A retroviral link to vertebrate myelination
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE237744 | GEO | 2024/02/14
REPOSITORIES: GEO
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Project description:The synarcual is a specialized adaptation of the anterior axial skeleton comprising a putatively fused array of vertebral elements characteristic of jawed vertebrate (gnathostome) clades such as batoid and chimaeroid chondrichthyans, as well as a fossil group known as the placoderms. Placoderms represent the phylogenetically most basal jawed vertebrates and the presence of a synarcual in these and chondrichthyans may suggest a conserved vertebral type for jawed vertebrates, predating the divergence of stem and crown gnathostomes. Alternatively, synarcuals may have evolved independently in these lineages, exhibiting a remarkable case of morphological convergence. We investigated the early development of the cervicothoracic synarcual of an emerging model chondrichthyan, the Little skate Leucoraja erinacea, by combining x-ray computed tomography, classical histology, and a de novo transcriptome assembly for two developmental stages of the skate synarcual and post-synarcual axial skeletal elements.
2019-06-01 | GSE121572 | GEO
Project description:Whereas the gill chambers of extant jawless vertebrates (lampreys and hagfish) open directly into the environment, jawed vertebrates have evolved skeletal appendages that promote the unidirectional flow of oxygenated water over the gills. A major anatomical difference between the two jawed vertebrate lineages is the presence of a single operculum covering a large common gill cavity in bony fishes versus separate covers for each gill chamber in cartilaginous fishes. Here we find that these divergent gill cover patterns correlate with the pharyngeal arch expression of Pou3f3 orthologs, and we identify a deeply conserved Pou3f3 arch enhancer that is present in nearly all jawed vertebrates but undetectable in lampreys. Despite only minor sequence differences, bony fish and cartilaginous fish versions of this enhancer are sufficient to drive the respective single versus multiple gill arch expression. In zebrafish, loss of Pou3f3 gene function or its conserved enhancer disrupts gill cover formation. Conversely, forced expression of Pou3f3b in the gill arches generates ectopic skeletal elements reminiscent of the multiple gill covers of cartilaginous fish. Emergence and modification of this ancient Pou3f3 enhancer may thus have contributed to the acquisition and diversification of gill covers during early gnathostome evolution.
2020-06-17 | GSE140636 | GEO
Project description:Myelinating glia in the auditory system enclose auditory nerve fibers, providing an insulating effect that facilitates rapid transfer of auditory information from the ear to the brain. Here we show that noise exposure at the levels sufficient for inducing hearing loss cause a rapid cellular and molecular response on myelinating glia that precedes neuron degeneration. The response is characterized by inflammatory response, myelin dysmorphology and widespread changes in myelin-related gene expression. Another characteristic was change in expression of the quaking gene (QKI), which encodes a group of RNA binding proteins that are enriched in myelinating glia. Changes in QKI were accompanied by changes in numerous known and potential QKI target genes, including many genes associated with myelination. Our results implicate QKI as a critical early component in the noise response, influencing glia dysfunction that leads to auditory nerve demyelination and, ultimately, sensorineural hearing loss.
2018-04-12 | GSE100365 | GEO
Project description:he neural crest is an embryonic stem cell population unique to vertebrates whose expansion and diversification are thought to have promoted vertebrate evolution by enabling emergence of novel cell types and structures like jaws and peripheral ganglia2. While basal vertebrates have sensory ganglia, convention has it that trunk sympathetic chain ganglia arose only in jawed vertebrates. In contrast, here we report the presence of trunk sympathetic neurons in the sea lamprey, Petromyzon marinus, an extant jawless vertebrate. These neurons arise from sympathoblasts near the dorsal aorta that undergo noradrenergic specification via a transcriptional program homologous to that described in gnathostomes. Lamprey sympathoblasts populate the extracardiac space and extend along the length of the trunk in bilateral streams, expressing the catecholamine biosynthetic pathway enzymes tyrosine hydroxylase and dopamine -hydroxylase. CM-DiI lineage tracing analysis further confirmed that these cells derive from the trunk neural crest. RNA-seq of isolated ammocete trunk sympathoblasts revealed gene profiles characteristic of sympathetic neuron function. Our findings challenge prevailing dogma which posits that sympathetic ganglia are a gnathostome innovation, instead suggesting that a late-developing rudimentary sympathetic nervous system may have been characteristic of the earliest vertebrates.
