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Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients

ABSTRACT: Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients

PROVIDER: PRJNA541855 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10162200.fastq.gz	Fastqsanger.gz
	SRR10162201.fastq.gz	Fastqsanger.gz
	SRR10162202.fastq.gz	Fastqsanger.gz
	SRR10162203.fastq.gz	Fastqsanger.gz
	SRR10162204.fastq.gz	Fastqsanger.gz

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Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients

Project description:Speciation is associated with substantial rewiring of the regulatory circuitry underlying the expression of genes. Determining which of these changes are biologically relevant and underlie the emergence of the human brain or its unique susceptibility to neural disease has been challenging. Here we annotate changes to gene regulatory elements at cell type resolution in the brains of multiple primate species spanning most of primate evolution. We identify a unique set of regulatory elements that emerged in hominins prior to the separation of humans and chimpanzees. We demonstrate that these hominin gains disproportionally affect oligodendrocyte function after postnatal development and are preferentially affected in the brains of autism spectrum disorder patients. Our data provide a roadmap of regulatory rewiring across primate evolution providing insight into the genomic changes that underlie the emergence of the brain and its susceptibility to neural disease.

2019-12-20 | GSE130871 | GEO

Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients.

Project description: Not available

| S-EPMC6965079 | biostudies-literature

Hominin-specific NOTCH2NL genes affect Notch signaling and cortical neurogenesis

Project description:Genetic changes causing brain size expansion in human evolution have remained elusive. Notch signaling is essential for radial glia stem cell proliferation and a determinant of neuronal number in the mammalian cortex. We find three paralogs of human-specific NOTCH2NL are highly expressed in radial glia. Functional analysis reveals different alleles of NOTCH2NL have varying potencies to enhance Notch signaling by interacting directly with NOTCH receptors. Consistent with a role in Notch signaling, NOTCH2NL ectopic expression delays differentiation of neuronal progenitors, while deletion accelerates differentiation. Furthermore, NOTCH2NL genes provide the breakpoints in typical cases of 1q21.1 distal deletion/duplication syndrome, where duplications are associated with macrocephaly and autism, and deletions with microcephaly and schizophrenia. Thus, the emergence of hominin-specific NOTCH2NL genes may have contributed to the rapid evolution of the larger hominin neocortex accompanied by loss of genomic stability at the 1q21.1 locus and a resulting recurrent neurodevelopmental disorder.

2018-02-26 | GSE111082 | GEO

A Pleistocene hominin enamel proteome from Homo antecessor

Project description:Hominin relationships and their dispersal throughout Eurasia during the Early and Middle Pleistocene are highly debated. The relationships between Early and Middle Pleistocene hominins, like Homo antecessor and Homo erectus, and hominin species that dominate the Late Pleistocene fossil record, like Homo sapiens, Neanderthals and Denisovans, are unclear. Here, we obtain enamel proteomes from Homo antecessor (Atapuerca, Spain) and Homo erectus (Dmanisi, Georgia), two key fossil assemblages that have a central role in models of Pleistocene hominin morphology, dispersal, and divergence. We recover endogenous ancient proteomes from the Atapuerca and Dmanisi hominins. In addition, our proteomic data indicates that the sampled Homo antecessor molar derives from a male hominin through amelogenin protein sexing. Our data includes preserved in vivo phosphorylation and enamel proteome proteolytic digestion.

2020-04-02 | PXD014342 | Pride

The TNH2 hominin enamel proteome

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De novo enhancer function in divergent hominin haplotypes

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Hominin brain size increase has emerged from within-species encephalization.

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Real-time quantitative PCR analysis of mouse brainstem oligodendrocytes, mouse cerebellum oligodendrocytes and baboon cerebellum oligodendrocytes

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DNA methylation data from newly emerged queens, newly emerged workers, adult nurses, adult foragers and adult reverted nurses Honeybees (Apis mellifera)

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Transcription profiling of rat perineuronal A2B5/OTMP+ oligodendrocytes

Project description:Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for â we speculate â a pathological eventuality. We posit that the signature molecules PDGFR-Î±Î², cytokine PDGF-CC, and the transcription factor Pea3 used â among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes. Experiment Overall Design: Flow Cytometry was used to isolate A2B5/OTMP+ oligodendrocytes from postnatal day 7 rat brain. 4 bioloical replicates were obtained. This data can be compared to the previously submitted oligodendrocyte expression data (GSE5940).

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