Project description:DNA methylation data from several primate species profiled on the mammalian methylation array (HorvathMammalMethylChip40) which focuses on highly conserved CpGs across mammalian species. We selected a total of 91 samples from animals representing 26 strepsirrhine species, in most cases, the entire lifespan, from immature (infant or juvenile) to senile stages: 68 samples from peripheral blood, 23 samples from skin Blood and skin samples from many different primates. We profiled the following species: Cheirogaleus medius (Fat-tailed dwarf lemur), Daubentonia madagascariensis (Aye-aye), Eulemur albifrons (White-headed lemur), Eulemur collaris (Collared brown lemur), Eulemur coronatus (Crowned lemur), Eulemur flavifrons (Blue-eyed black lemur), Eulemur fulvus (Brown lemur), Eulemur macaco (Black lemur), Eulemur mongoz (Mongoose lemur), Eulemur rubriventer (Red-bellied lemur), Eulemur rufus (Red-fronted lemur), Eulemur sanfordi (Sanford's brown lemur), Galago moholi (South African galago), Hapalemur griseus (Bamboo lemur), Lemur catta (Ring-tailed lemur), Loris tardigradus (Slender loris), Microcebus murinus (Gray mouse lemur), Mirza zaza (Northern giant mouse lemur), Nycticebus coucang (Slow loris), Otolemur crassicaudatus (Greater galago), Perodicticus potto (Potto), Propithecus diadema (Diademed sifaka), Propithecus tattersalli (Golden-crowned sifaka), Varecia rubra (Red ruffed lemur). Peripheral blood was collected through venipuncture with standard procedures, either during a routine veterinary procedure or at time of necropsy. Skin tissues were collected during necropsies.
Project description:Nucleotide excision repair is a primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair maps of the grey mouse lemur,Microcebus murinus, in comparison with human. We derived fibroblast cell lines from mouse lemur and exposed them to UV irradiation. Following repair events were captured genome-wide by XR-seq protocol 1 hour and 5 minutes after irradiation for cyclobutane pyrimidine dimers (CPD) and 6-4 pyrimidine-pyrimidone photoproducts ([6-4]PP), respectively. Mouse lemur repair profiles were analyzed in comparison with the equivalent human fibroblast datasets. We found that transcription-coupled repair levels for CPD repair differs between two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions between the primates are highly correlated. This correlation is stronger for the highly expressed genes as well as the genes sharing high homology. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts between two primates repair lesions more similarly relative to two distinct cell lines from human. These results suggest that mouse lemurs and humans, and possibly primates in general, share similar repair mechanism as well as genomic variance distribution.
Project description:Aging is accompanied by complex alterations in brain structure and functions, with growing evidence implicating the choroid plexus (CP) as a key regulator of cognitive and motor function. Here, we investigated age-related changes in the CP of the gray mouse lemur (Microcebus murinus), a non-human primate model that recapitulates human brain aging features. Lemurs of different ages underwent behavioral testing, followed by transcriptomic profiling and immunofluorescence analyses of lateral ventricle CP tissue. Behavioral assessments revealed age-related declines in motor coordination and exploratory drive, whereas working memory and visual discrimination remained largely preserved. Histological analysis showed no significant structural alterations in CP architecture. Transcriptomic profiling identified 1,519 upregulated and 1,682 downregulated genes with aging, highlighting increased interindividual heterogeneity, upregulation of immune- and transport-related pathways, and downregulation of signaling and intercellular communication processes. Functionally, AQP1 protein expression decreased with age without changes in mRNA levels, suggesting post-transcriptional regulation, whereas NKCC1 and TTR expression were largely maintained. Notably, reduced AQP1 expression correlated with age-related motor decline. These findings indicate that CP aging in the mouse lemur is characterized by selective functional vulnerability, immune activation, and transcriptional remodeling, yet essential barrier and secretory functions are largely preserved. Our results highlight a primate-like aging profile of the CP, providing insights into mechanisms by which CP dysfunction may contribute to age-related motor decline and altered brain homeostasis.
2026-02-02 | GSE317899 | GEO
Project description:Small RNA-sequencing of euthermic (control) and torpid gray mouse lemur (Microcebus murinus) skeletal muscle