TFEB Links Autophagy to Lysosomal Biogenesis
Open accessAbstract
Starvation activates a transcriptional program controlling autophagosome formation, lysosome fusion, and substrate degradation.
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TFE3 and TFEB are two major members of the MiT/TFE subfamily and are well characterized as master regulators of lysosome biogenesis and autophagy.
“Transcription factor E3 (TFE3) and transcription factor EB (TFEB) are two major members of the microphthalmia-transcription factor E (MiT/TFE) subfamily and well characterized as master regulators of lysosome biogenesis and autophagy1–4.”
From PDCD4 triggers α-synuclein accumulation and motor deficits via co-suppressing TFE3 and TFEB translation in a model of Parkinson’s disease (2024) · cites this paper as [1]
The Abstract (page not available in our copy) calls TFEB a master gene for lysosomal biogenesis and says it drives expression of autophagy and lysosomal genes. The paper does not establish the corresponding claim about TFE3 or identify TFE3 and TFEB as two major MiT/TFE subfamily members. (LLM, conf=0.88)
Experimental — accuracy not yet measuredA gene regulatory network named CLEAR (coordinated lysosomal enhancement and regulation) that controls both lysosome and autophagosome biogenesis was identified using a systems-biology approach.
“A gene regulatory network, named CLEAR (coordinated lysosomal enhancement and regulation) that controls both lysosome and autophagosome biogenesis was identified using a systemsbiology approach.[463][464][465]”
From Guidelines for the use and interpretation of assays for monitoring autophagy (2012) · cites this paper as [463]
The passage discussing CLEAR (section labeled Abstract; page unavailable) calls it the “Coordinated Lysosomal Expression and Regulation” network, not “enhancement and regulation.” The paper reports that TFEB co-regulates lysosome and autophagosome biogenesis, but it treats CLEAR as an existing network and does not say it identified the network using a systems-biology approach. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe authors identified 20 targets related to autophagy activation and validated them by qPCR: ATG10, ATG14, ATG16L1, ATG3, ATG4, ATG7, ATG9A, BCL2, GABARAP, GABARAPL1, MAP1LC3B, NBR1, OPTN, PINK1, SQSTM1, ULK1, ULK2, UVRAG, WDR45, WIPI1.
“In a first case, starting from experimental data available in the literature, we identified 20 targets related to autophagy activation and validated them by qPCR: ATG10, ATG14, ATG16L1, ATG3, ATG4, ATG7, ATG9A, BCL2, GABARAP, GABARAPL1, MAP1LC3B, NBR1, OPTN, PINK1, SQSTM1, ULK1, ULK2, UVRAG, WDR45, WIPI1 (Fig. 2) [18–27].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
The passage on autophagy-gene expression (section labelled Abstract; page unavailable) identifies UVRAG, WIPI, MAPLC3B and SQSTM1 as genes involved in autophagy, supporting part of the cited background for the target selection. It does not identify the citing authors’ full set of 20 targets. The sentence presents the qPCR validation as the citing authors’ own work, not as a result of this source. (LLM, conf=0.87)
Experimental — accuracy not yet measuredTFEB pathway is unaltered in response to hα-Syn in microglia, as shown by lack of change in nuclear TFEB intensity.
“NRF2 or TFEB pathways were unaltered as shown by the lack of change in the level of NQO-1 and HO-1, two major targets of NRF2, or the intensity of nuclear TFEB in response to hα-Syn46,47 (Supplementary Fig. 4i, j).”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [47]
TFEB activity is regulated by starvation, and can thus serve as a new tool for monitoring transcriptional regulation connected with autophagy.
“TFEB activity is regulated by starvation, 463 and can thus serve as a new tool for monitoring transcriptional regulation connected with autophagy.”
From Guidelines for the use and interpretation of assays for monitoring autophagy (2012) · cites this paper as [463]
Overexpression or post-translational activation of the gene encoding TFEB induces autophagy; TFEB is a transcriptional regulator of the biogenesis of both lysosomes and autophagosomes.
“For example, this can be achieved either through overexpression or post-translational activation of the gene encoding TFEB (see Transcriptional and translational regulation), a transcriptional regulator of the biogenesis of both lysosomes and autophagosomes.463,464”
From Guidelines for the use and interpretation of assays for monitoring autophagy (2012) · cites this paper as [463]
Tfeb regulates expression of lysosome biogenesis genes.
“This transcription factor regulates expression of lysosome biogenesis genes [31].”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [31]
Tfeb may be targeted by miR-155.
“we identified that Tfeb, transcription factor and modulator of lysosome biogenesis [31], may be targeted by miR-155.”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [31]
The activation list was derived from comparison of publications reporting conditions of gene up-regulation upon autophagy activation.
“A so called “activation list” has been derived from the comparison of publications, in which we reported conditions of gene up-regulation upon autophagy activation [18–27].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
The authors identified 26 targets to assess the state of lysosomal biogenesis.
