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Physical fields are increasingly proposed in the production of germinated grain foods, thus shorting the preparation cycle of high value-added sprouted grain foods. Here, pulsed light treatment (PLT) with 300 times at a single energy of 400 J was found to significantly promote the shoot length and gamma-aminobutyric acid (GABA) content in 8 varieties of germinated brown rice (GBR). Functional annotation analysis showed that the brown rice germination was promoted by the biosynthesis of phenylalanine, carbohydrate metabolism, and energy metabolism pathway. Moreover, PLT influenced the genes and metabolites involved in the GABA shunt and the polyamine degradation pathway, promoting the accumulation of GABA. Transcription factor OsbZIP56 was closely related to the transcript level of regulatory gene for germination and GABA enrichment. Furthermore, overexpression of OsbZIP56 in rice significantly promoted germination and GABA accumulation. These findings would be significant for improving the germination efficiency of edible seeds, promoting accumulation of active ingredients, and exploring gene functions in food materials.

Ionizing radiation (IR) is a conventional cancer therapeutic, to which cancer cells develop radioresistance with exposure. The residual cancer cells after radiation treatment also have increased metastatic potential. The mechanisms by which cancer cells develop radioresistance and gain metastatic potential are still unknown. In this study acute IR exposure induced cancer cell senescence and apoptosis, but after long-term IR exposure, cancer cells exhibited radioresistance. The proliferation of radioresistant cells was retarded, and most cells were arrested in G0/G1 phase. The radioresistant cells simultaneously showed resistance to further IR-induced apoptosis, premature senescence, and epithelial to mesenchymal transformation (EMT). Acute IR exposure steadily elevated CDC6 protein levels due to the attenuation of ubiquitination, while CDC6 overexpression was observed in the radioresistant cells because the insufficiency of CDC6 phosphorylation blocked protein translocation from nucleus to cytoplasm, resulting in subcellular protein accumulation when the cells were arrested in G0/G1 phase. CDC6 ectopic overexpression in CNE2 cells resulted in apoptosis resistance, G0/G1 cell cycle arrest, premature senescence, and EMT, similar to the characteristics of radioresistant CNE2-R cells. Targeting CDC6 with siRNA promoted IR-induced senescence, sensitized cancer cells to IR-induced apoptosis, and reversed EMT. Furthermore, CDC6 depletion synergistically repressed the growth of CNE2-R xenografts when combined with IR. The study describes for the first time cell models for IR-induced senescence, apoptosis resistance, and EMT, three major mechanisms by which radioresistance develops. CDC6 is a novel radioresistance switch regulating senescence, apoptosis, and EMT. These studies suggest that CDC6highKI67lowrepresents a new diagnostic marker of radiosensitivity, and CDC6 represents a new therapeutic target for cancer radiosensitization.