scholarly journals Long Non-coding RNA T-uc.189 Modulates Neural Progenitor Cell Fate by Regulating Srsf3 During Mouse Cerebral Cortex Development

2021 ◽  
Vol 15 ◽  
Author(s):  
Meng Zhang ◽  
Junjie Zhou ◽  
Li Jiao ◽  
Longjiang Xu ◽  
Lin Hou ◽  
...  
Keyword(s):  
Cell Fate ◽  
Ventricular Zone ◽  
Neural Progenitor Cell ◽  
Temporal Gene Expression ◽  
Non Coding Rna ◽  
Complex Process ◽  
Mouse Cerebral Cortex ◽  
Full Length Sequence ◽  
Long Non Coding Rna ◽  
The Brain

Neurogenesis is a complex process that depends on the delicate regulation of spatial and temporal gene expression. In our previous study, we found that transcribed ultra-conserved regions (T-UCRs), a class of long non-coding RNAs that contain UCRs, are expressed in the developing nervous systems of mice, rhesus monkeys, and humans. In this study, we first detected the full-length sequence of T-uc.189, revealing that it was mainly concentrated in the ventricular zone (VZ) and that its expression decreased as the brain matured. Moreover, we demonstrated that knockdown of T-uc.189 inhibited neurogenesis. In addition, we found that T-uc.189 positively regulated the expression of serine-arginine-rich splicing factor 3 (Srsf3). Taken together, our results are the first to demonstrate that T-uc.189 regulates the expression of Srsf3 to maintain normal neurogenesis during cortical development.

scholarly journals Long Non-Coding RNA (lncRNA) Roles in Cell Biology, Neurodevelopment and Neurological Disorders

2021 ◽  
Vol 7 (2) ◽  
pp. 36
Author(s):  
Vincenza Aliperti ◽  
Justyna Skonieczna ◽  
Andrea Cerase
Keyword(s):  
Neurological Disorders ◽  
Cell Biology ◽  
Neuronal Development ◽  
Altered Expression ◽  
Non Coding Rna ◽  
Complex Process ◽  
Novel Target ◽  
Long Non Coding Rna ◽  
The Brain

Development is a complex process regulated both by genetic and epigenetic and environmental clues. Recently, long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression in several tissues including the brain. Altered expression of lncRNAs has been linked to several neurodegenerative, neurodevelopmental and mental disorders. The identification and characterization of lncRNAs that are deregulated or mutated in neurodevelopmental and mental health diseases are fundamental to understanding the complex transcriptional processes in brain function. Crucially, lncRNAs can be exploited as a novel target for treating neurological disorders. In our review, we first summarize the recent advances in our understanding of lncRNA functions in the context of cell biology and then discussing their association with selected neuronal development and neurological disorders.

scholarly journals MiR-7 in Cancer Development

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 325
Author(s):  
Petra Korać ◽  
Mariastefania Antica ◽  
Maja Matulić
Keyword(s):  
Cell Fate ◽  
Dominant Role ◽  
Tumor Development ◽  
Mrna Translation ◽  
Cell Types ◽  
Fine Tuning ◽  
Non Coding Rna ◽  
Tumor Types ◽  
Different Cell Types ◽  
The Brain

MicroRNAs (miRNAs) are short non-coding RNA involved in the regulation of specific mRNA translation. They participate in cellular signaling circuits and can act as oncogenes in tumor development, so-called oncomirs, as well as tumor suppressors. miR-7 is an ancient miRNA involved in the fine-tuning of several signaling pathways, acting mainly as tumor suppressor. Through downregulation of PI3K and MAPK pathways, its dominant role is the suppression of proliferation and survival, stimulation of apoptosis and inhibition of migration. Besides these functions, it has numerous additional roles in the differentiation process of different cell types, protection from stress and chromatin remodulation. One of the most investigated tissues is the brain, where its downregulation is linked with glioblastoma cell proliferation. Its deregulation is found also in other tumor types, such as in liver, lung and pancreas. In some types of lung and oral carcinoma, it can act as oncomir. miR-7 roles in cell fate determination and maintenance of cell homeostasis are still to be discovered, as well as the possibilities of its use as a specific biotherapeutic.

scholarly journals Long non‐coding RNA s in corticogenesis: deciphering the non‐coding code of the brain

2015 ◽  
Vol 34 (23) ◽  
pp. 2865-2884 ◽  
Author(s):  
Julieta Aprea ◽  
Federico Calegari
Keyword(s):  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
The Brain

Regulation of bone marrow mesenchymal stem cell fate by long non-coding RNA

Bone ◽  
2020 ◽  
Vol 141 ◽  
pp. 115617
Author(s):  
Qiaoyue Guo ◽  
Qi Guo ◽  
Ye Xiao ◽  
Changjun Li ◽  
Yan Huang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Fate ◽  
Stem Cell Fate ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA Neat1 regulates adaptive behavioural response to stress in mice

2019 ◽  
Author(s):  
Michail S. Kukharsky ◽  
Natalia N. Ninkina ◽  
Haiyan An ◽  
Vsevolod Telezhkin ◽  
Wenbin Wei ◽  
...  
Keyword(s):  
Expression Analysis ◽  
Physiological Stress ◽  
Physiological Role ◽  
Cellular Stress Response ◽  
Adaptive Behaviour ◽  
Knockout Mouse Model ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
The Brain

