(100-61) Regulation of protein stability in light-stress signaling crosstalk: COP1-ERF1-SCE1 module fine-tunes stress response under light-dark cycle in Arabidopsis
Assistant Professor National Taiwan University Taipei, Taipei, Taiwan (Republic of China)
Body of Abstract: In times of global climate change, understanding the crosstalk between light signaling and stress defense might help developing the crops that optimally use the light information and are more stress-resistant. In response to abiotic stresses, plants have developed sophisticated transcriptional regulatory network to defend themselves. However, how plants utilize light information to optimize their growth under stress conditions remains largely unknown. ETHYLENE RESPONSE FACTOR 1 (ERF1) is an important transcription factor that integrates hormone crosstalk and stress responses. In our recent work, we have shown that ERF1 is unstable in the dark and its degradation is mediated by UBIQUITIN-CONJUGATING ENZYME 18. To further investigate whether there are other enzymes regulating ERF1’s stability, we performed yeast two-hybrid analyses and found SUMO-CONJUGATING ENZYME 1 (SCE1) and CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) can interact with ERF1. Using various in vitro and in vivo biochemical, genetic and stress-tolerance tests, we demonstrated that both COP1 and SCE1 regulate the stability of ERF1 under light-dark cycle. We also performed transcriptomic analyses to understand their common regulatory pathways. COP1 mediates ERF1 ubiquitination in the dark while SCE1 mediates ERF1 sumoylation in the light. ERF1 stability is positively regulated by SCE1 and negatively regulated by COP1. Upon abiotic stress, SCE1 plays a positive role in stress defense by regulating the expression of ERF1’s downstream genes, including DELTA-1-PYRROLINE-5-CARBOXYLATE SYNTHASE 1 (P5CS1) and OSMOTIN 34 (OSM34), whereas COP1 plays a negative role in stress response. Moreover, ERF1 also promotes photomorphogenesis and the expression of light-responsive genes. Our study reveals the molecular mechanism of how COP1 and SCE1 counteract to regulate ERF1’s stability and fine-tune light-stress signaling crosstalk.