Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/162435
Title: Formation of RNA G-wires by G₄C₂ repeats associated with ALS and FTD
Authors: Bose, Krishnashish
Maity, Arijit
Ngo, Khac Huy
Vandana, J. Jeya
Shneider, Neil A.
Phan, Anh Tuân
Keywords: Science::Biological sciences
Issue Date: 2022
Source: Bose, K., Maity, A., Ngo, K. H., Vandana, J. J., Shneider, N. A. & Phan, A. T. (2022). Formation of RNA G-wires by G₄C₂ repeats associated with ALS and FTD. Biochemical and Biophysical Research Communications, 610, 113-118. https://dx.doi.org/10.1016/j.bbrc.2022.03.162
Project: MOE2015-T2-1-092
Journal: Biochemical and Biophysical Research Communications 
Abstract: In the neurodegenerative disorders amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), expansion of the G4C2 hexanucleotide repeat in the gene C9orf72 is a most common known cause of the disease. Here we use atomic force microscopy (AFM) and gel electrophoresis to visualize the formation of higher-order structures by RNA G4C2 repeats in physiologically relevant conditions. For the RNA sequence r[G4C2G4], we observed G-wires with left-handed undulating features of 4.4-nm periodicity and a uniform height which is consistently higher than that of a duplex B-DNA. These higher-order structures were not degraded fully when treated with a mixture of RNase A and RNase T1. Similarly, higher-order structures were observed for sequences containing three or four G4C2 repeats, pointing towards their potential formation in longer sequence contexts. Our observations suggest that RNA G-quadruplex blocks and G-wires can accumulate in cells containing G4C2 repeat transcripts.
URI: https://hdl.handle.net/10356/162435
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2022.03.162
Rights: © 2022 Elsevier Inc. All rights reserved.
Fulltext Permission: none
Fulltext Availability: No Fulltext
Appears in Collections:SPMS Journal Articles

Page view(s)

52
Updated on Nov 26, 2022

Google ScholarTM

Check

Altmetric


Plumx

Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.