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Transcriptomic analysis of human Fragile X syndrome neurons reveals neurite growth modulation by the TGFβ/BMP pathway

ABSTRACT: Transcriptomic analysis of human Fragile X syndrome neurons reveals neurite growth modulation by the TGFβ/BMP pathway

PROVIDER: PRJNA849165 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19649475_1.fastq.gz	Fastqsanger.gz
	SRR19649475_2.fastq.gz	Fastqsanger.gz
	SRR19649476_1.fastq.gz	Fastqsanger.gz
	SRR19649476_2.fastq.gz	Fastqsanger.gz
	SRR19649477_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of human Fragile X syndrome neurons reveals neurite growth modulation by the TGFβ/BMP pathway

Project description:Isogenic hESC clones with and without the FX mutation that share the same genetic background were in vitro differentiated into neurons. FX neurons present delayed neuronal development and maturation with full FMRP silencing. Following enrichment of neurons in the culture by MACS, transcriptome analysis by RNA sequencing at different time points during differentiation demonstrated dysregulation of the TGFβ/BMP signaling pathway and genes related to the extracellular matrix. FX neurons showed decreased neurite outgrowth that was rescued by inhibition of the TGFβ/BMP signaling pathway, this treatment did not affect the outgrowth of control neurons. In FMRP expressing neurons the regulation of the TGFβ/BMP pathway allow typical neurite outgrowth and axonogenesis that will eventually result in normal neuronal network activity. In contrast, in FX neurons the lack of FMRP dysregulate members of the BMP signaling pathway associated with the ECM organization that in a yet unknown mechanism, reduces the guidance of axonal growth cones, leading to an aberrant neuronal network function. Overall, our results provide new insights into the molecular pathways by which loss of FMRP affects neuronal network development which probably leads to its aberrant function in FXS.

2022-08-31 | GSE206088 | GEO

Transcriptomic Analysis of Human Fragile X Syndrome Neurons Reveals Neurite Outgrowth Modulation by the TGFβ/BMP Pathway.

Project description:Fragile X Syndrome (FXS) is the main genetic reason for intellectual disability and is caused by the silencing of fragile X mental retardation protein (FMRP), an RNA-binding protein regulating the translation of many neuronal mRNAs. Neural differentiation of FX human embryonic stem cells (hESC) mimics the neurodevelopment of FXS fetuses and thus serves as a good model to explore the mechanisms underlining the development of FXS. Isogenic hESC clones with and without the FX mutation that share the same genetic background were in vitro differentiated into neurons, and their transcriptome was analyzed by RNA sequencing. FX neurons inactivating FMR1 expression presented delayed neuronal development and maturation, concomitant with dysregulation of the TGFβ/BMP signaling pathway, and genes related to the extracellular matrix. Migration assay showed decreased neurite outgrowth in FX neurons that was rescued by inhibition of the TGFβ/BMP signaling pathway. Our results provide new insights into the molecular pathway by which loss of FMRP affects neuronal network development. In FX neurons, the lack of FMRP dysregulates members of the BMP signaling pathway associated with ECM organization which, in a yet unknown mechanism, reduces the guidance of axonal growth cones, probably leading to the aberrant neuronal network function seen in FXS.

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Spatial transcriptomics reveals a role for sensory nerves in preserving cranial suture patency through modulation of BMP/TGFβ signaling

Project description:The patterning and ossification of the mammalian skeleton requires the coordinated actions of both intrinsic bone morphogens and extrinsic neurovascular signals, which function in a temporal and spatial fashion to control mesenchymal progenitor cell (MPC) fate. Here we show genetic inhibition of Tropomyosin receptor kinase A (TrkA) sensory nerve innervation of the developing cranium results in premature calvarial suture closure, associated with a decrease in suture MPC proliferation. In vitro, axons from peripheral afferent neurons derived from DRGs of wild type mice induce MPC proliferation in a spatially-restricted manner via a soluble factor when co-cultured in microfluidic chambers. Comparative spatial transcriptomic analysis of the cranial sutures in vivo confirmed a positive association between sensory axons and proliferative MPCs. SpatialTime analysis across the developing suture revealed regional-specific alterations in BMP and TGFβ signaling pathway transcripts in response to TrkA inhibition. RNA sequencing of DRG cell bodies following direct axonal co-culture with MPCs confirmed alterations in BMP/TGFβ signaling pathway transcripts. Among these, the BMP inhibitor FSTL1 (Follistatin-like 1) replicated key features of the neural-to-bone influence, including mitogenic and anti-osteogenic effects via inhibition of BMP/TGFβ signaling. Taken together, our results demonstrate that sensory nerve-derived signals, including FSTL1, function to coordinate cranial bone patterning by regulating MPC proliferation and differentiation in the suture mesenchyme.

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