Translational Insights from Cell-type variation across Amygdala Subnuclei in Rhesus Monkeys and Humans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1094867 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR28514113_1.fastq.gz | Fastqsanger.gz | |||
| SRR28514113_2.fastq.gz | Fastqsanger.gz | |||
| SRR28514114_1.fastq.gz | Fastqsanger.gz | |||
| SRR28514114_2.fastq.gz | Fastqsanger.gz |
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Project description:Theories of amygdala function are central to our understanding of psychiatric and neurodevelopmental disorders. However, our limited knowledge of the molecular and cellular composition of the amygdala impedes translational research aimed at developing new treatments and interventions. Here, we use single-nucleus RNA-sequencing from multiple amygdala subnuclei in both humans (n=3, Male) and rhesus macaques (n=3, Male) to begin to bridge the gap between preclinical rodent models and human disorders. Our results reveal substantial heterogeneity between regions, even when restricted to inhibitory or excitatory neurons. Consistent with prior work, our data highlight the complexities of individual marker genes for uniquely targeting specific cell-types. Cross-species analyses suggest the rhesus monkey model to be well-suited to understanding the human amygdala, but also identify limitations. For example, we identified a cell-cluster in the ventral lateral nucleus (vLA) of the amygdala that is enriched in humans, relative to rhesus macaques. Additionally, we identify specific cell-clusters with relative enrichment of disorder-related genes. These analyses point to the human-enriched vLa cell-cluster as relevant to ASD, potentially highlighting a vulnerability to neurodevelopmental disorders that has emerged in recent primate evolution. Further, we identified a cluster of cells expressing markers for intercalated cells (ITCs) that is enriched for genes reported in human genome-wide association studies of neuroticism, anxiety disorders, and depressive disorders. Together, these data shed light on the composition of the amygdala and identify specific cell-types that can be prioritized in basic science research to better understand human psychopathology and guide the development of potential treatments
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Project description:Type 2 diabetes mellitus (TM) is a severely metabolic disorder that affects above 10% worldwide population. Obesity is a major cause of insulin resistance and contributes to the development of TM. Liver is an essential metabolic organ that plays crucial roles in the pathogenesis of obesity and diabetes. However, the underlying mechanisms of liver in the transition of obesity to diabetes are not fully understood. Nonhuman primate (NHP) rhesus monkey is an appropriate animal for research of human diseases. Here, we first screened and selected three individual spontaneous and diabetic rhesus monkeys. Interestingly, the diabetic monkeys were obese with high BMI at beginning, but gradually lost their body weight during one-year observation. Furthermore, we performed a SILAC-based quantitative proteomics to identify proteins and signaling pathways with altered expression in the liver of obese and diabetic monkeys. Totally, 3509 proteins were identified and quantified, and of which 185 proteins displayed altered expression level. GO analysis revealed that the expression of proteins involved in fatty acids β-oxidation and galactose metabolism was increased in obese monkeys; while proteins involved in oxidative phosphorylation (OXPHOS) and branched chain amino acid (BCAA) degradation was upregulated in diabetic monkeys. In addition, we observed a mild impaired mitophagy and apoptosis in the liver of diabetic monkeys, suggesting a dysfunction of mitochondria and liver injury in the late onset of diabetics. Taken together, our liver proteomics may reveal a distinct metabolic transition from fatty acids β-oxidation in obese monkey to BCAA degradation in diabetic monkeys.
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