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Promoting axon regeneration by enhancing the non-coding function of the injury-responsive coding gene Gpr151

ABSTRACT: Promoting axon regeneration by enhancing the non-coding function of the injury-responsive coding gene Gpr151

PROVIDER: PRJNA742408 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14995043_1.fastq.gz	Fastqsanger.gz
	SRR14995044_1.fastq.gz	Fastqsanger.gz
	SRR14995045_1.fastq.gz	Fastqsanger.gz
	SRR14995046_1.fastq.gz	Fastqsanger.gz
	SRR14995047_1.fastq.gz	Fastqsanger.gz

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Promoting axon regeneration by enhancing the non-coding function of the injury-responsive coding gene Gpr151

Project description:Gene expression profiling in response to nerve injury has been mainly focused on protein functions of coding genes to understand mechanisms of axon regeneration and to identify targets of potential therapeutics for nerve repair. However, the protein functions of several highly injury-induced genes including Gpr151 for regulating the regenerative ability remain unclear. Here we present an alternative approach focused on non-coding functions of the coding genes, which led to the identification of the non-coding function of Gpr151 RNA interacting with RNA-binding proteins such as CSDE1. Gpr151 promotes axon regeneration by the function of its 5’- untranslated region (5’UTR) and expression of an engineered form of the 5’UTR improves regenerative capacity in vitro and in vivo in both sciatic nerve and optic nerve injury models. Our data suggest that searching injury-induced coding genes potentially functioning by their non-coding regions is required for the RNA-based gene therapy for improving axon regeneration.

2021-07-01 | GSE179145 | GEO

SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

Project description:During peripheral nerve (PN) development, unmyelinated axons (nmAs) initially form tight fascicles before being separated and enveloped by non-myelinating Schwann cells (nmSCs), which are essential for maintaining nmA integrity. The mechanism underlying this transition from axon-axon to axon-glia interactions remains unclear. Here, we found that inactivating nmSC-derived SEMA3B or its axonal receptor components in mice led to incomplete nmA separation and envelopment by nmSCs, leading to nmA dysfunction and inducing hyperalgesia and allodynia. Conversely, increasing SEMA3B levels in nmSCs accelerated nmA separation and envelopment. SEMA3B transiently promoted nmA defasciculation accompanied by cell adhesion molecule (CAM) endocytosis, thus facilitating subsequent CAM-mediated nmA-mSC association. Restoring SEMA3B expression post-PN injury promoted nmA-nmSC re-association and alleviated hyperalgesia and allodynia. We propose that SEMA3B-induced CAM turnover facilitates the switch from axon-axon to axon-glia interactions, promoting nmA envelopment by nmSCs, which may be exploited to alleviate PN injury-induced pain by accelerating the restoration of nmA integrity.

2025-04-09 | GSE294160 | GEO

SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

Project description:SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

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Activating injury-responsive genes with hypoxia enhances axon regeneration through neuronal HIF-1α

Project description:Injured peripheral neurons successfully activate a pro-regenerative transcriptional program to enable axon regeneration and functional recovery. How transcriptional regulators coordinate the expression of such programs remains unclear. Here we show that hypoxia-inducible factor 1α (HIF-1α) controls multiple injury-induced genes in sensory neurons and contribute to the pre-conditioning lesion effect. Knockdown of HIF-1α in vitro or conditional knockout in vivo impairs sensory axon regeneration. The HIF-1α target gene Vascular Endothelial Growth Factor A (VEGFA) is expressed in injured neurons and contributes to stimulate axon regeneration. Induction of HIF-1α using hypoxia enhances axon regeneration in vitro and in vivo in sensory neurons. Hypoxia also stimulates motor neuron regeneration and accelerates neuromuscular junction reinnervation. This study demonstrates that HIF-1α represents a critical transcriptional regulator in regenerating neurons and suggests hypoxia as a tool to stimulate axon regeneration.

2016-01-21 | GSE73415 | GEO

Genome-wide identification of Drought-responsive Regulatory Coding and Non-coding Transcripts from Oryza sativa L. by deep RNA sequencing

Project description:Abiotic environmental stresses cause serious economic losses in agriculture. These stresses include temperature extremes, high salinity and drought. To isolate drought-responsive novel coding and noncoding genes, we used the next generation sequencing method from three rice cultivars (wild type nipponbare, nipponbare AP2 transgenic plants, wild type vandana). 36 NGS data of mRNA-seq, small RNA-seq, riboZero-seq were analyzed. For the analyses of these data we constructed a TF-TG (Transcription Factor-Target Gene) network and an ap2 rooted cascading tree. Using these networks and tress we isolated lincRNAs, differentially expressed miRNAs and their targets. We identified several drought stress-related novel/function unknown coding transcripts (transcription factors and functional genes) and non-coding transcripts (small noncoding transcripts such as microRNA and long noncoding transcripts) from these database analyses and have constructed databases of drought stress-related coding and noncoding transcripts Identification of drought-responsive Regulatory Coding and Non-coding Transcripts from rice by deep RNA sequencing

