MétaCan
Menu
Back to cohort
Record W4389388944 · doi:10.1038/s41551-023-01132-z

Optimization of base editors for the functional correction of SMN2 as a treatment for spinal muscular atrophy

2023· article· en· W4389388944 on OpenAlexafffund
Christiano R. R. Alves, Leillani L. Ha, Rebecca Yaworski, Emma R Sutton, Cícera R. Lazzarotto, Kathleen A. Christie, Aoife Reilly, Ariane Beauvais, Roman M. Doll, Demitri de la Cruz, Casey A. Maguire, Kathryn J. Swoboda, Shengdar Q. Tsai, Rashmi Kothary, Benjamin P. Kleinstiver

Bibliographic record

VenueNature Biomedical Engineering · 2023
Typearticle
Languageen
FieldMedicine
TopicNeurogenetic and Muscular Disorders Research
Canadian institutionsOttawa HospitalUniversity of Ottawa
FundersNational Institute on Deafness and Other Communication DisordersNational Heart, Lung, and Blood InstituteCanadian Institutes of Health ResearchNational Cancer InstituteNational Institutes of HealthMuscular Dystrophy CanadaCharles A. King TrustSt. Jude Children's Research HospitalNational Institute of Neurological Disorders and StrokeMassachusetts General HospitalNational Institute of Allergy and Infectious DiseasesMuscular Dystrophy Association
KeywordsSMN1Spinal muscular atrophyExonSMA*BiologyMutationPoint mutationMotor neuronMolecular biologyGeneticsCancer researchGeneNeuroscienceSpinal cordComputer science

Abstract

fetched live from OpenAlex

Spinal muscular atrophy (SMA) is caused by mutations in SMN1. SMN2 is a paralogous gene with a C•G-to-T•A transition in exon 7, which causes this exon to be skipped in most SMN2 transcripts, and results in low levels of the protein survival motor neuron (SMN). Here we show, in fibroblasts derived from patients with SMA and in a mouse model of SMA that, irrespective of the mutations in SMN1, adenosine base editors can be optimized to target the SMN2 exon-7 mutation or nearby regulatory elements to restore the normal expression of SMN. After optimizing and testing more than 100 guide RNAs and base editors, and leveraging Cas9 variants with high editing fidelity that are tolerant of different protospacer-adjacent motifs, we achieved the reversion of the exon-7 mutation via an A•T-to-G•C edit in up to 99% of fibroblasts, with concomitant increases in the levels of the SMN2 exon-7 transcript and of SMN. Targeting the SMN2 exon-7 mutation via base editing or other CRISPR-based methods may provide long-lasting outcomes to patients with SMA. Optimized base editors targeting the exon-7 mutation in SMN2 restore expression of the survival motor neuron (SMN) protein to normal levels, as shown in mice with spinal muscular atrophy and in fibroblasts from patients with this genetic disease.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.001
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.001
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.015
GPT teacher head0.299
Teacher spread0.284 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations42
Published2023
Admission routes2
Has abstractyes

Explore more

Same venueNature Biomedical EngineeringSame topicNeurogenetic and Muscular Disorders ResearchFrench-language works237,207