scholarly journals In VitroEffects of Lead on Gene Expression in Neural Stem Cells and Associations between Up-regulated Genes and Cognitive Scores in Children

2017 ◽  
Vol 125 (4) ◽  
pp. 721-729 ◽  
Author(s):  
Peter J. Wagner ◽  
Hae-Ryung Park ◽  
Zhaoxi Wang ◽  
Rory Kirchner ◽  
Yongyue Wei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neural Stem Cells

Gene Expression Profiling of Neural Stem Cells and Identification of Regulators of Neural Differentiation During Cortical Development

Stem Cells ◽  
2011 ◽  
Vol 29 (11) ◽  
pp. 1817-1828 ◽  
Author(s):  
Toshiyuki Ohtsuka ◽  
Hiromi Shimojo ◽  
Mitsuhiro Matsunaga ◽  
Naoki Watanabe ◽  
Kohei Kometani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Neural Differentiation ◽  
Cortical Development

scholarly journals Single cell 3’UTR analysis identifies changes in alternative polyadenylation throughout neuronal differentiation and in autism

2020 ◽  
Author(s):  
Manuel Göpferich ◽  
Nikhil Oommen George ◽  
Ana Domingo Muelas ◽  
Alex Bizyn ◽  
Rosa Pascual ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Single Cell ◽  
Neuronal Differentiation ◽  
Mrna Translation ◽  
Autism Spectrum ◽  
Adult Brain ◽  
Control Of Gene Expression ◽  
Risk Genes

SUMMARYAutism spectrum disorder (ASD) is a neurodevelopmental disease affecting social behavior. Many of the high-confident ASD risk genes relate to mRNA translation. Specifically, many of these genes are involved in regulation of gene expression for subcellular compartmentalization of proteins1. Cis-regulatory motifs that often localize to 3’- and 5’-untranslated regions (UTRs) offer an additional path for posttranscriptional control of gene expression. Alternative cleavage and polyadenylation (APA) affect 3’UTR length thereby influencing the presence or absence of regulatory elements. However, APA has not yet been addressed in the context of neurodevelopmental disorders. Here we used single cell 3’end sequencing to examine changes in 3’UTRs along the differentiation from neural stem cells (NSCs) to neuroblasts within the adult brain. We identified many APA events in genes involved in neurodevelopment, many of them being high confidence ASD risk genes. Further, analysis of 3’UTR lengths in single cells from ASD and healthy individuals detected longer 3’UTRs in ASD patients. Motif analysis of modulated 3’UTRs in the mouse adult neurogenic lineage and ASD-patients revealed enrichment of the cytoplasmic and polyadenylation element (CPE). This motif is bound by CPE binding protein 4 (CPEB4). In human and mouse data sets we observed co-regulation of CPEB4 and the CPEB-binding synaptic adhesion molecule amyloid beta precursor-like protein 1 (APLP1). We show that mice deficient in APLP1 show aberrant regulation of APA, decreased number of neural stem cells, and autistic-like traits. Our findings indicate that APA is used for control of gene expression along neuronal differentiation and is altered in ASD patients.

scholarly journals Effect of Bmi1 over-expression on gene expression in adult and embryonic murine neural stem cells

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Mythily Ganapathi ◽  
Nathan C. Boles ◽  
Carol Charniga ◽  
Steven Lotz ◽  
Melissa Campbell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Over Expression

Abstract TP142: Post-Ischemic Cortical Excitability and Gene Expression are Modulated by Transplanted Human Neural Stem Cells

Stroke ◽  
2019 ◽  
Vol 50 (Suppl_1) ◽  
Author(s):  
Ricardo L Azevedo-Pereira ◽  
Tanya Weerakkody ◽  
Jennifer Vu ◽  
Fang Du ◽  
Xibin Liang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Cortical Excitability ◽  
Human Neural Stem Cells

Saturated fatty acid alters embryonic cortical neurogenesis through modulation of gene expression in neural stem cells

