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Lockd promotes myoblast proliferation and skeletal muscle regeneration through binding with Dhx36 to facilitate unwinding of 5’UTR rG4 and translation of Anp32e mRNA

ABSTRACT: Lockd promotes myoblast proliferation and skeletal muscle regeneration through binding with Dhx36 to facilitate unwinding of 5’UTR rG4 and translation of Anp32e mRNA

PROVIDER: PRJNA805521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17982676_1.fastq.gz	Fastqsanger.gz
	SRR17982676_2.fastq.gz	Fastqsanger.gz
	SRR17982677_1.fastq.gz	Fastqsanger.gz
	SRR17982677_2.fastq.gz	Fastqsanger.gz
	SRR17982678_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Lockd promotes myoblast proliferation and skeletal muscle regeneration through binding with DHX36 to facilitate unwinding of 5’UTR rG4 and translation of Anp32e mRNA

Project description:Adult muscle stem cells, also known as satellite cells (SCs) play pivotal roles in injury induced muscle regeneration and our knowledge of long non-coding RNA (lncRNA) functions in SCs remains limited. Here we identify a lncRNA, Lockd which is induced in activated SCs upon acute muscle injury. We demonstrate that Lockd promotes SC proliferation; deletion of Lockd leads to cell cycle arrest at G1/S phase. Consistently, in vivo repression of Lockd in mouse muscles hinders muscle regeneration process. Mechanistically, we uncover that Lockd lncRNA molecule directly interacts with an RNA helicase DHX36; structural probing further shows that the 5’end of the Lockd possesses the strongest binding activity with DHX36 protein. Furthermore, we demonstrate that Lockd stabilizes the interaction between DHX36 and EIF3B proteins; and synergistically this complex unwinds the RNA G-quadruplex (rG4) structure formed at the 5’UTR of Anp32e mRNA and promotes the translation of ANP32E protein which is required for myoblast cell proliferation. Altogether, our findings thus identify a regulatory circuitry consisting of Lockd/DHX36/Anp32e that functions to promote myoblast proliferation, thus enabling the acute injury induced muscle regeneration to progress.

2022-05-24 | PXD033658 |

System-wide analysis of Dhx36 function in skeletal muscle satellite cells reveals its binding with 5’UTR G4 structure to promote Gnai2 RNA translation

Project description:In this study, we deciphered the functions of Dhx36 and related molecular mechanisms in muscle stem cells and muscle regeneration. We found Dhx36 was highly induced in activated muscle stem cells during regeneration induced by injury. Conditional inactivation of Dhx36 in mouse muscle stem cells caused significant impaired regeneration, which was due to the dramatically decreased cell proliferation. Dhx36 was a well-known RNA helicase for binding/unwinding DNA/RNA G-quadruplexes and it was dominantly expressed in cytoplasm of proliferating myoblast. CLIP-seq was conducted to identify the mRNAs interacting with Dhx36 in myoblast cells. To examine whether Dhx36 regulates translation process, we also conducted polysome profiling followed by RNA-seq in WT and Dhx36 KO myoblast cells. This SuperSeries is composed of the SubSeries listed below.

2021-04-27 | GSE151124 | GEO

System-wide analysis of Dhx36 function in skeletal muscle satellite cells reveals its binding with 5’UTR G4 structure to promote Gnai2 RNA translation [Polysome profiling]

Project description:In this study, we deciphered the functions of Dhx36 and related molecular mechanisms in muscle stem cells and muscle regeneration. We found Dhx36 was highly induced in activated muscle stem cells during regeneration induced by injury. Conditional inactivation of Dhx36 in mouse muscle stem cells caused significant impaired regeneration, which was due to the dramatically decreased cell proliferation. Dhx36 was a well-known RNA helicase for binding/unwinding DNA/RNA G-quadruplexes and it was dominantly expressed in cytoplasm of proliferating myoblast. To examine whether Dhx36 regulates translation process, we conducted polysome profiling followed by RNA-seq in WT and Dhx36 KO myoblast cells.

2021-04-27 | GSE151123 | GEO

Lockd promotes myoblast proliferation and skeletal muscle regeneration through binding with Dhx36 to facilitate unwinding of 5’UTR rG4 and translation of Anp32e mRNA

Project description:polysome profiling in WT and Lockd KO myoblast cells

2022-02-14 | GSE196574 | GEO

System-wide analysis of Dhx36 function in skeletal muscle satellite cells reveals its binding with 5’UTR G4 structure to promote Gnai2 RNA translation [CLIP-seq]

Project description:In this study, we deciphered the functions of Dhx36 and related molecular mechanisms in muscle stem cells and muscle regeneration. We found Dhx36 was highly induced in activated muscle stem cells during regeneration induced by injury. Conditional inactivation of Dhx36 in mouse muscle stem cells caused significant impaired regeneration, which was due to the dramatically decreased cell proliferation. Dhx36 was a well-known RNA helicase for binding/unbinding DNA/RNA G-quadruplexes and it was dominantly expressed in cytoplasm of proliferating myoblast. Therefore CLIP-seq was conducted to identify the mRNAs interacting with Dhx36 in myoblast cells.

