ReviewTrends in genetics : TIG2022
Mitochondrial genome engineering coming-of-age.
Review in Trends in genetics : TIG, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Harnessing mitochondrial genome editing for crop improvement: principles and applications.aBIOTECH · 2026Review
- Reversible one-step acylation facilitates mitochondrial delivery of functional RNA.Chemical science · 2026Article
- Gene Therapy Tools for Diseases Caused by Mutations of the Mitochondrial Genome.International journal of molecular sciences · 2026Review
- From modeling to therapy: the efficient and precise tools for mitochondrial base editing.Science China. Life sciences · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Leveraging base excision repair for efficient adenine base editing of mitochondrial DNA.Nature biotechnology · 2026Article
- RAP proteins regulate apicoplast noncoding RNA processing in Plasmodium falciparum.Cell reports · 2025Article
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
- Engineered mitochondria in diseases: mechanisms, strategies, and applications.Signal transduction and targeted therapy · 2025Review
- Engineering a bacterial toxin deaminase from the DYW-family into a novel cytosine base editor for plants and mammalian cells.Genome biology · 2025Article
- Transfer of mitochondrial DNA into the nuclear genome during induced DNA breaks.Nature communications · 2024Article
- Herbicide-resistant plants produced by precision adenine base editing in plastid DNA.Nature plants · 2024Article
- Origins of tissue and cell-type specificity in mitochondrial DNA (mtDNA) disease.Human molecular genetics · 2024Review
- mitoTALEN reduces the mutant mtDNA load in neurons.Molecular therapy. Nucleic acids · 2024Article
- Base editing of organellar DNA with programmable deaminases.Nature reviews. Molecular cell biology · 2024Review
- The Roles of CircRNAs in Mitochondria.Journal of Cancer · 2024Review
- Emerging Multi-omic Approaches to the Molecular Diagnosis of Mitochondrial Disease and Available Strategies for Treatment and Prevention.Current genomics · 2024Review
- Challenges and opportunities to bridge translational to clinical research for personalized mitochondrial medicine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Nucleoside deaminases: the key players in base editing toolkit.Biophysics reports · 2023Article
- Efficient elimination of MELAS-associated m.3243G mutant mitochondrial DNA by an engineered mitoARCUS nuclease.Nature metabolism · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
Abstract
The mitochondrial genome has been difficult to manipulate because it is shielded by the organelle double membranes, preventing efficient nucleic acid entry. Moreover, mitochondrial DNA (mtDNA) recombination is not a robust system in most species. This limitation has forced investigators to rely on naturally occurring alterations to study both mitochondrial function and pathobiology. Because most pathogenic mtDNA mutations are heteroplasmic, the development of specific nucleases has allowed us to selectively eliminate mutant species. Several 'protein only' gene-editing platforms have been successfully used for this purpose. More recently, a DNA double-strand cytidine deaminase has been identified and adapted to edit mtDNA. This enzyme was also used as a component to adapt a DNA single-strand deoxyadenosine deaminase to mtDNA editing. These are major advances in our ability to precisely alter the mtDNA in animal cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.