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Book ; Thesis: Characterization of Scylla, Charybdis, and Lk6 as novel growth modulators of the insulin receptor and target of rapamycin signaling pathways in Drosophila

Reiling, Jan H

2005

Author's details	vorgelegt von Jan H. Reiling
Language	English
Size	1 CD-R, Ill, 12 cm
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Zürich, 2005
Note	Enthält Sonderdrucke
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Secretory stressors induce intracellular death receptor accumulation to control apoptosis.

van Raam, Bram J / Lacina, Tamara / Lindemann, Ralph K / Reiling, Jan H

Cell death & disease

2017 Volume 8, Issue 10, Page(s) e3069

Abstract: Disruption of the Golgi apparatus can induce a distinct form of programmed cell death that has not been thoroughly characterized. We found that pharmacological application of Golgi stress leads to induction of death receptors (DRs) 4 and 5. DR4 appears ... ...

Abstract	Disruption of the Golgi apparatus can induce a distinct form of programmed cell death that has not been thoroughly characterized. We found that pharmacological application of Golgi stress leads to induction of death receptors (DRs) 4 and 5. DR4 appears to be primarily responsible for the initiation of cell death downstream of Golgi stress, whereas DR5 seems to be more important for cell death triggered by endoplasmic reticulum (ER) stress in specific cancer cell lines. DR induction downstream of either Golgi or ER stress mainly causes intracellular accumulation of DR4 presumably at the Golgi, rather than increased expression on the cell surface. Nevertheless, cells treated with secretory pathway stressors displayed an increased susceptibility to TRAIL (tumor necrosis factor related apoptosis inducing ligand), the endogenous ligand of DR4/5, probably due to intracellular sequestration of the caspase-8 regulator CFLAR (caspase-8 and FADD-like apoptosis regulator). These findings have implications for the treatment of cancer with DR agonists and our general understanding of DR signaling while highlighting the role of the Golgi apparatus as a cell death signaling platform.
MeSH term(s)	Apoptosis/drug effects ; CASP8 and FADD-Like Apoptosis Regulating Protein/genetics ; Caspase 8/genetics ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; Endoplasmic Reticulum Stress/genetics ; Golgi Apparatus/drug effects ; Golgi Apparatus/genetics ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics
Chemical Substances	CASP8 and FADD-Like Apoptosis Regulating Protein ; CFLAR protein, human ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10A protein, human ; TNFRSF10B protein, human ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2017-10-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2017.466
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Article ; Online: Image-based drug screen identifies HDAC inhibitors as novel Golgi disruptors synergizing with JQ1.

Gendarme, Mathieu / Baumann, Jan / Ignashkova, Tatiana I / Lindemann, Ralph K / Reiling, Jan H

Molecular biology of the cell

2017 Volume 28, Issue 26, Page(s) 3756–3772

Abstract: The Golgi apparatus is increasingly recognized as a major hub for cellular signaling and is involved in numerous pathologies, including neurodegenerative diseases and cancer. The study of Golgi stress-induced signaling pathways relies on the selectivity ... ...

Abstract	The Golgi apparatus is increasingly recognized as a major hub for cellular signaling and is involved in numerous pathologies, including neurodegenerative diseases and cancer. The study of Golgi stress-induced signaling pathways relies on the selectivity of the available tool compounds of which currently only a few are known. To discover novel Golgi-fragmenting agents, transcriptomic profiles of cells treated with brefeldin A, golgicide A, or monensin were generated and compared with a database of gene expression profiles from cells treated with other bioactive small molecules. In parallel, a phenotypic screen was performed for compounds that alter normal Golgi structure. Histone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified as novel Golgi disruptors. Further analysis identified HDAC1/HDAC9 as well as BRD8 and DNA-PK as important regulators of Golgi breakdown mediated by HDAC inhibition. We provide evidence that combinatorial HDACi/(+)-JQ1 treatment spurs synergistic Golgi dispersal in several cancer cell lines, pinpointing a possible link between drug-induced toxicity and Golgi morphology alterations.
MeSH term(s)	Apoptosis/drug effects ; Azepines/pharmacology ; Cell Line, Tumor ; Drug Evaluation, Preclinical/methods ; Drug Synergism ; Gene Expression Profiling/methods ; Golgi Apparatus/drug effects ; Histone Deacetylase 1/genetics ; Histone Deacetylase 1/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Triazoles/pharmacology
Chemical Substances	(+)-JQ1 compound ; Azepines ; Histone Deacetylase Inhibitors ; Histones ; Triazoles ; HDAC1 protein, human (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2017-10-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E17-03-0176
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Article ; Online: Cell survival and protein secretion associated with Golgi integrity in response to Golgi stress-inducing agents.

