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Article ; Online: Hijacking intracellular membranes to feed autophagosomal growth.

Staiano, Leopoldo / Zappa, Francesca

2019 Volume 593, Issue 22, Page(s) 3120–3134

Abstract: Autophagy is widely considered as a housekeeping mechanism that enables cells to survive stress conditions and, in particular, nutrient deprivation. Autophagy begins with the formation of the phagophore that expands and closes around cytosolic material ... ...

Abstract	Autophagy is widely considered as a housekeeping mechanism that enables cells to survive stress conditions and, in particular, nutrient deprivation. Autophagy begins with the formation of the phagophore that expands and closes around cytosolic material and damaged organelles destined for degradation. The execution of this complex machinery is guaranteed by the coordinated action of more than 40 ATG (autophagy-related) proteins that control the entire process at different stages from the biogenesis of the autophagosome to cargo sequestration and fusion with lysosomes. Autophagosome biogenesis occurs at multiple intracellular sites, such as the endoplasmic reticulum (ER) and the plasma membrane. Soon after the formation of the phagophore, the nascent autophagosome progressively grows in size and ultimately closes by recruiting intracellular membranes. In this review, we focus on the contribution of three membrane sources - the ER, the ER-Golgi intermediate compartment, and the Golgi complex - to autophagosome biogenesis and expansion. We also highlight the interplay between the secretory pathway and autophagy in cells when nutrients are scarce.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy-Related Proteins/metabolism ; Endoplasmic Reticulum/metabolism ; Golgi Apparatus/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lysosomes/metabolism
Chemical Substances	Autophagy-Related Proteins
Language	English
Publishing date	2019-10-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13637
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Article: Hijacking intracellular membranes to feed autophagosomal growth

Staiano, Leopoldo / Zappa, Francesca

FEBS letters. 2019 Nov., v. 593, no. 22

2019

Abstract	Autophagy is widely considered as a housekeeping mechanism that enables cells to survive stress conditions and, in particular, nutrient deprivation. Autophagy begins with the formation of the phagophore that expands and closes around cytosolic material and damaged organelles destined for degradation. The execution of this complex machinery is guaranteed by the coordinated action of more than 40 ATG (autophagy‐related) proteins that control the entire process at different stages from the biogenesis of the autophagosome to cargo sequestration and fusion with lysosomes. Autophagosome biogenesis occurs at multiple intracellular sites, such as the endoplasmic reticulum (ER) and the plasma membrane. Soon after the formation of the phagophore, the nascent autophagosome progressively grows in size and ultimately closes by recruiting intracellular membranes. In this review, we focus on the contribution of three membrane sources – the ER, the ER–Golgi intermediate compartment, and the Golgi complex – to autophagosome biogenesis and expansion. We also highlight the interplay between the secretory pathway and autophagy in cells when nutrients are scarce.
Keywords	Golgi apparatus ; autophagosomes ; autophagy ; biogenesis ; endoplasmic reticulum ; lysosomes ; plasma membrane
Language	English
Dates of publication	2019-11
Size	p. 3120-3134.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13637
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Article ; Online: Phosphoinositides in the kidney.

Staiano, Leopoldo / De Matteis, Maria Antonietta

Journal of lipid research

2018 Volume 60, Issue 2, Page(s) 287–298

Abstract: Phosphoinositides (PIs) play pivotal roles in the regulation of many biological processes. The quality and quantity of PIs is regulated in time and space by the activity of PI kinases and PI phosphatases. The number of PI-metabolizing enzymes exceeds the ...