AbstractNEAT1 is a highly and ubiquitously expressed long non-coding RNA (lncRNA) which serves as an important regulator of cellular stress response. However, the physiological role of NEAT1 in the central nervous system (CNS) is still poorly understood. In the current study, we addressed this by characterising the CNS function in the Neat1 knockout mouse model (Neat1-/- mice), using a combination of behavioural phenotyping, electrophysiology and expression analysis. RNAscope® in situ hybridisation revealed that in wild-type mice, Neat1 is expressed evenly across the CNS, with high expression in glial cells and low expression in neurons. Loss of Neat1 in mice results in an inadequate reaction to physiological stress manifested as hyperlocomotion and panic escape response. In addition, Neat1-/- mice display deficits in social interaction and rhythmic patterns of activity but retain normal motor function and memory. Neat1-/- mice do not present with neuronal loss, overt neuroinflammation or gross synaptic dysfunction in the brain. However, cultured Neat1-/- neurons are characterised by hyperexcitability and dysregulated calcium homeostasis, and stress-induced neuronal activity is also augmented in Neat1-/- mice in vivo. Gene expression analysis showed that Neat1 may act as a weak positive regulator of multiple genes in the brain. Furthermore, loss of Neat1 affects alternative splicing of genes important for the CNS function and implicated in neurological diseases. Overall, our data suggest that Neat1 is involved in stress signaling in the brain and fine-tunes the CNS functions to enable adaptive behaviour in response to physiological stress.

scholarly journals An Evolving Role for the Long Non-Coding RNA H19 in Aging and Senescence

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 563-563
Author(s):  
Christian Sell ◽  
Manali Potnis
Keyword(s):  
Cell Cycle ◽  
Somatic Cell ◽  
Cell Fate ◽  
Cell Cycle Progression ◽  
Adult Stem Cells ◽  
Somatic Cells ◽  
Gene Transcript ◽  
Cell Fate Decisions ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract The long non-coding RNA (lncRNA) H19 is a maternally imprinted gene transcript that, in conjunction with the neighboring Igf2 gene, is critical in controlling embryonic growth. Loss of H19 results in fetal overgrowth associated with Beckwith Weidemann syndrome, while elevated H19 occurs in human cancers. In the adult, H19 functions in cancer cells where it promotes migration and is correlated with poor prognosis, and in adult stem cells where it is a key regulator of cell fate decisions during differentiation. While the function of H19 in primary somatic cells has not been defined, a reduction in the abundance of H19 has been reported during senescence in endothelial cells. Given the critical importance of H19 in cell fate decisions, it is likely that understanding the precise function of H19 in somatic cells in general and why reduced levels occur with cellular senescence will provide novel insights into both somatic cell maintenance and the senescence program. Towards this end, we examined the role of H19 in somatic cell growth using cardiac interstitial fibroblasts. Our results indicate that H19 is not only vital for somatic cell proliferation and survival, but that depletion of H19 leads to cell cycle arrest and the formation of abnormal nuclei resulting in senescent cells. We are defining both the upstream regulators of H19 and the downstream mediators of senescence following H19 depletion. Overall, these results indicate an essential role for H19 in cell cycle progression, chromatin structure, and possibly proper mitotic division.

Abstract 2517: Ewing sarcoma associated long non-coding RNA determines neural cell fate of the tumors

2016 ◽  
Author(s):  
Sheetal A. Mitra ◽  
Anirban P. Mitra ◽  
Jonathan D. Buckley ◽  
Timothy J. Triche
Keyword(s):  
Cell Fate ◽  
Ewing Sarcoma ◽  
Neural Cell ◽  
Non Coding Rna ◽  
Neural Cell Fate ◽  
Long Non Coding Rna

scholarly journals The activation of a Suv39h1-repressive antisense lncRNA by OCT4 couples the control of H3K9 methylation to pluripotency

2021 ◽  
Author(s):  
Laure D. Bernard ◽  
Agnès Dubois ◽  
Victor Heurtier ◽  
Almira Chervova ◽  
Alexandra Tachtsidi ◽  
...  
Keyword(s):  
Cell Fate ◽  
Es Cells ◽  
Embryonic Stem ◽  
H3k9 Methylation ◽  
Targeted Deletion ◽  
Mouse Es Cells ◽  
Non Coding Rna ◽  
Fate Restriction ◽  
In Cis ◽  
Long Non Coding Rna

Histone H3 Lysine 9 (H3K9) methylation, a characteristic mark of heterochromatin, is progressively implemented during development to contribute to cell fate restriction as differentiation proceeds. For instance, in pluripotent mouse Embryonic Stem (ES) cells the global levels of H3K9 methylation are rather low and increase only upon differentiation. Conversely, H3K9 methylation represents an epigenetic barrier for reprogramming somatic cells back to pluripotency. How global H3K9 methylation levels are coupled with the acquisition and loss of pluripotency remains largely unknown. Here, we identify SUV39H1, a major H3K9 di- and tri-methylase, as an indirect target of the pluripotency network of Transcription Factors (TFs). We find that pluripotency TFs, principally OCT4, activate the expression of an uncharacterized antisense long non-coding RNA to Suv39h1, which we name Suv39h1as. In turn, Suv39h1as downregulates Suv39h1 transcription in cis via a mechanism involving the modulation of the chromatin status of the locus. The targeted deletion of the Suv39h1as promoter region triggers increased SUV39H1 expression and H3K9me2 and H3K9me3 levels, leading to accelerated and more efficient commitment into differentiation. We report, therefore, a simple genetic circuitry coupling the global levels of H3K9 methylation to pluripotency in mouse ES cells.

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