Ignashkova, Tatiana I / Gendarme, Mathieu / Peschk, Katrin / Eggenweiler, Hans-Michael / Lindemann, Ralph K / Reiling, Jan H

Traffic (Copenhagen, Denmark)

2017 Volume 18, Issue 8, Page(s) 530–544

Abstract: The Golgi apparatus is part of the secretory pathway and of central importance for modification, transport and sorting of proteins and lipids. ADP-ribosylation factors, whose activation can be blocked by brefeldin A (BFA), play a major role in ... ...

Abstract	The Golgi apparatus is part of the secretory pathway and of central importance for modification, transport and sorting of proteins and lipids. ADP-ribosylation factors, whose activation can be blocked by brefeldin A (BFA), play a major role in functioning of the Golgi network and regulation of membrane traffic and are also involved in proliferation and migration of cancer cells. Due to high cytotoxicity and poor bioavailability, BFA has not passed the preclinical stage of drug development. Recently, AMF-26 and golgicide A have been described as novel inhibitors of the Golgi system with antitumor or bactericidal properties. We provide here further evidence that AMF-26 closely mirrors the mode of action of BFA but is less potent. Using several human cancer cell lines, we studied the effects of AMF-26, BFA and golgicide A on cell homeostasis including Golgi structure, endoplasmic reticulum (ER) stress markers, secretion and viability, and found overall a significant correlation between these parameters. Furthermore, modulation of ADP-ribosylation factor expression has a profound impact on Golgi organization and survival in response to Golgi stress inducers.
Language	English
Publishing date	2017-08
Publishing country	England
Document type	Journal Article
ZDB-ID	1483852-7
ISSN	1600-0854 ; 1398-9219
ISSN (online)	1600-0854
ISSN	1398-9219
DOI	10.1111/tra.12493
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Article ; Online: Increased mTORC1 signaling UPRegulates stress.

Reiling, Jan H / Sabatini, David M

Molecular cell

2008 Volume 29, Issue 5, Page(s) 533–535

Abstract: In this issue of Molecular Cell, Ozcan et al. (2008) show that the loss of the tuberous sclerosis tumor suppressor complex induces endoplasmic reticulum stress, leading to attenuation of insulin receptor signaling activity via the unfolded protein ... ...

Abstract	In this issue of Molecular Cell, Ozcan et al. (2008) show that the loss of the tuberous sclerosis tumor suppressor complex induces endoplasmic reticulum stress, leading to attenuation of insulin receptor signaling activity via the unfolded protein response.
MeSH term(s)	Animals ; Endoplasmic Reticulum/metabolism ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Multiprotein Complexes ; Neoplasms/metabolism ; Oxidative Stress ; Proteins ; Receptor, Insulin/metabolism ; Signal Transduction/physiology ; TOR Serine-Threonine Kinases ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Multiprotein Complexes ; Proteins ; Transcription Factors ; Tumor Suppressor Proteins ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Receptor, Insulin (EC 2.7.10.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2008-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2008.02.011
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Article ; Online: Golgi stress mediates redox imbalance and ferroptosis in human cells.

Alborzinia, Hamed / Ignashkova, Tatiana I / Dejure, Francesca R / Gendarme, Mathieu / Theobald, Jannick / Wölfl, Stefan / Lindemann, Ralph K / Reiling, Jan H

Communications biology

2018 Volume 1, Page(s) 210

Abstract: Cytotoxic activities of several Golgi-dispersing compounds including AMF-26/M-COPA, brefeldin A and golgicide A have previously been shown to induce autophagy or apoptosis. Here, we demonstrate that these Golgi disruptors also trigger ferroptosis, a non- ... ...

