between development and immunity can be ensured by MAP Kinase homeostasis reflecting the availability of upstream receptors, thereby providing a novel view on signal specificity.
细胞感知并整合多种信号以协调发育和防御。植物气孔发育的受体激酶信号通路与免疫通路共享一些组分。确保它们信号特异性的机制仍不清楚。利用化学遗传学方法，我们在此报告鉴定出一种小分子kC9，它通过抑制经典的ERECTA受体激酶途径触发过度的气孔分化。kC9结合并抑制下游的丝裂原活化蛋白激酶MPK6，扰乱其与底物的相互作用。引人注目的是，细菌鞭毛蛋白肽激活免疫信号会消除kC9对气孔发育的影响。免疫信号对气孔发育的这种交叉激活依赖于免疫受体FLS2，并且即使在没有kC9的情况下，如果ERECTA家族受体数量变得不足也会发生。此外，增殖的气孔谱系细胞易受免疫信号渗透的影响。我们的研究结果表明，发育和免疫之间的信号特异性可以通过反映上游受体可用性的丝裂原活化蛋白激酶稳态来确保，从而为信号特异性提供了新的视角。
