Melatonin enhances the tolerance to iron deficiency stress through scavenging ROS in apple

Iron (Fe) is an essential micronutrient for plants. Fe deficiency, resulting from poor availability induced by its insolubility in most soils, severely affects the growth and yield of apple (Malus domestica Borkh.). Except for the application of an Fe nutrition agent, there is a lack of efficient and environmently-friendly ways to relieve plants from Fe deficiency in a modern orchard. Here, we observed that melatonin (MT), as an efficient reactive oxygen species (ROS) scavenger, could alleviate the chlorosis of leaves in apple under Fe deficiency, following increased Fe content, decreased chlorophyll degradation and stable photosynthetic rate. Exogenous melatonin induced the synthesis of endogenous melatonin and improved the activities of antioxidant enzymes, which decreased the oxidative damage induced by Fe deficiency through properly scavenging O2•− and H2O2. In addition, exogenous melatonin promoted the expression of its synthetase genes, but decreased their protein level, inferring post-transcriptional regulation. In brief, melatonin improved the tolerance to Fe deficiency through ROS migration and chloroplast protection in apple. This work uncovered the role of melatonin on Fe deficiency tolerance and also provided a potential way to relieve plants from Fe deficiency stress for apple production

RP11-495P10.1 promotes HCC cell proliferation by regulating reprogramming of glucose metabolism and acetylation of the NR4A3 promoter via the PDK1/PDH axis

The incidence and related death of hepatocellular carcinoma (HCC) have increased over the past decades. However, the molecular mechanisms underlying HCC pathogenesis are not fully understood. Long noncoding RNA (lncRNA) RP11-495P10.1 has been proven to be closely associated with the progression of prostate cancer, but its role and specific mechanism in HCC are still unknown. Here, we identify that RP11-495P10.1 is highly expressed in HCC tissues and cells and contributes to the proliferation of HCC cells. Moreover, this study demonstrates that RP11-495P10.1 affects the proliferation of HCC by negatively regulating the expression of nuclear receptor subfamily 4 group a member 3 (NR4A3). Glycometabolism reprogramming is one of the main characteristics of tumor cells. In this study, we discover that RP11-495P10.1 regulates glycometabolism reprogramming by changing the expression of pyruvate dehydrogenase kinase 1 (PDK1) and pyruvate dehydrogenase (PDH), thus contributing to the proliferation of HCC cells. Furthermore, knockdown of RP11-495P10.1 increases enrichment of H3K27Ac in the promoter of NR4A3 by promoting the activity of PDH and the production of acetyl-CoA, which leads to the increased transcription of NR4A3. Altogether, RP11-495P10.1 promotes HCC cell proliferation by regulating the reprogramming of glucose metabolism and acetylation of the NR4A3 promoter via the PDK1/PDH axis, which provides an lncRNA-oriented therapeutic strategy for the diagnosis and treatment of HCC