No abstract

Background: UHRF1 is an important epigenetic regulator connecting DNA methylation and histone methylations. Results: PHD-H3 interaction is independent of the TTD, whereas TTD-H3K9me3 interaction the PHD. Conclusion: Both TTD and PHD are essential for specific recognition of H3K9me3 by human UHRF1. Significance: This work reveals how UHRF1 recognizes H3K9me3, which is important for its cellular localization and DNA methylation.

Melatonin, an indoleamine widely found in animals and plants, is considered as a candidate phytohormone that affects responses to a variety of biotic and abiotic stresses. In plants, melatonin has a similar action to that of the auxin indole-3-acetic acid (IAA), and IAA and melatonin have the same biosynthetic precursor, tryptophan. Salt stress results in the rapid accumulation of melatonin in plants. Melatonin enhances plant resistance to salt stress in two ways: one is via direct pathways, such as the direct clearance of reactive oxygen species; the other is via an indirect pathway by enhancing antioxidant enzyme activity, photosynthetic efficiency, and metabolite content, and by regulating transcription factors associated with stress. In addition, melatonin can affect the performance of plants by affecting the expression of genes. Interestingly, other precursors and metabolite molecules associated with melatonin can also increase the tolerance of plants to salt stress. This paper explores the mechanisms by which melatonin alleviates salt stress by its actions on antioxidants, photosynthesis, ion regulation, and stress signaling.

Recently, an connection between Short-chain fatty acids (SCFAs) produced by intestinal microbiota and kidney has been revealed. The aim of this study was to explore whether SCFAs or their specific G protein-coupled receptors 43 (GPR43) agonist inhibit oxidative stress and inflammatory response in glomerular mesangial cells (GMCs) induced by high glucose and lipopolysaccharide (LPS). Our research showed that treatment with SCFAs, especially acetate and butyrate, or GPR43 agonist significantly inhibited GMCs proliferation induced by high glucose and LPS, and then reversed the production of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased levels of antioxidant enzyme superoxide dismutase (SOD). Furthermore, SCFAs or GPR43 agonist obviously increased the protein expression of GPR43 induced by high glucose and LPS, but diminished the expression of adhesion molecule intercellular adhesion molecule-1 (ICAM-1), and then decreased the proinflammatory cytokine monocyte chemoattractant protein (MCP-1) and interleukin-1β (IL-1β) release from GMCs stimulated by the high glucose and LPS. These combined results support the hypothesis that SCFAs or GPR43 agonist can inhibit oxidative stress and inflammation of GMCs induced by high glucose and LPS, suggesting that SCFAs induced signaling pathway may act as new therapeutic targets of diabetic nephropathy (DN).