Tillage intensities largely affect soil compaction dynamics in agro-ecosystems. However, the contribution of tillage intensities on compaction changes in underground peanut (Arachis hypogaea) fields has not been quantified. We thus aimed to better understand the role of soil tillage intensities in mitigation of compaction stress for peanuts. Using three field tillage experiments in major Chinese peanut producing areas, we quantified the effects of (1) no tillage, (2) shallow (20 cm) plowing, (3) deep (30 cm) plowing and (4) deep (30 cm) loosening on changes in soil bulk density at 0–10 cm, 10–20 cm and 20–30 cm depths, roots and pods growth, and nutrient accumulation. Results showed that tillage management effectively mitigated soil compaction stress for peanut growth and production. Greater beneficial improvement for the underground growth of roots and pods, and N accumulation ranked as deep plowing > shallow plowing and deep loosening. Respective increases of 7.5% and 4.6% in root biomass productions and peanut yields were obtained when soil bulk density was decreased by 0.1 g cm−3. Our results suggest that the mitigation of soil compaction stress by deep plowing could be a key tillage strategy for increasing peanut yields in the field.
Background: Dysregulation of fatty acid (FA) metabolism is involved in hepatocellular carcinoma (HCC) development. Non-POU domain-containing octamer binding protein (NONO), known as the component of nuclear paraspeckles, has recently been found to promote HCC progression. In this study, we investigated the functions of NONO in regulating de novo FA synthesis and its underling mechanism during HCC development. Methods: The roles of NONO in HCC development by applying gene function loss analysis in HCC cells were detected by quantitative real-time polymerase chain reaction, cell proliferation, and cell invasion assays. The underlying mechanism of NONO in HCC development was examined by western blotting, subcellular fractionation, RNAbinding protein immunoprecipitation-sequencing, chromatin immunoprecipitation, co-immunoprecipitation and mass spectrometry. The effect of NONO on tumorigenesis in vivo was performed with a subcutaneous xenograft mouse model of HCC. Results: NONO promotes HCC progression by interacting with and increasing ATP-citrate lyase (ACLY) mRNA to enhance FA biosynthesis. Furthermore, NONO promotes ACLY expression through enhancing nuclear ACLY mRNA stability in Diethylnitrosamine-stimulated HCC cells, not related to nuclear paraspeckles. Moreover, we find that NONO/ SFPQ (Splicing factor proline and glutamine rich) heterodimer is essential for NONO interacting with ACLY mRNA in DEN stimulated HCC cells. In addition, NONO, Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) and ACLY expressions contribute HCC development in mice and are related to poor survival. Conclusion: NONO promotes HCC progression by enhancing FA biosynthesis through interacting with ACLY mRNA and provide a novel potential target for HCC therapy.
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