Project description:Japanese macaques learn to use rakes to acquire food, and this learning is associated with rapid electrophysiological and morphological changes in the brain. To examine the molecular mechanisms of these plastic changes, we performed comprehensive gene expression analysis with a cDNA microarray and identified many candidate genes.
Project description:Japanese macaques learn to use rakes to acquire food, and this learning is associated with rapid electrophysiological and morphological changes in the brain. To examine the molecular mechanisms of these plastic changes, we performed comprehensive gene expression analysis with a cDNA microarray and identified many candidate genes. We compared gene expressions between experimental (Rhesus_E) and control (Rhesus_C) animals from Surrounding areas of the lateral sulcus. We also compared gene expressions between experimental (IPS_E) and control (IPS_C) animals from Surrounding areas of the Intraparietal sulcus.
Project description:We performed gene expression profiling of total RNA from brain samples derived from BSE-infected versus non-infected cynomolgus macaques (Macaca fascicularis). Total RNA from brain samples derived from 7 BSE-infected (6 intracerebrally, 1 orally infected) versus 5 non-infected controls were compared using GeneChip Rhesus macaque Genome Array.
Project description:Background: Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease. Results: Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques. Conclusions: We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration. Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. In a second approach, ERV-K-(HML-2) RNA and protein expression was analysed in extracts from the same cynomolgus macaques.
Project description:Macaque species share over 93% genome homology with humans and develop many disease phenotypes similar to those of humans, making them valuable animal models for the study of human diseases (e.g.,HIV and neurodegenerative diseases). However, the quality of genome assembly and annotation for several macaque species lags behind the human genome effort. To close this gap and enhance functional genomics approaches, we employed a combination of de novo linked-read assembly and scaffolding using proximity ligation assay (HiC) to assemble the pig-tailed macaque (Macaca nemestrina) genome. This combinatorial method yielded large scaffolds at chromosome-level with a scaffold N50 of 127.5 Mb; the 23 largest scaffolds covered 90% of the entire genome. This assembly revealed large-scale rearrangements between pig-tailed macaque chromosomes 7, 12, and 13 and human chromosomes 2, 14, and 15. We subsequently annotated the genome using transcriptome and proteomics data from personalized induced pluripotent stem cells (iPSCs) derived from the same animal. Reconstruction of the evolutionary tree using whole genome annotation and orthologous comparisons among three macaque species, human and mouse genomes revealed extensive homology between human and pig-tailed macaques with regards to both pluripotent stem cell genes and innate immune gene pathways. Our results confirm that rhesus and cynomolgus macaques exhibit a closer evolutionary distance to each other than either species exhibits to humans or pig-tailed macaques. These findings demonstrate that pig-tailed macaques can serve as an excellent animal model for the study of many human diseases particularly with regards to pluripotency and innate immune pathways.
Project description:Aging is a major risk factor for various forms of disease. An enhanced understanding of the physiological mechanisms related to aging is urgently needed. Nonhuman primates (NHPs) have the closest genetic relationship to humans, making them an ideal model to explore the complicated aging process. Multiomics analysis of NHP peripheral blood offers a promising approach to evaluate new therapies and biomarkers. Here, we explored the mechanisms of aging using proteomics (serum and serum-derived exosomes [SDEs]) in rhesus monkey (Macaca mulatta) blood.