2018 ◽  
Vol 62 ◽  
pp. 230-246 ◽  
Author(s):  
Mustafa T. Ardah ◽  
Shama Parween ◽  
Divya S. Varghese ◽  
Bright Starling Emerald ◽  
Suraiya A. Ansari
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Fatty Acid ◽  
Neural Stem Cells ◽  
Saturated Fatty Acid ◽  
Cortical Neurogenesis ◽  
Modulation Of Gene Expression

scholarly journals Icariin promotes cell proliferation and regulates gene expression in human neural stem cells in vitro

2016 ◽  
Vol 14 (2) ◽  
pp. 1316-1322 ◽  
Author(s):  
Pan Yang ◽  
Yun-Qian Guan ◽  
Ya-Li Li ◽  
Li Zhang ◽  
Lan Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Neural Stem Cells ◽  
Human Neural Stem Cells

A MEIS1 Dependent Genetic Program in Leukemia Associated with Cell Cycle Entry and ‘Stemness’

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 746-746
Author(s):  
Ashish Kumar ◽  
Baolin Wu ◽  
John H. Kersey
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Cell Line ◽  
Fusion Proteins ◽  
Leukemia Cells ◽  
Self Renewal ◽  
Knock Down ◽  
Cell Cycle Entry

Abstract The HOX co-factor MEIS1 is expressed in several leukemias, especially those involving MLL-gene rearrangements. Experimental data have demonstrated that MLL-fusion proteins induce the expression of MEIS1 in hematopoietic cells along with increased self-renewal and recent murine experiments indicate that MEIS1 is central to the growth-promoting effects of MLL fusion proteins. However, the cellular and molecular pathways that are regulated by MEIS1 are unknown. We studied the effect of MEIS1 knock-down in a cell line derived from a leukemic MLL-AF9 knock-in mouse. Transduction of this cell line (4166) with MEIS1-shRNA bearing lentivirus led to significant reduction in MEIS1 expression compared to cells transduced with control virus. The MEIS1 knock-down cells displayed decreased cell cycle entry, while terminal myeloid differentiation and apoptosis were enhanced. To characterize the molecular effects of MEIS1 knock-down, we performed gene expression profiling of leukemia cells with and without MEIS1 expression. We extracted RNA from 5 separate experiments where 4166 cells were transduced with vector control or MEIS1 shRNA for 48 hours and analyzed gene expression profiles using Affymetrix 430 2.0 whole genome arrays. We used a regularized two-sample paired t-test to select genes that were differentially expressed among the two groups. At a false discovery rate (FDR) of ≤ 5%, 1053 probe sets displayed decreased expression with MEIS1 knockdown, while 296 probe sets showed increased expression. Analysis of gene ontology (GO) terms by DAVID (Database for Annotation, Visualization and Integrated Discovery) revealed that the list of genes down-regulated with MEIS1 knock-down was significantly enriched in genes associated with the cell cycle and its regulation (Cdk2, Cdk6, Cdkn3, Ccna2, Cdc7, Cdc42, Rbl1, Wee1) and DNA replication (Brca1, Cdc6, Cdt1, Gmnn, Mcm4, Mcm5, Mcm8). Conversely, the genes displaying increased expression with MEIS1 knockdown were associated with inhibition of proliferation eg. Cdkn1a (p21), Btg2, Btg3 and pro-apoptotic effects such as Bax. A search of the Molecular Signatures Database for previously published profiles that overlap with our list of MEIS1-dependent genes revealed that the profile of MEIS1 knockdown in our murine leukemia cells significantly overlapped with that of neural stem cells. Specifically, of the 1838 genes expressed highly in neural stem cells compared to differentiated brain and bone marrow cells (Ramalho-Santos et al, Science 2002), 155 showed an overlap with the 594 genes in our MEIS1-dependent set (594 gene identifiers contained in 1053 probe sets; p = 3.27 e−28, hypergeometric distribution). This list of 155 genes included MEIS1 and several of the cell cycle and DNA replication-associated genes. These results reveal a core self-renewal genetic program shared by leukemia and neural stem cells that is regulated by MEIS1. Activation of MEIS1 in leukemia and possibly brain tumors could thus enhance self-renewal via the up-regulation of the above common genes. Overall, our results show that MEIS1 regulates cell cycle entry in murine MLL-AF9 leukemia, an effect that enhances self-renewal in other cells as well.

Sign in / Sign up

Export Citation Format

Share Document