In prokaryotic and eukaryotic cells, the 39-59-exonucleolytic decay and processing of RNAs are essential for RNA metabolism. However, the understanding of the mechanism of 39-59-exonucleolytic decay in plants is very limited. Here, we report the characterization of an Arabidopsis (Arabidopsis thaliana) transfer DNA insertional mutant that shows severe growth defects in early seedling growth, including delayed germination and cotyledon expansion, thinner yellow/pale-green leaves, and a slower growth rate. High-efficiency thermal asymmetric interlaced polymerase chain reaction analysis showed that the insertional locus was in the sixth exon of AT4G27490, encoding a predicted 39-59-exonuclease, that contained a conserved RNase phosphorolytic domain with high similarity to RRP41, designated RRP41L. Interestingly, we detected highly accumulated messenger RNAs (mRNAs) that encode seed storage protein and abscisic acid (ABA) biosynthesis and signaling pathway-related protein during the early growth stage in rrp41l mutants. The mRNA decay kinetics analysis for seed storage proteins, 9-cis-epoxycarotenoid dioxygenases, and ABA INSENSITIVEs revealed that RRP41L catalyzed the decay of these mRNAs in the cytoplasm. Consistent with these results, the rrp41l mutant was more sensitive to ABA in germination and root growth than wild-type plants, whereas overexpression lines of RRP41L were more resistant to ABA in germination and root growth than wild-type plants. RRP41L was localized to both the cytoplasm and nucleus, and RRP41L was preferentially expressed in seedlings. Altogether, our results showed that RRP41L plays an important role in seed germination and early seedling growth by mediating specific cytoplasmic mRNA decay in Arabidopsis.
Introduction: To investigate antitumor activity and mechanism of flavonoids from Alpinia officinarum Hance against gastric cancer. Methods: Transplanted mouse fore-stomach carcinoma (MFC) tumor mice were divided into six groups: control group, model group, low dose (20 mg/kg), middle dose (40 mg/kg), and high dose (80 mg/kg) groups of TFAO and 5-Fu group. Mice were treated with TFAO or 5-Fu for 14 days, except those of control and model group. Tumor inhibitory rate, spleen, and thymus index were calculated. Contents of proliferating cell nuclear antigen, MMP-9, vascular endothelial growth factor, IL-1β, IL-6, and IL-17 in serum were detected. Effect of galangin on BGC-823 cell growth was detected. Cell apoptosis and cell cycle distribution were measured. Enzyme activity of Caspase-3, Caspase-8, and Caspase-9 was detected. Western blot was used to detect STAT3, Bcl-2, Bax, Caspase-3, Caspase-8, Caspase-9, CyclinB1, and CyclinD1 protein expression in BGC-823 cell. Results: Compared with model group, tumor weight of mice decreased significantly ( p < .01) in 5-Fu group, low dose, middle dose, and high dose group of TFAO; thymus index of mice decreased significantly ( p < .05) in 5-Fu group; and spleen index decreased significantly ( p < .05) in low dose and middle dose groups of TFAO. Compared with model group, levels of PCNA, MMP-9, IL-1β, and IL-6 in serum of mice decreased obviously ( p < .01) in all administration groups; levels of VEGF in serum of mice decreased obviously ( p < .01) in low dose and high dose group of TFAO and 5-Fu group; and levels of IL-17 in serum of mice decreased significantly ( p < .01) in low-dose and middle-dose groups of TFAO and 5-Fu group. Galangin could inhibit BGC-823 cell growth; accelerate apoptosis; block cell cycle; increase cell Caspase-3, Caspase-8, and Caspase-9 enzyme activity; upregulate expression of Caspase-3, Caspase-8, Caspase-9, and Bax; and downregulate expression of STAT3, CyclinB1, CyclinD1, and Bcl-2 protein. Conclusion: Flavonoids from A. officinarum showed antitumor activity in gastric cancer. Mechanisms may be associated with inhibition of tumor angiogenesis, tumor cell proliferation, and cancer-associated inflammation.
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