2024-02-22 | GSE246248 | GEO
Project description:Understanding the regulation of oligodendrocyte development and myelination in the central nervous system (CNS) is essential, not only to facilitate myelin repair but also to define the role of oligodendrocytes in maintaining axonal integrity. In vitro studies have implicated astrocytes in influencing multiple aspects of oligodendrocytes and their precursors, however the in vivo role of astrocytes in myelination and myelin repair remain poorly defined. We show that astrocyte ablation during postnatal spinal cord development resulted in a concomitant delay in myelination, demonstrating a critical role for astrocytes in promoting developmental myelination. By contrast, in the adult CNS, localized ablation of astrocytes 2 days after a demyelinating insult resulted in increased numbers of oligodendrocytes and accelerated remyelination in both the spinal cord and the corpus callosum. Microarray analysis reveals astrocytic NF-kB signaling pathway as a major contributor to pathological events occurring after demyelination. We suggest that the localized functions of astrocytes are fundamentally different during developmental myelination and myelin repair. Astrocytes are critical for developmental myelination, however in a demyelinating environment they are detrimental to myelin repair.
2017-08-01 | GSE60276 | GEO
Project description:16 divergent jawed vertebrate species Targeted Locus (Loci)
| PRJNA254214 | ENA
Project description:Background Methylation of CG dinucleotides constitutes a critical system of epigenetic memory in bony vertebrates, where it modulates gene expression and suppresses transposon activity. The genomes of studied vertebrates are pervasively hypermethylated, with the exception of regulatory elements such as transcription start sites (TSSs), where the presence of methylation is associated with gene silencing. This system is not found in the sparsely methylated genomes of invertebrates, and establishing how it arose during early vertebrate evolution is impeded by a paucity of epigenetic data from basal vertebrates. Methods We perform whole-genome bisulfite sequencing to generate the first genome-wide methylation profiles of a cartilaginous fish, the elephant shark Callorhinchus milii. Employing these to determine the elephant shark methylome structure and its relationship with expression, we compare this with higher vertebrates and an invertebrate chordate using published methylation and transcriptome data. Results Like higher vertebrates, the majority of elephant shark CG sites are highly methylated, and methylation is abundant across the genome rather than patterned in the mosaic configuration of invertebrates. This global hypermethylation includes transposable elements and the bodies of genes at all expression levels. Significantly, we document an inverse relationship between TSS methylation and expression in the elephant shark, supporting the presence of the repressive regulatory architecture shared by higher vertebrates. Conclusions Our demonstration that methylation patterns in a cartilaginous fish are characteristic of higher vertebrates imply the conservation of this epigenetic modification system across jawed vertebrates separated by 465 million years of evolution. In addition, these findings position the elephant shark as a valuable model to explore the evolutionary history and function of vertebrate methylation.
2017-03-24 | GSE96683 | GEO
Project description:The NuRD complex is required for efficient and timely myelination in the peripheral nervous system. ChIP-chip assays were performed on rat sciatic nerve at P15, a peak timepoint of myelination, for binding of Chd4 to genes involved in regulating myelin formation. This experiment includes two custom ChIP-chip design incorporating many genes that are dynamically regulated during myelination. The antibodies used in this platform were Chd3/4 (Santa Cruz sc-11378) Chd4 (gift from Paul Wade), Mta2 (Santa Cruz sc-9447), and Nab2 (Santa Cruz sc-22815). Chd4 ChIP samples from experimental and input samples were hybridized.
2011-07-25 | E-GEOD-30890 | biostudies-arrayexpress
Project description:Chromatin organization is critical for cell growth, differentiation, and disease development, however, its functions in peripheral myelination and myelin repair remain elusive. Here we observed a global diminution of chromatin accessibility during Schwann cell differentiation and demonstrated that the chromatin organizer CCCTC-binding factor (CTCF) is critical for Schwann cell myelination and myelin regeneration after nerve injury. Inhibition of Ctcf or its deletion blocked Schwann cell differentiation at the pre-myelinating stage, whereas overexpression of CTCF promoted the myelination program. CTCF establishes the chromatin interaction loop between promoters and regulatory elements to promote expression of key pro-myelinogenic factors such as EGR2. In addition, CTCF interacts with SUZ12, a component of polycomb-repressive-complex 2, to repress expression of immature Schwann cell-associated regulators including HES1, RSPO2, and CALCA. Together, our findings reveal the dual role of CTCF-dependent chromatin organization in promoting myelinogenic programs and recruiting chromatin-repressive complexes to block differentiation inhibitors to control peripheral myelination and myelin repair.
2020-06-22 | GSE138117 | GEO
Project description:Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/?-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and ?-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair. ChIP-seq was performed to identify Olig2 direct target genes in oligodendrocytes during oligodendrocyte differentiation.
2012-08-31 | E-GEOD-40506 | biostudies-arrayexpress