Large scale rice germplasm screening for identification of novel brown planthopper resistance sources.

Rice (Oryza sativa L.) is a staple food crop globally. Brown planthopper (Nilaparvata lugens Stål, BPH) is the most destructive insect that threatens rice production annually. More than 40 BPH resistance genes have been identified so far, which provide valuable gene resources for marker-assisted breeding against BPH. However, it is still urgent to evaluate rice germplasms and to explore more new wide-spectrum BPH resistance genes to combat newly occurring virulent BPH populations. To this end, 560 germplasm accessions were collected from the International Rice Research Institute (IRRI), and their resistance to current BPH population of China was examined. A total of 105 highly resistant materials were identified. Molecular screening of BPH resistance genes in these rice germplasms was conducted by developing specific functional molecular markers of eight cloned resistance genes. Twenty-three resistant germplasms were found to contain none of the 8 cloned BPH resistance genes. These accessions also exhibited a variety of resistance mechanisms as indicated by an improved insect weight gain (WG) method, suggesting the existence of new resistance genes. One new BPH resistance gene, Bph44(t), was identified in rice accession IRGC 15344 and preliminarily mapped to a 0-2 Mb region on chromosome 4. This study systematically sorted out the corresponding relationships between BPH resistance genes and germplasm resources using a functional molecular marker system. Newly explored resistant germplasms will provide valualble donors for the identification of new resistance genes and BPH resistance breeding programs. Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-023-01416-x.

Alzheimer's risk factor FERMT2 promotes the progression of colorectal carcinoma via Wnt/ß-catenin signaling pathway and contributes to the negative correlation between Alzheimer and cancer.

Increasing evidence from epidemiological studies indicate that Alzheimer's disease (AD) has a negative relationship with the incidence of cancers. Whether the Alzheimer's genetic risk factor, named as fermitin family homolog-2 (FERMT2), plays a pivotal part in the progressive process of colorectal carcinoma (CRC) yet remains unclear. This study revealed that FERMT2 was upregulated in CRC tissues which predicted an unfavorable outcome of CRC using the PrognoScan web tool. FERMT2 was co-expressed with a variety of genes have been linked with CRC occurrence and implicated in the infiltration of immune cell in CRC tissues. Overexpressing FERMT2 promoted CRC progression with upregulation of Wnt/ß-catenin signaling. Knockdown of FERMT2 suppressed the cell multiplication, colony formation rate, migration and invasion, along with the epithelial to mesenchymal transition (EMT) with downregulation Wnt/ß-catenin proteins in cells of CRC, while overexpressing ß-catenin reversed the inhibitory effects of silencing FERMT2 on the migration or invasion of CRC cells. Furthermore, Aß1-42 treated HT22 cells induced downregulation of FERMT2 and inhibited the migration, invasion and EMT in co-cultured CT26 cells through Wnt/ß-catenin signaling. Our results revealed that the downregulated FERMT2 gene during AD is prominently activated in CRC, which promotes its progression via Wnt/ß-catenin pathway.

Advanced glycation end products induce Aß1-42 deposition and cognitive decline through H19/miR-15b/BACE1 axis in diabetic encephalopathy.