2021-04-27 | GSE151122 | GEO

DHX36 binding induces RNA structurome remodeling and regulates RNA abundance via m6A/YTHDF1

Project description:RNA structure constitutes a new layer of gene regulatory mechanisms. RNA binding proteins can modulate RNA secondary structures, thus participating in post-transcriptional regulation. The DEAH-box helicase 36 (DHX36) is known to bind and unwind RNA G-quadruplex (rG4) structure but the transcriptome-wide RNA structure remodeling induced by DHX36 binding and the impact on RNA fate remain poorly understood. Here, we investigate the RNA structurome alteration induced by DHX36 depletion. Our findings reveal that DHX36 binding induces structure remodeling not only at the localized binding sites but also on the entire mRNA transcript most pronounced in3’UTR regions. DHX36 binding increase structural accessibility at 3’UTRs which is correlated with decreased post-transcriptional mRNA abundance. Further analyses and experiments uncover that DHX36 binding sites are enriched for N6-methyladenosine (m6A) modification and YTHDF1 binding; and DHX36 induced structural change may facilitate YTHDF1 binding to m6A sites leading to RNA degradation. Altogether, our findings uncover the structural remodeling effect of DHX36 binding and its impact on RNA abundance through regulating m6A dependent YTHDF1 binding.

2024-10-03 | GSE264642 | GEO

Transcriptomic RNA structure mapping unveils the structure dynamic induced by DHX36 binding (RBNS)

Project description:RNA binding proteins can modulate RNA secondary structures, thus participating in post-transcriptional regulation. The DEAH-box helicase 36 (DHX36) has a remarkable ability to bind and unwind RNA G-quadruplex (rG4) and duplex. However, the transcriptome-wide RNA structure dynamic induced by DHX36 and how structure change subsequently influences RNA fate remain poorly understood. Here, we first identify the endogenous binding sites and specificity of DHX36 based on binding profiles. Next, we capture in vivo RNA structuromes to investigate the structure change of DHX36-bound mRNAs following DHX36 knockout. DHX36 induces structure remodeling on not only the localized binding sites but also the other sites across the entire mRNA especially in 3’UTR. DHX36-induced more accessible structures of 3’UTR are revealed to correlate with post-transcriptional mRNA decrease. Furthermore, we demonstrate that DHX36 binding sites are enriched for N6-methyladenosine (m6A) modification and YTHDF1 binding. Finally, we experimentally validate that YTHDF1 binding is repelled to DHX36 loss-induced structure inaccessibility and YTHDF1 loss-induced mRNA stabilization could be a source of DHX36 loss-induced mRNA increase. Altogether, our findings uncover the effect of DHX36 binding on in vivo mRNA structure and propose a plausible mechanism of how RNA secondary structure change involves in post-transcriptional regulation through orchestrating YTHDF1 binding.

2024-10-03 | GSE237159 | GEO

Transcriptomic RNA structure mapping unveils the structure dynamic induced by DHX36 binding (Structure-seq)

2024-10-03 | GSE237160 | GEO

Anp32e is a histone chaperone that removes H2A.Z from chromatin

Project description:We report a genome wide enrichment, redistribution and accumulation of H2A.Z at specific chromatin control regions, in particular at enhancers and insulators, in mouse embryonic fibroblasts depleted for Anp32e (MEFs Anp32e-/-). H2A.Z ChIP-seq in MEFs WT (+/+) or KO (-/-) for Anp32e.

2014-01-22 | E-GEOD-51579 | biostudies-arrayexpress

SMaRT lncRNA controls translation of a G-quadruplex containing mRNA antagonizing the DHX36 helicase

Project description:Guanine-quadruplexes (G4) present in RNA and DNA exert a number of different functions in the nucleus and in the cytoplasm. However, the molecular mechanisms of G4-mediated regulation are still poorly understood. We describe a regulatory circuitry operating in the early phases of muscle differentiation in which a long non coding RNA (SMaRT) base pairs with a G4-containing mRNA (Mlx-g) and represses its translation in an antagonistic way with the RNA helicase DHX36. MLX-g is required to allow the nuclear translocation of the MLX-a and b dimerization partners and to control proper myogenesis. We show that by controlling MLX-g, lnc-SMaRT is able to regulate the overall quantity of nuclear MLX proteins and their transcriptional output. Therefore, the circuitry composed by lnc-SMaRT, Mlx-g and Dhx36 not only plays an important role in the control of myogenesis but unravels a molecular mechanism where G4 structures and G4 unwinding activities are controlled in vivo.

2020-03-18 | GSE128486 | GEO

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