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Updated: May 31, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor (LATS) Biosensor
Published on: September 13, 2018
The STE20/Hippo kinase SIK1 interacts with COI1 and negatively regulates the response to jasmonic acid
Qinying Wang1, Pingping Zhang1, Yi Yang1
1State Key Laboratory of Microbial Metabolism & Joint International Research Laboratory of Metabolic and Developmental Sciences, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Abstract:
The Hippo signaling pathway is a highly conserved pathway in metazoans that limits organ size by restricting tissue overgrowth. This pathway is named after one of its key components, the Ste20 family protein kinase Hippo (Hpo). We previously identified SIK1 in Arabidopsis as a functional orthologue of Hpo and Ste20 and found that the sik1 mutant has smaller lateral organs due to cell cycle exit failure and delayed onset of cell expansion. The plant hormone jasmonic acid (JA) can limit cell proliferation and organ growth, and studies including our own have shown a potential association between SIK1 and JA. In this study, we investigated whether SIK1 is involved in JA biosynthesis, signaling, or response. We found that under normal growth conditions, JA levels and responses were elevated in sik1. However, the JA biosynthetic mutants aos and opr3, as well as the JA receptor mutant coi1, could not suppress the dwarf phenotype of sik1, indicating that the elevated JA response was not the cause of the reduced organ size in sik1. On the other hand, sik1, aos sik1, and opr3 sik1 mutants were all hypersensitive to exogenous JA in primary root elongation, whereas coi1 sik1, like coi1, was insensitive to JA. Furthermore, we found that SIK1 interacts with COI1 both in vitro and in vivo, and negatively regulates the JA response. RNA sequencing analyses further validated that the dwarf phenotype of sik1 was not a result of elevated JA response, but rather, may be due to a failure in cell cycle exit as we had previously reported. Our findings revealed two separate roles of SIK1; it plays a direct positive role in organ size control and a negative role in JA response which is achieved at least partially through its interaction with COI1.
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