OBJECTIVE: Diabetic encephalopathy (DE), a chronic complication of diabetes, is characterized by decline of cognitive function. The molecular mechanism of DE remains unclear. The purpose of this study is to evaluate the roles of advanced glycation end products (AGEs) in the pathogenesis of DE and investigate its underlying mechanisms in this process. METHODS: DE rats were developed by incorporating a high-fat diet and streptozotocin injection followed by the Morris Water Maze test. HT-22 cells were used to mimic the in vitro neuronal injuries of DE. Expression levels of long non-coding RNA H19, miR-15b and ß-site amyloid precursor protein cleaving enzyme 1 (BACE1) mRNA in the hippocampus of DE rats or HT-22 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The levels of BACE1 proteins were analyzed by western blotting or immunohistochemical staining. The contents of Aß1-42 in supernatant of the cell culture were analyzed by enzyme-linked immu-nosorbent assay (ELISA). The relationship between H19 or BACE1 and miR-15b was verified with dual-luciferase reporter assay. RESULTS: We found that the accumulation of Aß1-42 and the phosphorylation of Tau (Ser404) were increased in the hippocampus CA3 regionof DE rats. MiR-15b was downregulated while H19 and BACE1 were upregulated in the hippocampus CA3 regionof DE rats and AGEs-treated HT-22 cells. The expression of BACE1 protein was negatively regulated by miR-15b at the post-transcriptional level in HT-22 cells. In vivo, administration of miR-15b mimics by the intranasal delivery markedly decreased the BACE1 protein in hippocampal CA3 region and improved the cognitive decline in DE rats. Besides, the luciferase activity assay confirmed the binding site of miR-15b to both the 3'-untranslated region (3'-UTR) of BACE1 mRNA and H19. Then, miR-15b inhibitor reversed H19 knockdown-mediated decrease of Aß1-42 level in AGEs-treated HT-22 cells. CONCLUSION: These results suggested that AGEs induced Aß1-42 deposition andcognitive decline through H19/miR-15b/ BACE1 axis in DE.

Crosstalk Between Gut Microflora and Vitamin D Receptor SNPs Are Associated with the Risk of Amnestic Mild Cognitive Impairment in a Chinese Elderly Population.

BACKGROUND: The interactions between environmental factors and genetic variants have been implicated in the pathogenesis of Alzheimer's disease (AD). The altered gut microbiota (GM) and vitamin D deficiency are closely associated with the higher risk of AD. OBJECTIVE: This study was performed to evaluate whether the crosstalk between GM and single nucleotide polymorphisms (SNPs) of vitamin D receptor (VDR) or vitamin D binding protein (VDBP) have a link with the risk of amnestic mild cognitive impairment (aMCI) in the Chinese elderly population. METHODS: A total of 171 aMCI patients and 261 cognitive normal controls (NC) were enrolled in this study. Six tag SNPs of VDR and VDBP were genotyped by PCR-RFLP. The serum levels of vitamin D, Aß1-42, and p-tau (181P) were determined by using of ELISA kits. The alterations in the GM were analyzed by full-length 16S ribosomal RNA (rRNA) gene sequencing. RESULTS: The frequencies of AG genotype and A allele of VDR rs1544410 in aMCI group were significantly higher than that in NC group (genotype: p = 0.002, allele: p = 0.003). Patients with aMCI showed an abnormal GM composition compared with NC group. Interestingly, significant differences in GM composition were found between aMCI and NC group among individuals with AG genotype, as well as between individuals with AG and GG genotype of VDR rs1544410 among patients with aMCI. CONCLUSION: These results implicated that the crosstalk between gut microflora and vitamin D receptor variants are associated with the risk of aMCI in Chinese elderly population.

Advanced Glycosylation End Products Induced Synaptic Deficits and Cognitive Decline Through ROS-JNK-p53/miR-34c/SYT1 Axis in Diabetic Encephalopathy.

BACKGROUND: miR-34c has been found to be implicated in the pathological process of Alzheimer's disease, diabetes, and its complications. OBJECTIVE: To investigate the underlying mechanisms of miR-34c in the pathogenesis of diabetic encephalopathy (DE). METHODS: Diabetes mellitus rats were developed by incorporating a high-fat diet and streptozotocin injection. Morris water maze test and novel object recognition test were used to assess the cognitive function of rats. Expression of miR-34c were detected by fluorescence in situ hybridization and qRT-PCR. Immunofluorescence and western blot were used to evaluate synaptotagmin 1 (SYT1) and AdipoR2 or other proteins. Golgi staining was performed to investigate dendritic spine density. RESULTS: The increased miR-34c induced by advanced glycation end-products (AGEs) was mediated by ROS-JNK-p53 pathway, but not ROS-Rb-E2F1 pathway, in hippocampus of DE rats or in HT-22 cells. miR-34c negatively regulated the expression of SYT1, but not AdipoR2, in hippocampal neurons. miR-34c inhibitor rescued the AGE-induced decrease in the density of dendritic spines in primary hippocampal neurons. Administration of AM34c by the intranasal delivery increased the hippocampus levels of SYT1 and ameliorated the cognitive function in DE rats. The serum levels of miR-34c were increased in patients with DE comparing with normal controls. CONCLUSION: These results demonstrated that AGE-induced oxidative stress mediated increase of miR-34c through ROS-JNK-p53 pathway, resulting in synaptic deficits and cognitive decline by targeting SYT1 in DE, and the miR-34c/SYT1 axis could be considered as a novel therapeutic target for DE patients.

