Melatonin is known to involve multiple physiological actions in plants. Herein, we found that exogenous melatonin inhibited the Arabidopsis seedling growth through the elevated abscisic acid (ABA) levels, and the elevated ABA was ascribed to the upregulation of 9‐cis‐epoxycarotenoid dioxygenase genes (NCEDs) in the ABA biosynthesis pathway. We also found that the overexpression lines of the melatonin receptor gene PMTR1 (also known as Cand2) yielded smaller seeds and germinated slower than the wild type, whereas PMTR1‐knockout mutants produced larger seeds and germinated faster than the wild type. During the seed development, the accumulation peak of ABA was higher in the PMTR1‐knockout mutant, while it was lower in the PMTR1‐overexpression line than that in the wild type. In the dry seeds and imbibed seeds, the PMTR1‐overexpression line accumulated higher ABA levels, while the PMTR1‐knockout contained less ABA than the wild type. In summary, our findings suggest that PMTR1 is involved in ABA‐mediated seed development and germination in Arabidopsis.

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Postmeiotic development is a unique characteristic of flowering plants. During the development, microspores undergo two cycles of mitosis (PMI and PMII) and a subsequent maturation process to finally produce the mature pollen, but the mechanism underlying the development is still largely unknown. Here, we report on the roles of a novel gene, RA68, in postmeiotic pollen development in Oryza sativa. RA68 was expressed preferentially in shoots and flowers. In flowers, the transcript persisted from the floral organ differentiation to the mature pollen stages and showed preferential accumulation in male meiocytes, developing pollen and tapetal cells. RA68-deficient RNAi lines showed reduced seed setting and pollen viability but not an aberrant phenotype in vegetative organs. Knockdown of RA68 led to arrested PMI, smaller pollen grains with little or no starch, and aborted pollen but not severely distruped male meiosis. Additionally, no abnormality of anther wall development was observed in RA68-RNAi lines. RA68 may be required for postmeiotic pollen development by affecting PMI and starch accumulation.

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Background Spinal cord injury (SCI) is the most serious complication of spinal injury, often leading to severe dysfunction of the limbs below the injured segment. Conventional therapy approaches are becoming less and less effective, and gene therapy is a new research direction by now. Methods The Sprague-Dawley rats were haphazardly assigned to two groups, namely sham group and SCI model group, and lncRNA H19 and miR-370-3p levels were investigated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Correlation between lncRNA H19 and miR-370-3p was ascertained by luciferase report assay and RT-qPCR. After transfection with si-H19, miR-370-3p inhibitor, negative controls (NC), or both, primary spinal neurons were subjected to the simulation of lipopolysaccharide (LPS) for inducing in vitro model of SCI. Cell viability, apoptotic rate, caspase-3 activity, Bax and Bcl-2 protein, ROS generation, TNF-α, IL-1β, and IL-6 protein, as well as IκBα and p65 phosphorylation ratio were evaluated adopting 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), apoptosis, caspase-3 activity, ROS generation, and western blot assays, thereby searching for the specific action mechanism on LPS-induced spinal never injury. Results SCI resulted in lncRNA H19 higher expression and miR-370-3p lower expression. LPS simulation raised a series of cellular biological changes, such as decreased viability, promoted apoptosis, generated ROS, and released inflammatory factors. lncRNA H19 inhibition reversed above LPS-induced changes. Besides, as the downstream target of lncRNA H19, miR-370-3p was oppositely regulated by lncRNA H19. The above biological changes induced by lncRNA H19 inhibition were reversed by miR-370-3p upregulation. Moreover, lncRNA H19 inhibition could block NF-κB pathway through miR-370-3p upregulation. Conclusion Inhibition of lncRNA H19/miR-370-3p mitigated spinal neuron apoptosis in an in vitro model of SCI. This provided the possibility for clinical use of gene therapy.