Abstract	Phosphoinositides (PIs) play pivotal roles in the regulation of many biological processes. The quality and quantity of PIs is regulated in time and space by the activity of PI kinases and PI phosphatases. The number of PI-metabolizing enzymes exceeds the number of PIs with, in many cases, more than one enzyme controlling the same biochemical step. This would suggest that the PI system has an intrinsic ability to buffer and compensate for the absence of a specific enzymatic activity. However, there are several examples of severe inherited human diseases caused by mutations in one of the PI enzymes, although other enzymes with the same activity are fully functional. The kidney depends strictly on PIs for physiological processes, such as cell polarization, filtration, solute reabsorption, and signal transduction. Indeed, alteration of the PI system in the kidney very often results in pathological conditions, both inherited and acquired. Most of the knowledge of the roles that PIs play in the kidney comes from the study of KO animal models for genes encoding PI enzymes and from the study of human genetic diseases, such as Lowe syndrome/Dent disease 2 and Joubert syndrome, caused by mutations in the genes encoding the PI phosphatases, OCRL and INPP5E, respectively.
MeSH term(s)	Animals ; Humans ; Kidney/cytology ; Kidney/metabolism ; Kidney/pathology ; Kidney Diseases/drug therapy ; Kidney Diseases/metabolism ; Molecular Targeted Therapy ; Phosphatidylinositols/metabolism
Chemical Substances	Phosphatidylinositols
Language	English
Publishing date	2018-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R089946
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Article ; Online: Author Correction: The VersaLive platform enables microfluidic mammalian cell culture for versatile applications.

Nocera, Giovanni Marco / Viscido, Gaetano / Criscuolo, Stefania / Brillante, Simona / Carbone, Fabrizia / Staiano, Leopoldo / Carrella, Sabrina / di Bernardo, Diego

Communications biology

2022 Volume 5, Issue 1, Page(s) 1090

Language	English
Publishing date	2022-10-13
Publishing country	England
Document type	Published Erratum
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-04059-4
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Article ; Online: The VersaLive platform enables microfluidic mammalian cell culture for versatile applications.

Nocera, Giovanni Marco / Viscido, Gaetano / Criscuolo, Stefania / Brillante, Simona / Carbone, Fabrizia / Staiano, Leopoldo / Carrella, Sabrina / di Bernardo, Diego

Communications biology

2022 Volume 5, Issue 1, Page(s) 1034

Abstract: Microfluidic-based cell culture allows for precise spatio-temporal regulation of microenvironment, live cell imaging and better recapitulation of physiological conditions, while minimizing reagents' consumption. Despite their usefulness, most ... ...

Abstract	Microfluidic-based cell culture allows for precise spatio-temporal regulation of microenvironment, live cell imaging and better recapitulation of physiological conditions, while minimizing reagents' consumption. Despite their usefulness, most microfluidic systems are designed with one specific application in mind and usually require specialized equipment and expertise for their operation. All these requirements prevent microfluidic-based cell culture to be widely adopted. Here, we designed and implemented a versatile and easy-to-use perfusion cell culture microfluidic platform for multiple applications (VersaLive) requiring only standard pipettes. Here, we showcase the multiple uses of VersaLive (e.g., time-lapse live cell imaging, immunostaining, cell recovery, cell lysis, plasmid transfection) in mammalian cell lines and primary cells. VersaLive could replace standard cell culture formats in several applications, thus decreasing costs and increasing reproducibility across laboratories. The layout, documentation and protocols are open-source and available online at https://versalive.tigem.it/ .
MeSH term(s)	Animals ; Cell Culture Techniques ; Mammals ; Microfluidics ; Names ; Reproducibility of Results
Language	English
Publishing date	2022-09-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03976-8
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Article ; Online: The 5-phosphatase OCRL in Lowe syndrome and Dent disease 2.

De Matteis, Maria Antonietta / Staiano, Leopoldo / Emma, Francesco / Devuyst, Olivier

Nature reviews. Nephrology

2017 Volume 13, Issue 8, Page(s) 455–470

Abstract: Lowe syndrome is an X-linked disease that is characterized by congenital cataracts, central hypotonia, intellectual disability and renal Fanconi syndrome. The disease is caused by mutations in OCRL, which encodes an inositol polyphosphate 5-phosphatase ( ... ...

