In Arabidopsis, phytochrome (phy) A, phyB, and cryptochrome 1 (cry1) are representative far‐red, red, and blue light photoreceptors, respectively. Members of the SUPPRESSOR OF PHYA‐105 (SPA) protein family (SPA1–SPA4) form E3 ubiquitin ligase complexes with CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), which mediates the degradation of photomorphogenesis‐promoting factors to desensitize light signaling. SPA2 has been reported to promote seedling etiolation in the dark. However, the unique roles of SPA2 and its three functional domains in suppressing photomorphogenesis under different light conditions are largely unknown. Here, we demonstrate that overexpression of the full‐length or the central coiled‐coil and C‐terminal WD‐repeat domains of SPA2 cause hyper‐etiolation phenotypes under several light conditions. The SPA2 central coiled‐coil and C‐terminal WD‐repeat domains are necessary and sufficient for repressing seedling de‐etiolation, cotyledon unfolding, and promoting hypocotyl negative gravitropism under several light conditions. Furthermore, phyA, phyB, cry1, and COP1 repress protein accumulation or nuclear translocation of SPA2 through direct interactions with its kinase‐like and coiled‐coil domains located in the N‐terminus in response to far‐red, red, and blue light treatments, respectively. Taken together, our results demonstrate that SPA2 functions under multiple light conditions; moreover, light‐activated photoreceptors rapidly suppress SPA2 activity via direct interactions in response to different light treatments.

Flowering time is a key determinant of yield and regional adaptation in crops and is largely controlled by light signalling. In this study, we identified two maize orthologs of Arabidopsis CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), designated ZmCOP1a and ZmCOP1b, which activate light signalling and reduce plant height. Loss‐of‐function mutants of ZmCOP1a and ZmCOP1b flowered early, whereas overexpression of either gene significantly delayed flowering under both long‐ and short‐day conditions. Mechanistically, both ZmCOP1a and ZmCOP1b interacted with and stabilised the C2C2‐CO‐like transcription factor ZmCOL3. Together, they upregulated key repressors of flowering ( ZmPRR37 , ZmPRR95 , ZmCCA1 and ZmCCT9 ), leading to suppression of florigen genes ( ZCN7 , ZCN8 and ZCN12 ) and floral meristem identity genes ( ZMM3 , ZMM4 and ZMM15 ). Field trials demonstrated that overexpression of ZmCOP1a or ZmCOP1b reduced starch content but increased protein levels, kernel numbers and kernel length, width and weight. In contrast, overexpression of ZmCOL3 decreased both starch and protein content. Collectively, our results demonstrate that the ZmCOP1s–ZmCOL3 module is a key regulator of flowering time and source–sink reallocation, providing valuable genetic targets for breeding high‐yield, high‐quality maize with optimised flowering time and enhanced carbon and nitrogen allocation.