Ontology highlight
ABSTRACT:
PROVIDER: PRJNA521407 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8547520.fastq.gz | Fastqsanger.gz | |||
| SRR8547521.fastq.gz | Fastqsanger.gz | |||
| SRR8547522.fastq.gz | Fastqsanger.gz | |||
| SRR8547523.fastq.gz | Fastqsanger.gz | |||
| SRR8547524.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:Aging is the primary risk factor of neurodegenerative disorders such as Alzheimer's disease (AD). However, the molecular events occurring during brain aging are extremely complex and still largely unknown. For a better understanding of these age-associated modifications, animal models as close as possible to humans are needed. We thus analyzed the transcriptome of the temporal cortex of the primate Microcebus murinus using human oligonucleotide microarrays (Affymetrix). Gene expression profiles were assessed in the temporal cortex of 6 young adults, 10 healthy old animals and 2 old, "AD-like" animals that presented b-amyloid plaques and cortical atrophy, which are pathognomonic signs of AD in humans. Gene expression data of the 14,911 genes that were detected in at least 3 samples were analyzed. By SAM (significance analysis of microarrays), we identified 47 genes that discriminated young from healthy old and "AD-like" animals. These findings were confirmed by principal component analysis (PCA). ANOVA of the expression data from the three groups identified 695 genes (including the 47 genes previously identified by SAM and PCA) with significant changes of expression in old and "AD-like" in comparison to young animals. About one third of these genes showed similar changes of expression in healthy aging and in M-bM-^@M-^\AD-likeM-bM-^@M-^] animals, whereas more than two thirds showed opposite changes in these two groups in comparison to young animals. Hierarchical clustering analysis of the 695 markers indicated that each group had distinct expression profiles which characterized each group, especially the "AD-like" group. Functional categorization showed that most of the genes that were up-regulated in healthy old and down-regulated in "AD-like" animals belonged to metabolic pathways, particularly protein synthesis. These data suggest the existence of compensatory mechanisms during physiological brain aging that disappear in M-bM-^@M-^\AD-likeM-bM-^@M-^] animals. These results open the way to new exploration of physiological and M-bM-^@M-^\AD-likeM-bM-^@M-^] aging in primates. Microcebus murinus were divided in 3 groups: the first group included 6 young adults (4 females and 2 males), the second included 10 healthy old animals (7 females and 3 males) and the third one was composed by 2 "AD-like" old females. Since Microcebus murinus microarrays do not exist, we decided to use Affymetrix human genome chips (HG U133 plus 2), since studies have illustrated the feasibility of detecting non-human primate brain transcripts using human genome chips.
2011-04-01 | E-GEOD-21779 | biostudies-arrayexpress
Project description:Grey mouse lemurs (Microcebus murinus) are a primate species, which exhibits strong physiological seasonality in response to environmental energetic constraint. They notably accumulate large amounts of lipid reserves during early winter, which are thereafter mobilized during late winter, when food availability is very low. In addition, they develop glucose intolerance in late winter only. To decipher how the hepatic mechanisms may support such metabolic flexibility, we analyzed the liver proteome of captive lemurs, which seasonal regulations of metabolism and reproduction are comparable to their wild counterparts, during the phases of either constitution or use of fat reserves.
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Project description:Mouse lemurs are basal primates that rely on chemo- and acoustic signalling for social interactions in their dispersed social systems. We examined the urinary protein content of two mouse lemurs species, within and outside the breeding season, to assess candidates used in species discrimination, reproductive or competitive communication. Urine from Microcebus murinus and Microcebus lehilahytsara contain a predominant 10kDa protein, expressed in both species by some, but not all, males during the breeding season, but at very low levels by females. Mass spectrometry of the intact proteins confirmed the protein mass and revealed a 30 Da mass difference between proteins from the two species. Tandem mass spectrometry after digestion with three proteases and sequencing de novo defined the complete protein sequence and located an Ala/Thr difference between the two species that explained the 30 Da mass difference. The protein (mature form: 87 amino acids) is an atypical member of the whey acidic protein family (WFDC12). Seasonal excretion of this protein, species difference and male-specific expression during the breeding season suggest that it may have a function in intra- and/or intersexual chemical signalling in the context of reproduction, and could be a cue for sexual selection and species recognition.
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Project description:Parkinson disease (PD) is a neurodegenerative disease primarily associated with impaired movement affecting elderly people. To improve the understanding of the pathogenesis and to develop new therapies, we have developed a non-human primate model of PD using the lemurian Microcebus murinus (Mim). In this study, we tested the potential of canine adenovirus type 2 (CAV-2) as vector for gene transfer in the Mim brain by analyzing the gene expression changes in three regions involved in motor control: striatum, frontal cortex and midbrain. The CAV-2 viruses were injected in the right striatum of young adult females, 2 years old. CAV-2 vectors preferentially transduce neurons in the primate brain and were carried by axonal transport to afferent structures in both hemispheres. The gene expression changes were analyzed at 2 critical times after infection by CAV-2: an acute time effect at 24h and a delayed time effect at 28 days post infection. In addition, the gene expression was compared in the ipsilateral side versus the contralateral side, and with a non-infected brain samples using human Affymetrix microarrays. The transcriptomic data were analyzed by Significance Analysis of Microarrays (SAM) to identify genes differentially expressed when comparing brain samples in the 3 conditions. The data were also analyzed by ANOVA one way and by Principal Component Analysis (PCA). The results have shown that the transduction of CAV2 in neurons induced specific changes. These changes differed during the immediate and the long-term-point. Gene expression changes were detected in transcriptional regulation, in synaptic transmission, in cellular trafficking and in immune response. More precisely, in the short term, CAV2 activated genes involved in a non-specific innate immune response. In the long term, CAV2 induced an adaptive tolerant immune response. Gene expression changes in the frontal cortex of Microcebus murinus induced by Canine adenovirus type 2 (CAV-2)
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