ArticleDisease models & mechanisms
The mitochondrial import gene tomm22 is specifically required for hepatocyte survival and provides a liver regeneration model.
Article in Disease models & mechanisms. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 37 citations in OpenAlex.
- Mitochondrial protein Mrpl13 regulates zebrafish liver development through the mTORC1-mitochondrial homeostasis pathway.Communications biology · 2026Article
- Targeting TOMM40 and TOMM22 to Rescue Statin-Impaired Mitochondrial Function, Dynamics, and Mitophagy in Skeletal Myotubes.International journal of molecular sciences · 2025Article
- Article
- Structure of the intact Tom20 receptor in the human translocase of the outer membrane complex.PNAS nexus · 2024Article
- Lineage tracing identifies heterogeneous hepatoblast contribution to cell lineages and postembryonic organ growth dynamics.PLoS biology · 2023Article
- Review
- Low Expression of Mitofusin 1 Gene Leads to Mitochondrial Dysfunction and Embryonic Genome Activation Failure in Ovine-Bovine Inter-Species Cloned Embryos.International journal of molecular sciences · 2022Article
- Review
- All routes lead to Rome: multifaceted origin of hepatocytes during liver regeneration.Cell regeneration (London, England) · 2021Review
- Atomic structure of human TOM core complex.Cell discovery · 2020Article
- Macrophages in Zebrafish Models of Liver Diseases.Frontiers in immunology · 2019Review
- Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in zebrafish.PLoS genetics · 2018Article
- Article
- Making It New Again: Insight Into Liver Development, Regeneration, and Disease From Zebrafish Research.Current topics in developmental biology · 2017Review
- Zebrafish: an important tool for liver disease research.Gastroenterology · 2015Review
- The lure of zebrafish in liver research: regulation of hepatic growth in development and regeneration.Current opinion in genetics & development · 2015Review
- Identification of Annexin A4 as a hepatopancreas factor involved in liver cell survival.Developmental biology · 2014Article
- Tom70 serves as a molecular switch to determine pathological cardiac hypertrophy.Cell research · 2014Article
- Zebrafish models of human liver development and disease.Comprehensive Physiology · 2013Review
- Hepatic stellate cells in liver development, regeneration, and cancer.The Journal of clinical investigation · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Understanding liver development should lead to greater insights into liver diseases and improve therapeutic strategies. In a forward genetic screen for genes regulating liver development in zebrafish, we identified a mutant--oliver--that exhibits liver-specific defects. In oliver mutants, the liver is specified, bile ducts form and hepatocytes differentiate. However, the hepatocytes die shortly after their differentiation, and thus the resulting mutant liver consists mainly of biliary tissue. We identified a mutation in the gene encoding translocase of the outer mitochondrial membrane 22 (Tomm22) as responsible for this phenotype. Mutations in tomm genes have been associated with mitochondrial dysfunction, but most studies on the effect of defective mitochondrial protein translocation have been carried out in cultured cells or unicellular organisms. Therefore, the tomm22 mutant represents an important vertebrate genetic model to study mitochondrial biology and hepatic mitochondrial diseases. We further found that the temporary knockdown of Tomm22 levels by morpholino antisense oligonucleotides causes a specific hepatocyte degeneration phenotype that is reversible: new hepatocytes repopulate the liver as Tomm22 recovers to wild-type levels. The specificity and reversibility of hepatocyte ablation after temporary knockdown of Tomm22 provides an additional model to study liver regeneration, under conditions where most hepatocytes have died. We used this regeneration model to analyze the signaling commonalities between hepatocyte development and regeneration.
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.