<i>lncrps25</i> play an essential role in motor neuron development through controlling the expression of <i>olig2</i> in zebrafish

Gao, Tianheng; Li, Jingyun; Li, Nan; Gao, Yan; Yu, Lingling; Zhuang, Sisi; Zhao, Yanling; Dong, Xiaohua

doi:10.1002/jcp.29237

Cited by 12 publications

(12 citation statements)

References 35 publications

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“…For instance, the lncRNA lncrps25 is located near the S25 gene (which encodes a ribosomal protein) and it shares high sequence similarity with the 3' UTR of neuronal regeneration-related protein (NREP) in zebrafish. Loss of lncrps25 reduces locomotion behavior by regulating pMN development and Olig2 expression [48]. Additionally, depletion of an MN-enriched lncRNA, i.e.…”

Section: Role Of Lncrnas In Regulating Neural Progenitorsmentioning

confidence: 99%

Functional Roles of Long Non-coding RNAs in Motor Neuron Development and Disease

Chen

2020

J Biomed Sci

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Long non-coding RNAs (lncRNAs) have gained increasing attention as they exhibit highly tissue-and cell-type specific expression patterns. LncRNAs are highly expressed in the central nervous system and their roles in the brain have been studied intensively in recent years, but their roles in the spinal motor neurons (MNs) are largely unexplored. Spinal MN development is controlled by precise expression of a gene regulatory network mediated spatiotemporally by transcription factors, representing an elegant paradigm for deciphering the roles of lncRNAs during development. Moreover, many MN-related neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA), are associated with RNA metabolism, yet the link between MN-related diseases and lncRNAs remains obscure. In this review, we summarize lncRNAs known to be involved in MN development and disease, and discuss their potential future therapeutic applications.

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Section: Role Of Lncrnas In Regulating Neural Progenitorsmentioning

confidence: 99%

Functional Roles of Long Non-coding RNAs in Motor Neuron Development and Disease

Chen

2020

J Biomed Sci

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“…Olig2 is part of the Olig gene family that encode for basic helix‐loop‐helix transcription factors that are required for MN and oligodendrocyte development (Lu et al., 2002; Park et al., 2002). Based on the effect of lncrps25 depletion, and lncrps25 and olig2 expression patterns, it was proposed that lncrps25: olig2 interactions occur at the neural plate stage to eventually affect MN development (Gao et al., 2020). However, the precise mechanistic details of this lncRNA–mRNA pathway remain to be defined.…”

Section: Lncrnas In Motor Neuron Developmentmentioning

confidence: 99%

Long non‐coding RNAs in motor neuron development and disease

Vangoor

Gomes-Duarte

Pasterkamp

2020

Journal of Neurochemistry

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Long non‐coding RNAs (lncRNAs) are RNAs that exceed 200 nucleotides in length and that are not translated into proteins. Thousands of lncRNAs have been identified with functions in processes such as transcription and translation regulation, RNA processing, and RNA and protein sponging. LncRNAs show prominent expression in the nervous system and have been implicated in neural development, function and disease. Recent work has begun to report on the expression and roles of lncRNAs in motor neurons (MNs). The cell bodies of MNs are located in cortex, brainstem or spinal cord and their axons project into the brainstem, spinal cord or towards peripheral muscles, thereby controlling important functions such as movement, breathing and swallowing. Degeneration of MNs is a pathological hallmark of diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. LncRNAs influence several aspects of MN development and disruptions in these lncRNA‐mediated effects are proposed to contribute to the pathogenic mechanisms underlying MN diseases (MNDs). Accumulating evidence suggests that lncRNAs may comprise valuable therapeutic targets for different MNDs. In this review, we discuss the role of lncRNAs (including circular RNAs [circRNAs]) in the development of MNs, discuss how lncRNAs may contribute to MNDs and provide directions for future research.

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“…Similarly, Cat7 enhances the suppressive activity of the PRC1 suppressive machinery on the TF Hb9 , to guarantee its early repression along MN fate determination (Ray et al , 2016 ). Finally, in zebrafish, lncrps25 is necessary for the expression of the TF Olig2 , involved in MN and oligodendrocyte differentiation (Gao et al , 2020 ).…”

Section: Introductionmentioning

confidence: 99%

A multifunctional locus controls motor neuron differentiation through short and long noncoding RNAs

et al. 2022

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The transition from dividing progenitors to postmitotic motor neurons (MNs) is orchestrated by a series of events, which are mainly studied at the transcriptional level by analyzing the activity of specific programming transcription factors. Here, we identify a posttranscriptional role of a MN-specific transcriptional unit (MN2) harboring a lncRNA (lncMN2-203) and two miRNAs (miR-325-3p and miR-384-5p) in this transition. Through the use of in vitro mESC differentiation and single-cell sequencing of CRISPR/Cas9 mutants, we demonstrate that lncMN2-203 affects MN differentiation by sponging miR-466i-5p and upregulating its targets, including several factors involved in neuronal differentiation and function. In parallel, miR-325-3p and miR-384-5p, co-transcribed with lncMN2-203, act by repressing proliferation-related factors. These findings indicate the functional relevance of the MN2 locus and exemplify additional layers of specificity regulation in MN differentiation.

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lncrps25 play an essential role in motor neuron development through controlling the expression of olig2 in zebrafish

Cited by 12 publications

References 35 publications

Functional Roles of Long Non-coding RNAs in Motor Neuron Development and Disease

Functional Roles of Long Non-coding RNAs in Motor Neuron Development and Disease

Long non‐coding RNAs in motor neuron development and disease

A multifunctional locus controls motor neuron differentiation through short and long noncoding RNAs

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