Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development

Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Chenghao Li [verfasserIn] Xinrui Shi [verfasserIn] Jiaying Yang [verfasserIn] Ke Li [verfasserIn] Lijun Dai [verfasserIn] Yan Zhang [verfasserIn] Meng Zhou [verfasserIn] Jianzhong Su [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	RNA editing Retinal development Non-synonymous Bipolar cells Retinal ganglion cells

Übergeordnetes Werk:	In: Computational and Structural Biotechnology Journal - Elsevier, 2013, 20(2022), Seite 2648-2656
Übergeordnetes Werk:	volume:20 ; year:2022 ; pages:2648-2656

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.csbj.2022.05.029

Katalog-ID:	DOAJ020833288

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520			\|a Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown how RNA editing regulates its development. Here, a genome-wide screening of high-confidence RNA editing events were performed to decipher the dynamic transcriptome regulation by RNA editing during mouse retinal development. 2000 high-confidence editing sites across eight developmental stages of retina were called. Three unique patterns (RNA-editinghigh pattern, RNA-editingmedium pattern and RNA-editinglow pattern) were identified by clustering these editing sites based on their editing level during retinal development. Editing events from RNA-editinghigh pattern were significantly associated with glutamate receptors and regulated synaptic transmission. Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. Together, our results provide novel insights into mechanism of post-transcriptional regulation during retinal development and help to develop novel RNA editing-guided therapeutic strategies for retinal disorders.
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allfieldsSound	10.1016/j.csbj.2022.05.029 doi (DE-627)DOAJ020833288 (DE-599)DOAJd15e5d7b17d645c9ae687455c21d8c91 DE-627 ger DE-627 rakwb eng TP248.13-248.65 Chenghao Li verfasserin aut Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown how RNA editing regulates its development. Here, a genome-wide screening of high-confidence RNA editing events were performed to decipher the dynamic transcriptome regulation by RNA editing during mouse retinal development. 2000 high-confidence editing sites across eight developmental stages of retina were called. Three unique patterns (RNA-editinghigh pattern, RNA-editingmedium pattern and RNA-editinglow pattern) were identified by clustering these editing sites based on their editing level during retinal development. Editing events from RNA-editinghigh pattern were significantly associated with glutamate receptors and regulated synaptic transmission. Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. Together, our results provide novel insights into mechanism of post-transcriptional regulation during retinal development and help to develop novel RNA editing-guided therapeutic strategies for retinal disorders. RNA editing Retinal development Non-synonymous Bipolar cells Retinal ganglion cells Biotechnology Xinrui Shi verfasserin aut Jiaying Yang verfasserin aut Ke Li verfasserin aut Lijun Dai verfasserin aut Yan Zhang verfasserin aut Meng Zhou verfasserin aut Jianzhong Su verfasserin aut In Computational and Structural Biotechnology Journal Elsevier, 2013 20(2022), Seite 2648-2656 (DE-627)731890086 (DE-600)2694435-2 20010370 nnns volume:20 year:2022 pages:2648-2656 https://doi.org/10.1016/j.csbj.2022.05.029 kostenfrei https://doaj.org/article/d15e5d7b17d645c9ae687455c21d8c91 kostenfrei http://www.sciencedirect.com/science/article/pii/S2001037022001854 kostenfrei https://doaj.org/toc/2001-0370 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2022 2648-2656
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callnumber-first	T - Technology
author	Chenghao Li
spellingShingle	Chenghao Li misc TP248.13-248.65 misc RNA editing misc Retinal development misc Non-synonymous misc Bipolar cells misc Retinal ganglion cells misc Biotechnology Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
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topic_title	TP248.13-248.65 Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development RNA editing Retinal development Non-synonymous Bipolar cells Retinal ganglion cells
topic	misc TP248.13-248.65 misc RNA editing misc Retinal development misc Non-synonymous misc Bipolar cells misc Retinal ganglion cells misc Biotechnology
topic_unstemmed	misc TP248.13-248.65 misc RNA editing misc Retinal development misc Non-synonymous misc Bipolar cells misc Retinal ganglion cells misc Biotechnology
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title	Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
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title_full	Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
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title_sort	genome-wide characterization of rna editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
callnumber	TP248.13-248.65
title_auth	Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
abstract	Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown how RNA editing regulates its development. Here, a genome-wide screening of high-confidence RNA editing events were performed to decipher the dynamic transcriptome regulation by RNA editing during mouse retinal development. 2000 high-confidence editing sites across eight developmental stages of retina were called. Three unique patterns (RNA-editinghigh pattern, RNA-editingmedium pattern and RNA-editinglow pattern) were identified by clustering these editing sites based on their editing level during retinal development. Editing events from RNA-editinghigh pattern were significantly associated with glutamate receptors and regulated synaptic transmission. Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. Together, our results provide novel insights into mechanism of post-transcriptional regulation during retinal development and help to develop novel RNA editing-guided therapeutic strategies for retinal disorders.
abstractGer	Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown how RNA editing regulates its development. Here, a genome-wide screening of high-confidence RNA editing events were performed to decipher the dynamic transcriptome regulation by RNA editing during mouse retinal development. 2000 high-confidence editing sites across eight developmental stages of retina were called. Three unique patterns (RNA-editinghigh pattern, RNA-editingmedium pattern and RNA-editinglow pattern) were identified by clustering these editing sites based on their editing level during retinal development. Editing events from RNA-editinghigh pattern were significantly associated with glutamate receptors and regulated synaptic transmission. Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. Together, our results provide novel insights into mechanism of post-transcriptional regulation during retinal development and help to develop novel RNA editing-guided therapeutic strategies for retinal disorders.
abstract_unstemmed	Adenosine-to-inosine (A-to-I) RNA editing leads to functional change of neurotransmitter receptor which is essential for neurotransmission and normal neuronal development. As a highly accessible part of central nervous system, retina has been extensively studied, however, it remains largely unknown how RNA editing regulates its development. Here, a genome-wide screening of high-confidence RNA editing events were performed to decipher the dynamic transcriptome regulation by RNA editing during mouse retinal development. 2000 high-confidence editing sites across eight developmental stages of retina were called. Three unique patterns (RNA-editinghigh pattern, RNA-editingmedium pattern and RNA-editinglow pattern) were identified by clustering these editing sites based on their editing level during retinal development. Editing events from RNA-editinghigh pattern were significantly associated with glutamate receptors and regulated synaptic transmission. Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. Together, our results provide novel insights into mechanism of post-transcriptional regulation during retinal development and help to develop novel RNA editing-guided therapeutic strategies for retinal disorders.
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title_short	Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development
url	https://doi.org/10.1016/j.csbj.2022.05.029 https://doaj.org/article/d15e5d7b17d645c9ae687455c21d8c91 http://www.sciencedirect.com/science/article/pii/S2001037022001854 https://doaj.org/toc/2001-0370
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up_date	2024-07-03T17:16:45.869Z
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Interestingly, most non-synonymous high-editing sites were mapped to ion channel genes of glutamatergic synapse which were associated with neurotransmission by controlling ion channel permeability and affecting exocytosis. Meanwhile, these non-synonymous editing sites were evolutionarily conserved and exhibited a consistently increasing editing levels between mouse and human retinal development. Single-cell RNA-seq data analysis revealed that RNA editing events prefer to occur in two main cell types including bipolar and amacrine cells. Genes with non-synonymous high-editing sites were enriched in both bipolar cells and retina ganglion cells, which may mediate retina ganglion cell differentiation by altering channel ion permeability. 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Genome-wide characterization of RNA editing highlights roles of high editing events of glutamatergic synapse during mouse retinal development

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