Abstract	Lowe syndrome is an X-linked disease that is characterized by congenital cataracts, central hypotonia, intellectual disability and renal Fanconi syndrome. The disease is caused by mutations in OCRL, which encodes an inositol polyphosphate 5-phosphatase (OCRL) that acts on phosphoinositides - quantitatively minor constituents of cell membranes that are nonetheless pivotal regulators of intracellular trafficking. In this Review we summarize the considerable progress made over the past decade in understanding the cellular roles of OCRL in regulating phosphoinositide balance along the endolysosomal pathway, a fundamental system for the reabsorption of proteins and solutes by proximal tubular cells. We discuss how studies of OCRL have led to important discoveries about the basic mechanisms of membrane trafficking and describe the key features and limitations of the currently available animal models of Lowe syndrome. Mutations in OCRL can also give rise to a milder pathology, Dent disease 2, which is characterized by renal Fanconi syndrome in the absence of extrarenal pathologies. Understanding how mutations in OCRL give rise to two clinical entities with differing extrarenal manifestations represents an opportunity to identify molecular pathways that could be targeted to develop treatments for these conditions.
MeSH term(s)	Animals ; Clathrin-Coated Vesicles ; Disease Models, Animal ; Endocytosis ; Genetic Diseases, X-Linked/genetics ; Humans ; Inositol Polyphosphate 5-Phosphatases/genetics ; Kidney Tubules, Proximal/cytology ; Mutation ; Nephrolithiasis/genetics ; Oculocerebrorenal Syndrome/genetics ; Phosphoric Monoester Hydrolases/genetics
Chemical Substances	Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; OCRL protein, human (EC 3.1.3.36) ; Inositol Polyphosphate 5-Phosphatases (EC 3.1.3.56)
Language	English
Publishing date	2017-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2017.83
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Article ; Online: RagD auto-activating mutations impair MiT/TFE activity in kidney tubulopathy and cardiomyopathy syndrome.

Nature communications

2023 Volume 14, Issue 1, Page(s) 2775

Abstract: Heterozygous mutations in the gene encoding RagD GTPase were shown to cause a novel autosomal dominant condition characterized by kidney tubulopathy and cardiomyopathy. We previously demonstrated that RagD, and its paralogue RagC, mediate a non-canonical ...

Abstract	Heterozygous mutations in the gene encoding RagD GTPase were shown to cause a novel autosomal dominant condition characterized by kidney tubulopathy and cardiomyopathy. We previously demonstrated that RagD, and its paralogue RagC, mediate a non-canonical mTORC1 signaling pathway that inhibits the activity of TFEB and TFE3, transcription factors of the MiT/TFE family and master regulators of lysosomal biogenesis and autophagy. Here we show that RagD mutations causing kidney tubulopathy and cardiomyopathy are "auto- activating", even in the absence of Folliculin, the GAP responsible for RagC/D activation, and cause constitutive phosphorylation of TFEB and TFE3 by mTORC1, without affecting the phosphorylation of "canonical" mTORC1 substrates, such as S6K. By using HeLa and HK-2 cell lines, human induced pluripotent stem cell-derived cardiomyocytes and patient-derived primary fibroblasts, we show that RRAGD auto-activating mutations lead to inhibition of TFEB and TFE3 nuclear translocation and transcriptional activity, which impairs the response to lysosomal and mitochondrial injury. These data suggest that inhibition of MiT/TFE factors plays a key role in kidney tubulopathy and cardiomyopathy syndrome.
MeSH term(s)	Humans ; Autophagy/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; HeLa Cells ; Induced Pluripotent Stem Cells/metabolism ; Kidney/metabolism ; Lysosomes/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mutation
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; RRAGD protein, human
Language	English
Publishing date	2023-05-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38428-2
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Article ; Online: Loss of the batten disease protein CLN3 leads to mis-trafficking of M6PR and defective autophagic-lysosomal reformation.

Nature communications

2023 Volume 14, Issue 1, Page(s) 3911

Abstract: Batten disease, one of the most devastating types of neurodegenerative lysosomal storage disorders, is caused by mutations in CLN3. Here, we show that CLN3 is a vesicular trafficking hub connecting the Golgi and lysosome compartments. Proteomic analysis ... ...

