植物在发育过程中或暴露于不利条件时已经进化出器官脱落的机制。1不受控制的花瓣脱落,水果,或叶子会损害农业生产力。2,3,4,5尽管它对脱落进程很重要,我们对IDA信号通路及其调控的理解仍然不完整。IDA分泌到质外体,其中它被受体HAESA(HAE)和HAESA-LIKE2(HSL2)和体细胞胚胎发生受体激酶(SERK)共同受体感知。6,7,8,9这些质膜受体通过未知的机制激活丝裂原活化蛋白激酶(MAPK)的细胞内级联10,11,12此处,我们将油菜素类固醇信号激酶(BSKs)描述为拟南芥花器官脱落的调节因子。BSK1定位于脱落区细胞的质膜,它与HAESA受体相互作用以调节脱落。此外,我们证明YODA(YDA)在其他MAPKKs中在控制HAESA/BSK复合物下游的脱落中起着主导作用。这个激酶轴,包含富含亮氨酸的重复受体激酶,一个BSK,还有一个图形,已知调节气孔模式,早期胚胎发育,和免疫。10,13,14,15,16尽管通过共同效应子进行信号传导,但如何获得特定的细胞应答尚不清楚。我们表明,已鉴定的BSK1的脱落促进等位基因也增强了其他BSK介导的途径中的受体信号传导,建议信号机制的保守性。此外,我们提供了遗传证据支持BSK1功能与其激酶活性在几个发育过程中的独立性。一起,我们的研究结果表明,BSK1通过植物发育多个方面的保守机制促进质膜受体激酶和MAPKKs之间的信号传导。
Plants have evolved mechanisms to abscise organs as they develop or when exposed to unfavorable conditions.1 Uncontrolled abscission of petals, fruits, or leaves can impair agricultural productivity.2,3,4,5 Despite its importance for abscission progression, our understanding of the
IDA signaling pathway and its regulation remains incomplete.
IDA is secreted to the apoplast, where it is perceived by the receptors HAESA (HAE) and HAESA-LIKE2 (HSL2) and somatic embryogenesis receptor kinase (SERK) co-receptors.6,7,8,9 These plasma membrane receptors activate an intracellular cascade of mitogen-activated protein kinases (MAPKs) by an unknown mechanism.10,11,12 Here, we characterize brassinosteroid signaling kinases (BSKs) as regulators of floral organ abscission in Arabidopsis. BSK1 localizes to the plasma membrane of abscission zone cells, where it interacts with HAESA receptors to regulate abscission. Furthermore, we demonstrate that YODA (YDA) has a leading role among other MAPKKKs in controlling abscission downstream of the HAESA/BSK complex. This kinase axis, comprising a leucine-rich repeat receptor kinase, a BSK, and an MAPKKK, is known to regulate stomatal patterning, early embryo development, and immunity.10,13,14,15,16 How specific cellular responses are obtained despite signaling through common effectors is not well understood. We show that the identified abscission-promoting allele of BSK1 also enhances receptor signaling in other BSK-mediated pathways, suggesting conservation of signaling mechanisms. Furthermore, we provide genetic evidence supporting independence of BSK1 function from its kinase activity in several developmental processes. Together, our findings suggest that BSK1 facilitates signaling between plasma membrane receptor kinases and MAPKKKs via conserved mechanisms across multiple facets of plant development.