The pentatricopeptide repeat protein DG1 promotes the transition to bilateral symmetry during Arabidopsis embryogenesis through GUN1-mediated plastid signals.

During Arabidopsis embryogenesis, the transition of the embryo's symmetry from radial to bilateral between the globular and heart stage is a crucial event, involving the formation of cotyledon primordia and concurrently the establishment of a shoot apical meristem (SAM). However, a coherent framework of how this transition is achieved remains to be elucidated. In this study, we investigated the function of DELAYED GREENING 1 (DG1) in Arabidopsis embryogenesis using a newly identified dg1-3 mutant. The absence of chloroplast-localized DG1 in the mutants led to embryos being arrested at the globular or heart stage, accompanied by an expansion of WUSCHEL (WUS) and SHOOT MERISTEMLESS (STM) expression. This finding pinpoints the essential role of DG1 in regulating the transition to bilateral symmetry. Furthermore, we showed that this regulation of DG1 may not depend on its role in plastid RNA editing. Nevertheless, we demonstrated that the DG1 function in establishing bilateral symmetry is genetically mediated by GENOMES UNCOUPLED 1 (GUN1), which represses the transition process in dg1-3 embryos. Collectively, our results reveal that DG1 functionally antagonizes GUN1 to promote the transition of the Arabidopsis embryo's symmetry from radial to bilateral and highlight the role of plastid signals in regulating pattern formation during plant embryogenesis.

WUSCHEL RELATED HOMEOBOX5 and 7 maintain callus development by promoting cell division in Arabidopsis.

In tissue culture, a high concentration of auxin in the callus induction medium (CIM) stimulates cell division and subsequent callus formation, which acquires root primordium-like characteristics necessary for cell pluripotency. In Arabidopsis, WUSCHEL-RELATED HOMEOBOX5 (WOX5) and its closest homolog WOX7, which are abundant in the middle cell layer of mature callus, play a crucial role in maintaining pluripotency by promoting auxin accumulation and enhancing cytokinin sensitivity. However, the mechanism by which WOX5/7 regulate callus formation remains unclear. In this study, we found that mutations in WOX5/7 resulted in a significant down-regulation of genes involved in the G2M and S phases during callus induction. Loss-of-function mutants of WOX5/7 exhibited reduced callus formation, which was correlated with decreased expression of CYCB1;1 compared to the wild-type. Furthermore, we provided evidence that WOX5 physically interacts with PHYTOCHROME A SIGNAL TRANSDUCTION1 (PAT1), which spatio-temporally co-expresses with WOX5 in early-induced callus, and up-regulates a subset of cycle-regulating genes targeted by PAT1. Collectively, our findings suggest a critical role for the WOX5-PAT1 protein complex in regulating cell cycle progression, thereby promoting the continuous growth capacity of pluripotent callus.

Growth inhibition and induction of apoptosis in SGC­7901 human gastric cancer cells by evodiamine.

Evodiamine is one of the major bioactive compounds isolated and purified from the fruit of Fructus Evodiae. Numerous studies have indicated that evodiamine exhibits activity against human tumor cells. In the present study, the effect of evodiamine on the proliferation and apoptosis of SGC-7901 human gastric cancer cells and the correlative mechanisms were investigated. This may provide further experimental evidence of the pharmacological actions of evodiamine and a strategy for its use as a novel chemotherapeutic drug. Following treatment with evodiamine, the typical morphological changes of apoptosis were observed in human SGC-7901 cells. Cell cycle analysis indicated that evodiamine induced G2/M phase arrest in SGC-7901 cells and flow cytometry revealed that evodiamine induced apoptosis. Analysis of the enzymatic activity demonstrated that evodiamine increased the activity of caspase-3, -8 and -9 in SGC-7901 cells. The protein expression of caspase-3, -8 and -9 and Bax increased, and the expression of Bcl-2 decreased following treatment with evodiamine. These results suggest that evodiamine is able to inhibit the proliferation of SGC-7901 cells by inhibiting the cell cycle at G2/M phase and inducing apoptosis in SGC-7901 cells by activating caspase-3, -8 and -9, and altering the expression of caspase-3, Bax and Bcl-2.