Abstract	Batten disease, one of the most devastating types of neurodegenerative lysosomal storage disorders, is caused by mutations in CLN3. Here, we show that CLN3 is a vesicular trafficking hub connecting the Golgi and lysosome compartments. Proteomic analysis reveals that CLN3 interacts with several endo-lysosomal trafficking proteins, including the cation-independent mannose 6 phosphate receptor (CI-M6PR), which coordinates the targeting of lysosomal enzymes to lysosomes. CLN3 depletion results in mis-trafficking of CI-M6PR, mis-sorting of lysosomal enzymes, and defective autophagic lysosomal reformation. Conversely, CLN3 overexpression promotes the formation of multiple lysosomal tubules, which are autophagy and CI-M6PR-dependent, generating newly formed proto-lysosomes. Together, our findings reveal that CLN3 functions as a link between the M6P-dependent trafficking of lysosomal enzymes and lysosomal reformation pathway, explaining the global impairment of lysosomal function in Batten disease.
MeSH term(s)	Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Neuronal Ceroid-Lipofuscinoses/genetics ; Neuronal Ceroid-Lipofuscinoses/metabolism ; Receptor, IGF Type 2/genetics ; Receptor, IGF Type 2/metabolism ; Proteomics ; Molecular Chaperones/metabolism ; Lysosomes/metabolism ; Hydrolases/metabolism ; Autophagy
Chemical Substances	Membrane Glycoproteins ; Receptor, IGF Type 2 ; Molecular Chaperones ; Hydrolases (EC 3.-) ; CLN3 protein, human
Language	English
Publishing date	2023-07-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-39643-7
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Article ; Online: The SGLT2 inhibitor dapagliflozin improves kidney function in glycogen storage disease XI.

Science translational medicine

2023 Volume 15, Issue 720, Page(s) eabn4214

Abstract: Glycogen storage disease XI, also known as Fanconi-Bickel syndrome (FBS), is a rare autosomal recessive disorder caused by mutations in ... ...

Abstract	Glycogen storage disease XI, also known as Fanconi-Bickel syndrome (FBS), is a rare autosomal recessive disorder caused by mutations in the
MeSH term(s)	Humans ; Mice ; Animals ; Fanconi Syndrome/genetics ; Fanconi Syndrome/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Glucose ; Kidney/metabolism ; Glycogen
Chemical Substances	dapagliflozin (1ULL0QJ8UC) ; Sodium-Glucose Transporter 2 Inhibitors ; Glucose (IY9XDZ35W2) ; Glycogen (9005-79-2)
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abn4214
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Article ; Online: Transcriptional regulation of the Ciona Gsx gene in the neural plate.

Hudson, Clare / Esposito, Rosaria / Palladino, Antonio / Staiano, Leopoldo / Ferrier, David / Faure, Emmanuel / Lemaire, Patrick / Yasuo, Hitoyoshi / Spagnuolo, Antonietta

Developmental biology

2018 Volume 448, Issue 2, Page(s) 88–100

Abstract: The ascidian neural plate consists of a defined number of identifiable cells organized in a grid of rows and columns, representing a useful model to investigate the molecular mechanisms controlling neural patterning in chordates. Distinct anterior brain ... ...

Abstract	The ascidian neural plate consists of a defined number of identifiable cells organized in a grid of rows and columns, representing a useful model to investigate the molecular mechanisms controlling neural patterning in chordates. Distinct anterior brain lineages are specified via unique combinatorial inputs of signalling pathways with Nodal and Delta-Notch signals patterning along the medial-lateral axis and FGF/MEK/ERK signals patterning along the anterior-posterior axis of the neural plate. The Ciona Gsx gene is specifically expressed in the a9.33 cells in the row III/column 2 position of anterior brain lineages, characterised by a combinatorial input of Nodal-OFF, Notch-ON and FGF-ON. Here, we identify the minimal cis-regulatory element (CRE) of 376 bp, which can recapitulate the early activation of Gsx. We show that this minimal CRE responds in the same way as the endogenous Gsx gene to manipulation of FGF- and Notch-signalling pathways and to overexpression of Snail, a mediator of Nodal signals, and Six3/6, which is required to demarcate the anterior boundary of Gsx expression at the late neurula stage. We reveal that sequences proximal to the transcription start site include a temporal regulatory element required for the precise transcriptional onset of gene expression. We conclude that sufficient spatial and temporal information for Gsx expression is integrated in 376 bp of non-coding cis-regulatory sequences.
MeSH term(s)	Animals ; Base Sequence ; Ciona/genetics ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Neural Plate/metabolism ; Receptors, Notch/metabolism ; Response Elements/genetics ; Sequence Deletion ; Signal Transduction/genetics ; Snail Family Transcription Factors/metabolism ; Time Factors ; Transcription, Genetic
Chemical Substances	Gsx protein, Ciona intestinalis ; Homeodomain Proteins ; Receptors, Notch ; Snail Family Transcription Factors
Language	English
Publishing date	2018-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2018.12.013
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