NDLI: Lamin A/C Is Required for ChAT-Dependent Neuroblastoma Differentiation

Content Provider	Springer Nature Link
Author	Guglielmi, Loredana Nardella, Marta Musa, Carla Iannetti, Ilaria Arisi, Ivan D’Ofrio, Mara Storti, Andrea Valentini, Alessandra Cacci, Emanuele Biagioni, Stefa Augusti Tocco, Gabriella D’Agna, Igea Felsani, Armando
Copyright Year	2016
Abstract	The mouse neuroblastoma N18TG2 clone is unable to differentiate and is defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. The engagement of the 2/4 cells in the neuronal developmental program was confirmed by the increase of the expression level of several differentiation-related genes and by the reduction of the amount of transcripts of cell cycle genes. At the same time, we observed a massive reorganization of cytoskeletal proteins in terms of gene expression, with the accumulation of the nucleoskeletal lamina component Lamin A/C in differentiating cells. The increase of the Lmna transcripts induced by ChAT expression in 2/4 cells was mimicked treating the parental N18TG2 cells with the acetylcholine receptor agonist carbachol, thus demonstrating the direct role played by this receptor in neuron nuclei maturation. Conversely, a treatment of 2/4 cells with the muscarinic receptor antagonist atropine resulted in the reduction of the amount of Lmna RNA. Finally, the hypothesis that Lmna gene product might play a crucial role in the ChAT-dependent molecular differentiation cascade was strongly supported by Lmna knockdown in 2/4 cells leading to the downregulation of genes involved in differentiation and cytoskeleton formation and to the upregulation of genes known to regulate self-renewal and stemness.
Starting Page	3729
Ending Page	3744
Page Count	16
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	54
Issue Number	5
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2016-05-25
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Differentiation Neuroblastoma Choline acetyltransferase LMNA Gene expression Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Calreticulin Regulates VEGF-A in Neuroblastoma Cells

Effects of AF64A on Gene Expression of Choline Acetyltransferase (ChAT) in the Septo-Hippocampal Pathway and Striatum In Vivo

Phenotype-dependent susceptibility of cholinergic neuroblastoma cells to neurotoxic inputs

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

SVCT2 Overexpression in Neuroblastoma Cells Induces Cellular Branching that is Associated with ERK Signaling

Gene Expression Profile of NF-κB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid

NRF2 Mediates Neuroblastoma Proliferation and Resistance to Retinoic Acid Cytotoxicity in a Model of In Vitro Neuronal Differentiation

Expression of the Parkinson’s Disease-Associated Gene Alpha-Synuclein is Regulated by the Neuronal Cell Fate Determinant TRIM32

Tinospora cordifolia Induces Differentiation and Senescence Pathways in Neuroblastoma Cells

Lamin A/C Is Required for ChAT-Dependent Neuroblastoma Differentiation

Similar Documents

Calreticulin Regulates VEGF-A in Neuroblastoma Cells

Effects of AF64A on Gene Expression of Choline Acetyltransferase (ChAT) in the Septo-Hippocampal Pathway and Striatum In Vivo

Phenotype-dependent susceptibility of cholinergic neuroblastoma cells to neurotoxic inputs

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

SVCT2 Overexpression in Neuroblastoma Cells Induces Cellular Branching that is Associated with ERK Signaling

Gene Expression Profile of NF-κB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid

NRF2 Mediates Neuroblastoma Proliferation and Resistance to Retinoic Acid Cytotoxicity in a Model of In Vitro Neuronal Differentiation

Expression of the Parkinson’s Disease-Associated Gene Alpha-Synuclein is Regulated by the Neuronal Cell Fate Determinant TRIM32

Tinospora cordifolia Induces Differentiation and Senescence Pathways in Neuroblastoma Cells

Lamin A/C Is Required for ChAT-Dependent Neuroblastoma Differentiation