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LncRNAs are widely involved in various biological processes of plants. Recent evidences indicated that lncRNAs could act as competing endogenous RNAs (ceRNAs) to adsorb complementary miRNAs in a type of target mimicry, thereby indirectly regulating the target genes of miRNAs. In this study, a lncRNA, lncRNA08489 was identified to be the ceRNA of miR482e-3p in tomato plants. The expression patterns of lncRNA08489 and miR482e-3p showed opposite trends after tomato plants infected with Phytophthora infestans. In tomato leaves overexpressing lncRNA08489 (OE08489), the expression level of miR482e-3p decreased and its target gene, NBS-LRR increased. After infection with P. infestans , the resistance of OE08489 plants was stronger than that of the wild type, and the reactive oxygen species (ROS) scavenging ability of OE08489 plants was significantly improved. Taken together, these results indicated that lncRNA08489 acted as a ceRNA to decoy miR482e-3p and regulate the expression of NBS-LRR to enhance tomato resistance through ROS-scavenging system. • LncRNA08489 modulated the accumulation of NBS-LRR through decoying miR482e-3p. • LncRNA08489 acted as a positive regulator of tomato resistance to Phytophthora infestans infection. • Overexpressing lncRNA08489 tomato increased the ROS-scavenging. [ABSTRACT FROM AUTHOR]

SlmiR482e-3p is involved in tomato– Phytophthora infestans interactions. In this study, we evaluated the function of the complementary strand slmiR482e-5p. In transgenic plants slMIR482e , slmiR482e-3p, and slmiR482e-5p overexpression increased susceptibility to P. infestans infection, while slmiR482e-3p and slmiR482e-5p silencing increased resistance. Additionally, sllncRNA39298 inhibited slmiR482e-5p expression and increased resistance to P. infestans. Upon P. infestans infection, reactive oxygen species accumulation was higher in leaves overexpressing slMIR482e , slmiR482e-3p, and slmiR482e-5p and lower in sllncRNA39298-overexpressing leaves than in wild-type leaves. These results support the functional importance of complementary strand miRNAs and reveal the roles of slmiR482e-5p and sllncRNA39298 in tomato disease resistance. • miR482e-5p and miR482e-3p coordinately regulate tomato resistance to P. infestans. • lncRNA39298 enhances tomato resistance to P. infestans by decoying miR482e-5p. • miR482e-3p, miR482e-5p, and lncRNA39298 regulate ROS scavenging in tomato. [ABSTRACT FROM AUTHOR]

Ultraviolet B (UVB) irradiation causes skin inflammation and apoptosis. Mitochondria are highly dynamic and undergo constant fusion and fission that are essential for maintaining physiological functions of cells. Although dysfunction of mitochondria has been implicated in skin damages, little is known about the roles of mitochondrial dynamics in these processes. UVB irradiation increases abnormal mitochondrial content but decreases mitochondrial volume in immortalized human keratinocyte HaCaT cells. UVB irradiation resulted in marked upregulation of mitochondrial fission protein dynamin-related protein 1 (DRP1) and downregulation of mitochondrial outer membrane fusion proteins 1 and 2 (MFN1 and MFN2) in HaCaT cells. Mitochondrial dynamics was discovered to be crucial for NLRP3 inflammasome and cGAS-STING pathway activation, as well as the induction of apoptosis. Inhibition of mitochondrial fission by treatments with a DRP1 inhibitor, mdivi-1, or with DRP1-targeted siRNA, efficiently prevented UVB-induced NLRP3/cGAS-STING mediated pro-inflammatory pathways or apoptosis in the HaCaT cells, whereas inhibition of mitochondrial fusion with MFN1and 2 siRNA increased these pro-inflammatory pathways or apoptosis. The enhanced mitochondrial fission and reduced fusion caused the up-regulation of reactive oxygen species (ROS). Application of an antioxidant, N -acetyl- l -cysteine (NAC), which scavenges excessive ROS, attenuated inflammatory responses through suppressing NLRP3 inflammasome and cGAS-STING pathway activation, and rescued cells from apoptosis caused by UVB-irradiation. Together, our findings revealed the regulation of NLRP3/cGAS-STING inflammatory pathways and apoptosis by mitochondrial fission/fusion dynamics in UVB-irradiated HaCaT cells, providing a new strategy for the therapy of UVB skin injury. [Display omitted] • UVB perturbs mitochondrial fission/fusion dynamics in HaCaT cells. • Disturbed mitochondrial dynamics control the amount of mitochondria. • Disturbed mitochondrial dynamics regulate NLRP3/cGAS-STING mediated pro-inflammatory pathways and apoptosis. • ROS are responsible for pro-inflammatory pathways and apoptosis initiated by the dysregulated mitochondrial dynamics. [ABSTRACT FROM AUTHOR]