Germinating seeds undergo elaborate de-etiolation developmental transitions upon initial soil emergence. As central transcription factors promoting cotyledon greening, the abundance of ETHYLENE-INSENSITIVE 3 (EIN3) and PHYTOCHROME-INTERACTING FACTOR 3 (PIF3) are strictly controlled by physically associating themselves with the EIN3-BINDING F BOX PROTEINS 1 and 2 (EBF1/2) for ubiquitination. Here, we report that the B-box zinc-finger protein BBX32, as a positive regulator during seedling de-etiolation. BBX32 is robustly elevated during the dark-to-light transitions. Constitutively expressing BBX32 ultimately protects against severe photobleaching damage by synchronizing the accumulation of protochlorophyllide (Pchlide) and the differentiation of etioplast-chloroplast apparatus in buried seedlings. Specifically, BBX32 directly interacts with EIN3, PIF3 and EBF1/2. These associations disrupt the assembly of the SCFEBF1/2-EIN3/PIF3 E3 ligation protein complexes, thus dampening E3 ligase activity and robustly controlling EIN3/PIF3 stability. Under soil conditions, BBX32-ox largely rescues the greening deficiency of EBF1ox, and all EIN3ox/bbx32 seedlings override the bbx32 mutant defect and successfully turn green. Both biochemical findings and genetic evidence reveal a novel regulatory paradigm by which the B-box protein dampens the E3 ligase binding activity to achieve green seedlings upon changes in light or soil environmental conditions.

Soil salinization, a prevalent form of environmental stress, leads to significant soil desertification and impacts agricultural productivity by altering the internal soil environment, slowing cellular metabolism, and modifying cellular architecture. This results in a marked reduction in both the yield and diversity of crops. Maize, which is particularly susceptible to salt stress, serves as a critical model for studying these effects, making the elucidation of its molecular responses essential for crop improvement strategies. This study focuses on the phytochrome-interacting factor 3 (PIF3), previously known for its role in freezing tolerance, to assess its function in salt stress tolerance. Utilizing two transcript variants of maize ZmPIF3 (ZmPIF3.1 and ZmPIF3.2), we engineered Arabidopsis transgenic lines to overexpress these variants and analyzed their phenotypic, physiological, biochemical, and transcriptomic responses to salt stress. Our findings reveal that these transgenic lines displayed not only enhanced salt tolerance but also improved peroxide decomposition and reduced cellular membrane damage. Transcriptome analysis indicated significant roles of hormonal and Ca2+ signaling pathways, along with key transcription factors, in mediating the enhanced salt stress response. This research underscores a novel role for ZmPIF3 in plant salt stress tolerance, offering potential avenues for breeding salt-resistant crop varieties.