背景回顾：The embryonic cuticle integrity is critical for the embryo to separate from the neighboring endosperm. The sulfated TWISTED SEED1 (TWS1) peptide precursor generated in the embryo diffuses through gaps of the nascent cuticle to the surrounding endosperm where it is cleaved by ABNORMAL LEAF SHAPE1 (ALE1) and becomes an active mature form. The active TWS1 is perceived by receptor-like protein kinases GASSHO1 (GSO1) and GSO2 in the embryonic epidermal cells to start the downstream signaling and guide the formation of an intact embryonic cuticle. 

提出问题：However, the early signaling events after TWS1 is perceived by GSO1/2 are still unknown.

结果1-serk1/2/3表型：：Here, we report that serk1/2/3 embryos show cuticle defects similar to ale1, tws1, and gso1/2. 

结果2-SERKs与GSO1/2在同一通路发挥作用：Genetic and biochemical analyses were performed to dissect the signaling pathway mediated by SERKs during cuticle development. SERKs function with GSO1/2 in a common pathway to monitor the integrity of the embryonic cuticle. 

结果3-SERKs与GSO1/2互作：SERKs interact with GSO1/2, which can be enhanced dramatically by TWS1. 

结果4-SERKs与GSO1/2的磷酸化：The phosphorylation levels of SERKs and GSO1/2 rely on each other, and can respond to and be elevated by TWS1. 

结论：Our results demonstrate that SERKs may function as coreceptors of GSO1/2 to transduce the TWS1 signal and ultimately regulate embryonic cuticle integrity.

 摘 要 

胚胎角质层的完整性是胚胎与邻接胚乳分离的关键。胚胎中产生的硫酸化TWS1多肽前体通过新生角质层的缝隙扩散到周围的胚乳，接着会被ALE1切割，从而成为活跃的成熟态。胚胎表皮细胞中的类受体蛋白激酶GSO1和GSO2能够感知成熟的TWS1，从而启动下游信号并指导完整胚胎角质层的形成。然而，GSO1/2感知到TWS1后的早期信号事件仍然未知。本文中，作者发现serk1/2/3胚胎显示类似于ale1、tws1和gso1/2的角质层缺陷。作者进一步通过遗传和生化分析鉴定角质层发育过程中SERK介导的的信号转导通路。SERK与GSO1/2在同一个通路中发挥作用，以监测胚胎角质层的完整性。SERK与GSO1/2相互作用，并且这种互作会受到TWS1的显著增强。SERK和GSO1/2蛋白的磷酸化水平相互依赖，并且响应于TWS1增加磷酸化水平。本文的研究结果表明，SERK可能作为GSO1/2的共受体来传递TWS1信号，并最终调节胚胎角质层的完整性。