Abstract	Cytotoxic activities of several Golgi-dispersing compounds including AMF-26/M-COPA, brefeldin A and golgicide A have previously been shown to induce autophagy or apoptosis. Here, we demonstrate that these Golgi disruptors also trigger ferroptosis, a non-apoptotic form of cell death characterized by iron-dependent oxidative degradation of lipids. Inhibitors of ferroptosis not only counteract cell death, but they also protect from Golgi dispersal and inhibition of protein secretion in response to several Golgi stress agents. Furthermore, the application of sublethal doses of ferroptosis-inducers such as erastin and sorafenib, low cystine growth conditions, or genetic knockdown of SLC7A11 and GPX4 all similarly protect cells from Golgi stress and lead to modulation of ACSL4, SLC7A5, SLC7A11 or GPX4 levels. Collectively, this study suggests a previously unrecognized function of the Golgi apparatus, which involves cellular redox control and prevents ferroptotic cell death.
Language	English
Publishing date	2018-11-28
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-018-0212-6
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Article: The hypoxia-induced paralogs Scylla and Charybdis inhibit growth by down-regulating S6K activity upstream of TSC in Drosophila.

Reiling, Jan H / Hafen, Ernst

Genes & development

2004 Volume 18, Issue 23, Page(s) 2879–2892

Abstract: Diverse extrinsic and intrinsic cues must be integrated within a developing organism to ensure appropriate growth at the cellular and organismal level. In Drosophila, the insulin receptor/TOR/S6K signaling network plays a fundamental role in the control ... ...

Abstract	Diverse extrinsic and intrinsic cues must be integrated within a developing organism to ensure appropriate growth at the cellular and organismal level. In Drosophila, the insulin receptor/TOR/S6K signaling network plays a fundamental role in the control of metabolism and cell growth. Here we show that scylla and charybdis, two homologous genes identified as growth suppressors in an EP (enhancer/promoter) overexpression screen, act as negative regulators of growth. The simultaneous loss of both genes generates flies that are more susceptible to reduced oxygen concentrations (hypoxia) and that show mild overgrowth phenotypes. Conversely, scylla or charybdis overactivation reduces growth. Growth inhibition is associated with a reduction in S6K but not PKB/Akt activity. Together, genetic and biochemical analysis places Scylla/Charybdis downstream of PKB and upstream of TSC. Furthermore, we show that scylla and charybdis are induced under hypoxic conditions and that scylla is a target of Drosophila HIF-1 (hypoxia-inducible factor-1) like its mammalian counterpart RTP801/REDD1, thus establishing a potential cross-talk between growth and oxygen sensing.
MeSH term(s)	Amino Acid Sequence ; Animals ; Blotting, Western ; Drosophila/genetics ; Drosophila Proteins/biosynthesis ; Drosophila Proteins/chemistry ; Drosophila Proteins/genetics ; Drosophila Proteins/physiology ; Hypoxia/metabolism ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Ribosomal Protein S6 Kinases/metabolism ; Sequence Homology, Amino Acid
Chemical Substances	Drosophila Proteins ; Proto-Oncogene Proteins ; chrb protein, Drosophila ; scyl protein, Drosophila ; Akt1 protein, Drosophila (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases (EC 2.7.11.1)
Language	English
Publishing date	2004-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.322704
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Article: Off-target effects associated with long dsRNAs in Drosophila RNAi screens.

Moffat, Jason / Reiling, Jan H / Sabatini, David M

Trends in pharmacological sciences

2007 Volume 28, Issue 4, Page(s) 149–151

Abstract: Evidence of off-target effects (OTEs) associated with small interfering (si)RNAs (19-29bp) in mammalian cells has existed for several years. Two recent articles demonstrate that short sequences within long double-stranded (ds)RNAs frequently cause ... ...

Abstract	Evidence of off-target effects (OTEs) associated with small interfering (si)RNAs (19-29bp) in mammalian cells has existed for several years. Two recent articles demonstrate that short sequences within long double-stranded (ds)RNAs frequently cause undesirable OTEs in cultured Drosophila cells. These results reveal the potential for high false-positive rates in RNA interference (RNAi) screens using long dsRNAs and highlight the need for screening with multiple, non-overlapping long dsRNAs or siRNAs. Discovering multiple potent siRNAs with minimal off-target profiles for each target transcript will be invaluable for genome-based studies of gene function and for personalized RNAi therapeutics.
MeSH term(s)	Animals ; Drosophila/genetics ; Gene Library ; Genes, Insect/genetics ; RNA Interference ; RNA, Double-Stranded/genetics
Chemical Substances	RNA, Double-Stranded
Language	English
Publishing date	2007-04
Publishing country	England
Document type	Journal Article
ZDB-ID	282846-7
ISSN	1873-3735 ; 0165-6147
ISSN (online)	1873-3735
ISSN	0165-6147
DOI	10.1016/j.tips.2007.02.009
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Article ; Online: Golgi stress-induced transcriptional changes mediated by MAPK signaling and three ETS transcription factors regulate MCL1 splicing.

