ArticleBMC biology2020
Excess diacylglycerol at the endoplasmic reticulum disrupts endomembrane homeostasis and autophagy.
Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Atorvastatin Prevents Early Lipotoxic Remodelling in Right Ventricular Pacing-Induced Cardiomyopathy.CJC open · 2026Article
- Impaired Acetyl-CoA Compartmentalization Drives a Futile Lipogenic-Oxidative Cycle in N88S Seipinopathy.Cells · 2026Article
- Role of obesity and estrogen deficiency in non‑alcoholic fatty liver disease: Insights from a mouse model.Molecular medicine reports · 2025Article
- Hepatitis B Virus X Protein Upregulates SREBP2 to Modulate Autophagy in Hepatocellular Carcinoma.Cancer medicine · 2025Article
- Article
- N88S seipin-related seipinopathy is a lipidopathy associated with loss of iron homeostasis.Cell communication and signaling : CCS · 2025Article
- Exploring the interplay between yeast cell membrane lipid adaptation and physiological response to acetic acid stress.Applied and environmental microbiology · 2024Article
- Article
- Diacylglycerol metabolism and homeostasis in fungal physiology.FEMS yeast research · 2024Review
- Endoplasmic Reticulum Stress and Obesity.Advances in experimental medicine and biology · 2024Review
- Nitrogen limitation-induced adaptive response and lipogenesis in the Antarctic yeastFrontiers in microbiology · 2024Article
- Arf1 coordinates fatty acid metabolism and mitochondrial homeostasis.Nature cell biology · 2023Article
- Impact of interorganelle coordination between the conventional early secretory pathway and autophagy in cellular homeostasis and stress response.Frontiers in cell and developmental biology · 2023Review
- A Validated Set of Ascorbate Peroxidase-Based Organelle Markers for Electron Microscopy of Saccharomyces cerevisiae.mSphere · 2022Article
- Article
- DGAT1 activity synchronises with mitophagy to protect cells from metabolic rewiring by iron depletion.The EMBO journal · 2022Article
- The Human Milk Oligosaccharide 2'-Fucosyllactose Alleviates Liver Steatosis, ER Stress and Insulin Resistance by Reducing Hepatic Diacylglycerols and Improved Gut Permeability in Obese Ldlr-/-.Leiden Mice.Frontiers in nutrition · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWhen stressed, eukaryotic cells produce triacylglycerol (TAG) to store nutrients and mobilize autophagy to combat internal damage. We and others previously reported that in yeast, elimination of TAG synthesizing enzymes inhibits autophagy under nitrogen starvation, yet the underlying mechanism has remained elusive.
resultsHere, we show that disruption of TAG synthesis led to diacylglycerol (DAG) accumulation and its relocation from the vacuolar membrane to the endoplasmic reticulum (ER). We further show that, beyond autophagy, ER-accumulated DAG caused severe defects in the endomembrane system, including disturbing the balance of ER-Golgi protein trafficking, manifesting in bulging of ER and loss of the Golgi apparatus. Genetic or chemical manipulations that increase consumption or decrease supply of DAG reversed these defects. In contrast, increased amounts of precursors of glycerolipid synthesis, including phosphatidic acid and free fatty acids, did not replicate the effects of excess DAG. We also provide evidence that the observed endomembrane defects do not rely on Golgi-produced DAG, Pkc1 signaling, or the unfolded protein response.
conclusionsThis work identifies DAG as the critical lipid molecule responsible for autophagy inhibition under condition of defective TAG synthesis and demonstrates the disruption of ER and Golgi function by excess DAG as the potential cause of the autophagy defect.
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.