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Sciatic nerve injury-responsive differential mRNA profile and ribosome association efficiency of injury-induced mRNA

Project description:After nerve injury in the pheripheral nervous system, axon regeneration occurs through transcriptomic changes in neuronal cell bodies. To investigate which protein-coding transcripts are up-regulated and directed to ribosomes or not, we used RiboTag+/+;Advillin-Cre+ mice, expressing HA-tagged RPL22 specifically in sensory neurons, to profile their ribosome binding RNAs in nerve injured or uninjured dorsal root ganglion(DRG) tissues using HA-IP sequencing. We analyzed the results together with total RNA transcriptomics conducted under the same conditions. Through this analysis, we found mRNA of Gpr151 gene, one of the transcript that highly responds to injury but does not direct to the ribosomes, promoting axon regeneration by a non-coding RNA function.

2023-08-18 | GSE237046 | GEO

Sciatic nerve injury-responsive differential CSDE1 association efficiency of ribosomal protein coding mRNAs

Project description:Gpr151 is an injury-responsive gene that promotes axon regeneration through its interaction with the 5'UTR region of its mRNA transcripts and the RNA-binding protein CSDE1. We found that knocking down or overexpressing the 5'UTR of Gpr151 changes the ribosomal protein mRNA regulon regulated by CSDE1. After the sciatic nerve injury, the association between the ribosomal protein mRNA regulon and CSDE1 was enhanced at dorsal root ganglions(DRGs), but this enhancement was not observed in the AAV-shGpr151 injected mice. Overexpression of 5'UTRmut, which has increased binding affinity to CSDE1, enhanced the ribosomal protein mRNA regulon and its association with CSDE1 in embryonic DRG neurons.

2023-08-18 | GSE236910 | GEO

Epitranscriptomic m6A Regulation of Axon Regeneration in the Adult Mammalian Nervous System

Project description:N6-methyladenosine (m6A) affects multiple aspects of mRNA metabolism and regulates developmental transitions by promoting mRNA decay. Little is known about the role of m6A in the adult mammalian nervous system. Here we report that sciatic nerve lesion elevates levels of m6A-tagged transcripts encoding many regeneration-associated genes and protein translation machinery components in the adult mouse dorsal root ganglion (DRG). Single base resolution m6A-CLIP mapping further reveals a dynamic m6A landscape in the adult DRG upon injury. Loss of either m6A methyltransferase complex component Mettl14 or m6A-binding protein Ythdf1 globally attenuates injury induced protein translation in adult DRGs and reduces functional axon regeneration in the peripheral nervous system in vivo. Furthermore, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adult central nervous system is attenuated upon Mettl14 knockdown. Our study reveals a critical epitranscriptomic mechanism in promoting injury-induced protein synthesis and axon regeneration in the adult mammalian nervous system.

2018-01-17 | GSE106423 | GEO

Histone methyltransferase Ezh2 coordinates mammalian axon regeneration via regulation of key regenerative pathways (RRBS)

Project description:Current treatments for neurodegenerative diseases and neural injuries fall short of success. One primary reason is that neurons in the mammalian central nervous system (CNS) lose their regeneration ability as they mature. Here, we investigated the role of Ezh2, a histone methyltransferase, in regulation of mammalian axon regeneration. We found that Ezh2 declined in the mouse nervous system during maturation but was upregulated in adult dorsal root ganglion neurons to support spontaneous axon regeneration following peripheral nerve injury. In addition, overexpression of Ezh2 in retinal ganglion cells in the CNS promoted optic nerve regeneration via both histone methylation-dependent and -independent mechanisms. Further investigation revealed that Ezh2 supported axon regeneration by systematically silencing the transcription of genes regulating synaptic function and inhibiting axon regeneration, while simultaneously activating various axon regeneration promoting factors. In particular, our study demonstrated that the GABA transporter 2 encoded by the gene Slc6a13 acted downstream of Ezh2 to control axon regeneration. Our study suggested that modulating chromatin accessibility was a promising strategy to promote CNS axon regeneration.

2023-12-22 | GSE247319 | GEO

Axon-enriched lincRNA ALAE is required for axon elongation via regulating local mRNA translation

Project description:Long intergenic noncoding RNAs (lincRNAs) are critical regulators involved in diverse biological processes. However, the roles and related mechanisms of lincRNAs in axon development are largely unknown. To seek the axon-enriched lincRNAs in DRG neurons, we performed high-throughput RNA-seq of cultured rat dorsal root ganglion (DRG) neurons at P0 to profile lincRNAs. Profiling of highly expressed lincRNAs in RNA-seq and their enrichment in the axon of DRG neurons. We report a previously unappreciated axon-enriched lincRNA regulating axon elongation, thus referred to as ALAE. ALAE functionally associates with KHSRP for preventing KHSRP binding on Gap43 mRNA, thereby maintaining GAP43 synthesis and facilitating axon elongation.

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