Rathu Heenati (RHT) is a Sri Lankan rice cultivar that carries a brown planthopper (BPH) resistance gene, Bph3, and shows broad-spectrum resistance to all four biotypes of BPH. The BPH-resistance loci in RHT has been studied extensively and assigned to four different rice chromosomes (3, 4, 6, and 10) by different research groups, but the gene has not been cloned previously. An Affymetrix rice genome array containing 48,564 japonica and 1,260 indica sequences was used to analyze the potential resistance-related genes on the four chromosomes by comparative analysis of the differentially expressed genes between resistant and susceptible rice cultivars exposed to BPH attack. The microarray results showed that at least 17 genes related to induced resistance and at least 193 genes related to constitutive resistance in RHT. On chromosome 3, the AOC4 was hypothesized to be the most important candidate gene. On chromosome 6, no valuable candidate resistance gene was identified in the Bph3 localization region. In the three Quantitative trait locus regions of chromosomes 3, 4, and 10, the numbers of constitutive and induced resistance-related genes found were 17, 26, and 12, respectively. The major probe on chromosome 10 represents a constitutive expression gene with a very high absolute fold-change of 2,588.82. The microarray analysis indicated that BPH resistance in RHT is probably controlled by a series of resistance-related genes. This study provides valuable information for cloning, functional analysis and marker-assisted breeding of these BPH resistance genes.

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Objectives: Diabetes is an independent risk factor for dementia. Mitochondrial dysfunction is a critical player in diabetes and diabetic complications. The present study aimed to investigate the role of mitochondrial dynamic changes in diabetes-associated cognitive impairment.Methods: Cognitive functions were examined by novel object recognition and T-maze tests. Mice hippocampi were collected for electron microscopy and immunofluorescence examination. Neuron cell line HT22 and primary hippocampal neurons were challenged with high glucose in vitro. Mitotracker-Red CM-H2X ROS was used to detect mitochondrial-derived free radicals.Results: Diabetic mice exhibited memory loss and spatial disorientation. Electron microscopy revealed that diabetic mice had larger synaptic gaps, attenuated postsynaptic density and fewer dendritic spines in the hippocampus. More round-shape mitochondria were observed in hippocampal neurons in diabetic mice than those in control mice. In cultured neurons, high glucose induced a high phosphorylated level of dynamin-related protein 1 (DRP1) and increased oxidative stress, resulting in cell apoptosis. Inhibition of mitochondrial fission by Mdivi-1 and metformin significantly decreased oxidative stress and prevented cell apoptosis in cultured cells. Treatment of Mdivi-1 and metformin restored cognitive function in diabetic mice.Conclusion: Metformin restores cognitive function by inhibiting mitochondrial fission, reducing mitochondrial-derived oxidative stress, and mitigating neuron loss in hippocampi of diabetic mice. The protective effects of metformin shed light on the therapeutic strategy of cognitive impairment.