eprintid: 10203573
rev_number: 7
eprint_status: archive
userid: 699
dir: disk0/10/20/35/73
datestamp: 2025-01-20 11:19:16
lastmod: 2025-01-20 11:19:16
status_changed: 2025-01-20 11:19:16
type: article
metadata_visibility: show
sword_depositor: 699
creators_name: Kempthorne, Liam
creators_name: Vaizoglu, Deniz
creators_name: Cammack, Alexander J
creators_name: Carcolé, Mireia
creators_name: Roberts, Martha J
creators_name: Mikheenko, Alla
creators_name: Fisher, Alessia
creators_name: Suklai, Pacharaporn
creators_name: Muralidharan, Bhavana
creators_name: Kroll, François
creators_name: Moens, Thomas G
creators_name: Yshii, Lidia
creators_name: Verschoren, Stijn
creators_name: Hölbling, Benedikt V
creators_name: Moreira, Francisco C
creators_name: Katona, Eszter
creators_name: Coneys, Rachel
creators_name: de Oliveira, Paula
creators_name: Zhang, Yong-Jie
creators_name: Jansen, Karen
creators_name: Daughrity, Lillian M
creators_name: McGown, Alexander
creators_name: Ramesh, Tennore M
creators_name: Van Den Bosch, Ludo
creators_name: Lignani, Gabriele
creators_name: Rahim, Ahad A
creators_name: Coyne, Alyssa N
creators_name: Petrucelli, Leonard
creators_name: Rihel, Jason
creators_name: Isaacs, Adrian M
title: Dual-targeting CRISPR-CasRx reduces C9orf72 ALS/FTD sense and antisense repeat RNAs in vitro and in vivo
ispublished: pub
divisions: UCL
divisions: B02
divisions: C07
divisions: C08
divisions: D07
divisions: D09
divisions: D10
divisions: F81
divisions: F85
divisions: F86
divisions: F96
divisions: G10
keywords: C9orf72 Protein, Amyotrophic Lateral Sclerosis, Humans, Frontotemporal Dementia, Animals, CRISPR-Cas Systems, RNA, Antisense, Mice, HEK293 Cells, Induced Pluripotent Stem Cells, DNA Repeat Expansion, Disease Models, Animal, Neurons, Genetic Therapy
note: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
abstract: The most common genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is an intronic G4C2 repeat expansion in C9orf72. The repeats undergo bidirectional transcription to produce sense and antisense repeat RNA species, which are translated into dipeptide repeat proteins (DPRs). As toxicity has been associated with both sense and antisense repeat-derived RNA and DPRs, targeting both strands may provide the most effective therapeutic strategy. CRISPR-Cas13 systems mature their own guide arrays, allowing targeting of multiple RNA species from a single construct. We show CRISPR-Cas13d variant CasRx effectively reduces overexpressed C9orf72 sense and antisense repeat transcripts and DPRs in HEK cells. In C9orf72 patient-derived iPSC-neuron lines, CRISPR-CasRx reduces endogenous sense and antisense repeat RNAs and DPRs and protects against glutamate-induced excitotoxicity. AAV delivery of CRISPR-CasRx to two distinct C9orf72 repeat mouse models significantly reduced both sense and antisense repeat-containing transcripts. This highlights the potential of RNA-targeting CRISPR systems as therapeutics for C9orf72 ALS/FTD.
date: 2025-01-08
date_type: published
publisher: Springer Science and Business Media LLC
official_url: https://doi.org/10.1038/s41467-024-55550-x
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 2351605
doi: 10.1038/s41467-024-55550-x
medium: Electronic
pii: 10.1038/s41467-024-55550-x
lyricists_name: Rihel, Jason
lyricists_name: Rahim, Ahad
lyricists_name: Isaacs, Adrian
lyricists_name: Lignani, Gabriele
lyricists_name: Mikheenko, Alla
lyricists_id: JRIHE66
lyricists_id: ARAHI02
lyricists_id: AISAA22
lyricists_id: GLIGN08
lyricists_id: AMIKH76
actors_name: Gaisford, Simon
actors_name: Harris, Jean
actors_id: SGAIS88
actors_id: JAHAR68
actors_role: owner
actors_role: impersonator
funding_acknowledgements: 648716 - C9ND [EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)]; 217150/Z/19/Z [Wellcome Trust (Wellcome)]
full_text_status: public
publication: Nature Communications
volume: 16
article_number: 459
event_location: England
issn: 2041-1723
citation:        Kempthorne, Liam;    Vaizoglu, Deniz;    Cammack, Alexander J;    Carcolé, Mireia;    Roberts, Martha J;    Mikheenko, Alla;    Fisher, Alessia;                                                                                             ... Isaacs, Adrian M; + view all <#>        Kempthorne, Liam;  Vaizoglu, Deniz;  Cammack, Alexander J;  Carcolé, Mireia;  Roberts, Martha J;  Mikheenko, Alla;  Fisher, Alessia;  Suklai, Pacharaporn;  Muralidharan, Bhavana;  Kroll, François;  Moens, Thomas G;  Yshii, Lidia;  Verschoren, Stijn;  Hölbling, Benedikt V;  Moreira, Francisco C;  Katona, Eszter;  Coneys, Rachel;  de Oliveira, Paula;  Zhang, Yong-Jie;  Jansen, Karen;  Daughrity, Lillian M;  McGown, Alexander;  Ramesh, Tennore M;  Van Den Bosch, Ludo;  Lignani, Gabriele;  Rahim, Ahad A;  Coyne, Alyssa N;  Petrucelli, Leonard;  Rihel, Jason;  Isaacs, Adrian M;   - view fewer <#>    (2025)    Dual-targeting CRISPR-CasRx reduces C9orf72 ALS/FTD sense and antisense repeat RNAs in vitro and in vivo.                   Nature Communications , 16     , Article 459.  10.1038/s41467-024-55550-x <https://doi.org/10.1038/s41467-024-55550-x>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10203573/1/s41467-024-55550-x.pdf