“Hence, for the second sub-lists, we identified 26 targets to assess the state of lysosomal biogenesis (Fig. 2) at variance with the autophagy activation list, this sub-list has been realized by only comparing data from recent work, in which mRNA levels of lysosomal genes in response to autophagy enhancement were accurately and experimentally examined [15, 18, 19, 28–30].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
The restricted "induction list" for the prediction of autophagy activation state is made of 20 targets and was obtained by combining data from previous publications documenting increased mRNA expression following autophagy induction.
“The restricted “induction list” for the prediction of autophagy activation state, made by 20 targets, was obtained combining data from previous publications [18–27], in which have been documented the increase of the mRNA expression following autophagy induction.”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
The list for the evaluation of "lysosomal biogenesis" was created from literature by combining data that underwent preceding experimental validation.
“Similarly, the list for the evaluation of “lysosomal biogenesis” was created from literature by combining data that underwent preceding experimental validation [15, 18, 19, 28–30].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
NRF2 pathway is unaltered in response to hα-Syn in microglia, as shown by lack of change in NQO-1 and HO-1.
“NRF2 or TFEB pathways were unaltered as shown by the lack of change in the level of NQO-1 and HO-1, two major targets of NRF2, or the intensity of nuclear TFEB in response to hα-Syn46,47 (Supplementary Fig. 4i, j).”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [47]
The paper’s TFEB passages discuss nuclear translocation in response to starvation in HeLa cells, not hα-Syn exposure in microglia. Searches for NRF2, NQO-1, HO-1, microglia, and α-synuclein found no passage addressing whether the NRF2 pathway was unchanged under the claimed condition. (LLM, conf=0.77)
Experimental — accuracy not yet measuredThe lysosomal biogenesis list resulted from an extensive literature analysis combining data that underwent previous experimental validation.
“The “lysosomal biogenesis list” resulted instead from an extensive literature analysis, obtained by combining data that underwent previous experimental validation [15, 18, 19, 28–30].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [18]
The paper’s main text (indexed under Abstract; page unavailable) says the authors analyzed 51 previously reported autophagy genes and discusses the CLEAR network. Neither passage explains how a “lysosomal biogenesis list” was assembled. Searches for the list, literature analysis, and prior experimental validation found no passage establishing the claimed provenance. (LLM, conf=0.75)
Experimental — accuracy not yet measuredTFEB directs expression of autophagy and lysosomal genes comprising the CLEAR network by binding to a conserved promoter motif.
“Global regulation of the myriad effectors and phases of autophagy is overseen by TFEB (transcription factor EB), a basic helix-loop-helix leucine zipper that directs expression of autophagy and lysosomal genes comprising the coordinated lysosomal expression and regulation (CLEAR) network by binding to a conserved promoter motif [47,48].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [48]
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- Authors
- Settembre, C., Di Malta, C., Polito, V. A., Arencibia, M. G., Vetrini, F., Erdin, S., Erdin, S. U., Huynh, T., Medina, D., Colella, P., Sardiello, M., Rubinsztein, D. C., & Ballabio, A.
- Affiliations
- Baylor College of Medicine (US)
- Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131 Naples, Italy.
- Cambridge Institute for Medical Research, Wellcome Trust–Medical Research Council Building, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0XY, UK.
- Telethon Institute Of Genetics And Medicine (IT)
- Addenbrooke's Hospital (GB)
- Corresponding author
- Ballabio, Andrea
- ORCID
- Venue
- Science
- Published
- 2011-06-17
- Volume
- 332
- Issue
- 6036
- Pages
- 1429-1433
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3638014
- OpenAlex
- W1975200363
- Cited by
- 3,365
- References
- 33
- Citations by year
- 2026: 283 · 2025: 275 · 2024: 287 · 2023: 270 · 2022: 328 · 2021: 290 · 2020: 317 · 2019: 251 · 2018: 227 · 2017: 192 · 2016: 184 · 2015: 152 · 2014: 116 · 2013: 96 · 2012: 66
- FWCI
- 73.01
- Type
- journal article
- Language
- en
- Update notices
- correction (2025-12-18)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Acceda (Universidad de Las Palmas de Gran Canaria) (submittedVersion)
- Funders
- Wellcome Trust
- National Institute of Neurological Disorders and Stroke (R01NS078072)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD024064)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- TFEB, autophagy, lysosomal biogenesis, starvation, autophagosome-lysosome fusion, autophagosome formation, substrate degradation, serine phosphorylation, ERK2, mitogen-activated protein kinase, nutrient sensing, transcriptional regulation, nuclear localization
- MeSH terms
- Animals, Autophagy, Cell Nucleus, Cells, Cultured, Chlorocebus aethiops, Cytoplasm, Gene Expression Regulation, HeLa Cells, Humans, Liver, Lysosomes, Mice, Transgenic, Microtubule-Associated Proteins, Phagosomes, Phosphorylation, Transcription, Genetic, Up-Regulation, COS Cells, Mitogen-Activated Protein Kinase 1, MAP Kinase Signaling System, Active Transport, Cell Nucleus, RNA Interference, Mice, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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