ArticlePLoS genetics2021
Formimidoyltransferase cyclodeaminase prevents the starvation-induced liver hepatomegaly and dysfunction through downregulating mTORC1.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Trial
- Mitochondrial protein Mrpl13 regulates zebrafish liver development through the mTORC1-mitochondrial homeostasis pathway.Communications biology · 2026Article
- Article
- Gallbladder-derived retinoic acid signalling drives reconstruction of the damaged intrahepatic biliary ducts.Nature cell biology · 2025Article
- Establishment of a Lactylation-Related Gene Signature for Hepatocellular Carcinoma Applying Bulk and Single-Cell RNA Sequencing Analysis.International journal of genomics · 2025Article
- Prognostic alternative splicing and multi-omics characteristics reveal FTCD is a potential target of hepatocellular carcinoma.Discover oncology · 2024Article
- Embryonic Amoxicillin Exposure Has Limited Impact on Liver Development but Increases Susceptibility to NAFLD in Zebrafish Larvae.International journal of molecular sciences · 2024Article
- Exosome-Related FTCD Facilitates M1 Macrophage Polarization and Impacts the Prognosis of Hepatocellular Carcinoma.Biomolecules · 2023Article
- An inflammation-associated ferroptosis signature optimizes the diagnosis, prognosis evaluation and immunotherapy options in hepatocellular carcinoma.Journal of cellular and molecular medicine · 2023Article
- The MRN complex maintains the biliary-derived hepatocytes in liver regeneration through ATR-Chk1 pathway.NPJ Regenerative medicine · 2023Article
- Delayed First Feeding Chronically Impairs Larval Fish Growth Performance, Hepatic Lipid Metabolism, and Visceral Lipid Deposition at the Mouth-Opening Stage.Marine biotechnology (New York, N.Y.) · 2023Article
- Lipid metabolism and ageing in Caenorhabditis elegans: a complex interplay.Biogerontology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The liver is a crucial center in the regulation of energy homeostasis under starvation. Although downregulation of mammalian target of rapamycin complex 1 (mTORC1) has been reported to play pivotal roles in the starvation responses, the underpinning mechanisms in particular upstream factors that downregulate mTORC1 remain largely unknown. To identify genetic variants that cause liver energy disorders during starvation, we conduct a zebrafish forward genetic screen. We identify a liver hulk (lvh) mutant with normal liver under feeding, but exhibiting liver hypertrophy under fasting. The hepatomegaly in lvh is caused by enlarged hepatocyte size and leads to liver dysfunction as well as limited tolerance to starvation. Positional cloning reveals that lvh phenotypes are caused by mutation in the ftcd gene, which encodes the formimidoyltransferase cyclodeaminase (FTCD). Further studies show that in response to starvation, the phosphorylated ribosomal S6 protein (p-RS6), a downstream effector of mTORC1, becomes downregulated in the wild-type liver, but remains at high level in lvh. Inhibition of mTORC1 by rapamycin rescues the hepatomegaly and liver dysfunction of lvh. Thus, we characterize the roles of FTCD in starvation response, which acts as an important upstream factor to downregulate mTORC1, thus preventing liver hypertrophy and dysfunction.
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