Constitutive Photomorphogenic 1 Enhances ER Stress Tolerance in Arabidopsis

Abstract

Interaction between light signaling and stress response has been recently reported in plants. Here, we investigated the role of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), a key regulator of light signaling, in endoplasmic reticulum (ER) stress response in Arabidopsis. The cop1-4 mutant Arabidopsis plants were highly sensitive to ER stress induced by treatment with tunicarmycin (Tm). Interestingly, the abundance of nuclear-localized COP1 increased under ER stress conditions. Complementation of cop1-4 mutant plants with the wild-type or variant types of COP1 revealed that the nuclear localization and dimerization of COP1 are essential for its function in plant ER stress response. Moreover, the protein amount of ELONGATED HYPOCOTYL 5 (HY5), which inhibits bZIP28 to activate the unfolded protein response (UPR), decreased under ER stress conditions in a COP1-dependent manner. Accordingly, the binding of bZIP28 to the BIP3 promoter was reduced in cop1-4 plants and increased in hy5 plants compared with the wild type. Furthermore, introduction of the hy5 mutant locus into the cop1-4 mutant background rescued its ER stress-sensitive phenotype. Altogether, our results suggest that COP1, a negative regulator of light signaling, positively controls ER stress response by partially degrading HY5 in the nucleus.

COP1‐ERF1‐SCE1 regulatory module fine‐tunes stress response under light‐dark cycle in Arabidopsis

“…However, under prolonged treatment in seedlings, ABA-induced the nuclear translocation of COP1 and promoted salt stress tolerance by destabilising golden2-like1 protein to supress chloroplast development (Lee et al, 2021). Kang et al also reported that COP1 enhanced ER stress tolerance in Arabidopsis (Kang et al, 2021). It has also been reported that ACC treatment enhances COP1 nuclear localisation to promote hypocotyl elongation after 15 h of treatment in the light (Yu et al, 2013).…”

The E3 ubiquitin ligase COP1 regulates salt tolerance via GIGANTEA degradation in roots

“…The ecotype of plants used in all experiments was Arabidopsis thaliana Columbia‐0 (Col‐0). Mutants cop1‐4 (McNellis et al, 1994) and gi‐201 (Martin‐Tryon et al, 2007), along with transgenic lines 35S:COP1‐GFP/cop1‐4 (Lee et al, 2017), 35S:GI‐HA/gi‐2 (David et al, 2006), 35S:GI‐HA/cop1‐4 (Ahn et al, 2023), 35S:COP1 L105A ‐GFP/cop1‐4 , 35S:COP1 L170A ‐GFP/cop1‐4 and 35S:COP1 Cyt ‐GFP/cop1‐4 (Kang et al, 2021) used in this study have been previously described. Double mutants, gi‐201 cop1‐4 were obtained by genetic crossing, then verified by phenotypic inspection and Western blot analysis.…”

“…The ecotype of plants used in all experiments was Arabidopsis thaliana Columbia-0 (Col-0). Mutants cop1-4 (McNellis et al, 1994) andgi-201 (Martin-Tryon et al, 2007), along with transgenic lines 35S:COP1-GFP/cop1-4 (Lee et al, 2017), 35S:GI-HA/gi-2 (David et al, 2006), 35S:GI-HA/cop1-4 (Ahn et al, 2023), 35S:COP1 L105A -GFP/cop1-4, 35S:COP1 L170A -GFP/cop1-4 and 35S:COP1 Cyt -GFP/cop1-4 (Kang et al, 2021)…”

Post-translational modifications: emerging directors of cell-fate decisions during endoplasmic reticulum stress in Arabidopsis thaliana

“…ER stress response elements (ERSEs) are cis -acting DNA sequences in the promoter regions of genes targeted by UPR TFs [ 75 ], and the TF HY5 binds ERSEs preventing bZIP28 from binding and driving expression of downstream UPR genes [ 169 ]. COP1, an E3 ubiquitin ligase, relocates to the nucleus in ER stress, ubiquitinates HY5 and triggers its degradation, allowing bZIP28 to bind the ERSEs [ 169 , 170 ] ( Figure 4 ). Additionally, in mammalian cells experiencing chronic ER stress, ATF6 exhibits a reduction in its pro-life transcriptional activity due to SUMOylation in the nucleus likely operated by the E3 ligase PIAS1 [ 171 ].…”