Administration of miR-195 Inhibitor Enhances Memory Function Through Improving Synaptic Degradation and Mitochondrial Dysfunction of the Hippocampal Neurons in SAMP8 Mice.

BACKGROUND: Mitochondrial dysfunction is an early feature of Alzheimer's disease (AD) and miR-195 is involved in mitochondrial disorder through targeting MFN-2 protein in hippocampal neurons of AD. OBJECTIVE: To clarify if administration of miR-195 inhibitor could enhance the memory deficits through improving hippocampal neuron mitochondrial dysfunction in SAMP8 mice. METHODS: The expression of miR-195 was detected by RT-qPCR in primary hippocampal neurons and HT-22 cells treated with Aß1-42. Morris water maze (MWM) was used to assess the learning and memory function in SAMP8 mice administrated with antagomir-195. Transmission electron microscopy was employed to determine the morphological changes of synapses and mitochondria of hippocampus in SAMP8 mice. Mitochondrial respiration was measured using a high-resolution oxygraph. RESULTS: The expression of miR-195 were upregulated in the primary hippocampal neurons and HT-22 cells induced by Aß1-42. Inhibition of miR-195 ameliorated the mitochondrial dysfunction in HT-22 cells induced by Aß1-42, including mitochondrial morphologic damages, mitochondrial membrane potential, respiration function, and ATP production. Administration of antagomir-195 by the third ventricle injection markedly ameliorated the cognitive function, postsynaptic density thickness, length of synaptic active area, mitochondrial aspect ratio, and area in hippocampus of SAMP8 mice. Finally, antagomir-195 was able to promote an increase in the activity of respiratory chain complex CI and II in SAMP8 mice. CONCLUSION: This study demonstrated that miR-195 inhibitor ameliorated the cognitive impairment of AD mice by improving mitochondrial structure damages and dysfunction in the hippocampal neurons, which provide an experimental basis for further exploring the treatment strategy of AD.

Transcriptomic and proteomic analyses of the mechanisms of overwintering diapause in soybean pod borer (Leguminivora glycinivorella).

BACKGROUND: Soybean pod borer (Leguminivora glycinivorella) is an important soybean pest in north-eastern Asia, whose mature larvae overwinter in a diapause state. Disruption of winter diapause may be a valuable tool in pest management. However, the molecular mechanisms regulating diapause in this species have not yet been elucidated. RESULTS: We compared the transcriptomes and proteomes between diapause and mature larvae and between mature and newly developed pupae to identify the genes and proteins associated with diapause. Thirty-seven differentially expressed genes and their proteins changed synchronously between diapause and mature larvae and 82 changed synchronously between diapause larvae and newly developed pupae. Among these, genes involved in fatty acid biosynthesis and the longevity regulating pathway were up-regulated in diapause larvae and down-regulated in newly developed pupae, suggesting that they may regulate diapause. One fatty acid synthase (FAS) gene and two small heat shock genes (HSP19.8 and HSP18.9) were chosen for further functional analysis. After RNA interference (RNAi)-mediated knockdown of FAS, the survival of mature larvae was significantly lower than that of control larvae, but the mean developmental time from first-instar larva to adult remained unchanged. RNAi-mediated knockdown of HSP19.8 and HSP18.9 severely shortened the mean developmental time, causing approximately 50% larvae to develop directly into pupae. CONCLUSION: FAS and the small heat shock gene play roles in diapause regulation and larvae survival. This study provides important information that may assist in understanding the molecular regulatory mechanisms of overwintering diapause of this important agricultural insect pest. © 2020 Society of Chemical Industry.