Baumann, Jan / Ignashkova, Tatiana I / Chirasani, Sridhar R / Ramírez-Peinado, Silvia / Alborzinia, Hamed / Gendarme, Mathieu / Kuhnigk, Kyra / Kramer, Valentin / Lindemann, Ralph K / Reiling, Jan H

Molecular biology of the cell

2017 Volume 29, Issue 1, Page(s) 42–52

Abstract: The secretory pathway is a major determinant of cellular homoeostasis. While research into secretory stress signaling has so far mostly focused on the endoplasmic reticulum (ER), emerging data suggest that the Golgi itself serves as an important ... ...

Abstract	The secretory pathway is a major determinant of cellular homoeostasis. While research into secretory stress signaling has so far mostly focused on the endoplasmic reticulum (ER), emerging data suggest that the Golgi itself serves as an important signaling hub capable of initiating stress responses. To systematically identify novel Golgi stress mediators, we performed a transcriptomic analysis of cells exposed to three different pharmacological compounds known to elicit Golgi fragmentation: brefeldin A, golgicide A, and monensin. Subsequent gene-set enrichment analysis revealed a significant contribution of the ETS family transcription factors ELK1, GABPA/B, and ETS1 to the control of gene expression following compound treatment. Induction of Golgi stress leads to a late activation of the ETS upstream kinases MEK1/2 and ERK1/2, resulting in enhanced ETS factor activity and the transcription of ETS family target genes related to spliceosome function and cell death induction via alternate MCL1 splicing. Further genetic analyses using loss-of-function and gain-of-function experiments suggest that these transcription factors operate in parallel.
MeSH term(s)	A549 Cells ; Alternative Splicing/drug effects ; Alternative Splicing/genetics ; Apoptosis/drug effects ; Brefeldin A/pharmacology ; Cytoprotection/drug effects ; Gene Expression Profiling ; Gene Knockdown Techniques ; Golgi Apparatus/drug effects ; Golgi Apparatus/metabolism ; HEK293 Cells ; HeLa Cells ; Humans ; MAP Kinase Signaling System/drug effects ; Mitogen-Activated Protein Kinases/metabolism ; Monensin/pharmacology ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Proto-Oncogene Proteins c-ets/metabolism ; Pyridines/pharmacology ; Quinolines/pharmacology ; Small Molecule Libraries/pharmacology ; Spliceosomes/drug effects ; Spliceosomes/metabolism ; Stress, Physiological/drug effects ; Transcription, Genetic/drug effects ; Transcriptome/drug effects ; Transcriptome/genetics ; Up-Regulation/drug effects
Chemical Substances	Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-ets ; Pyridines ; Quinolines ; Small Molecule Libraries ; golgicide A ; Brefeldin A (20350-15-6) ; Monensin (906O0YJ6ZP) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2017-11-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E17-06-0418
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Article ; Online: TRAPPC13 modulates autophagy and the response to Golgi stress.

Ramírez-Peinado, Silvia / Ignashkova, Tatiana I / van Raam, Bram J / Baumann, Jan / Sennott, Erica L / Gendarme, Mathieu / Lindemann, Ralph K / Starnbach, Michael N / Reiling, Jan H

Journal of cell science

2017 Volume 130, Issue 14, Page(s) 2251–2265

Abstract: Tether complexes play important roles in endocytic and exocytic trafficking of lipids and proteins. In yeast, the multisubunit transport protein particle (TRAPP) tether regulates endoplasmic reticulum (ER)-to-Golgi and intra-Golgi transport and is also ... ...

Abstract	Tether complexes play important roles in endocytic and exocytic trafficking of lipids and proteins. In yeast, the multisubunit transport protein particle (TRAPP) tether regulates endoplasmic reticulum (ER)-to-Golgi and intra-Golgi transport and is also implicated in autophagy. In addition, the TRAPP complex acts as a guanine nucleotide exchange factor (GEF) for Ypt1, which is homologous to human Rab1a and Rab1b. Here, we show that human TRAPPC13 and other TRAPP subunits are critically involved in the survival response to several Golgi-disrupting agents. Loss of TRAPPC13 partially preserves the secretory pathway and viability in response to brefeldin A, in a manner that is dependent on ARF1 and the large GEF GBF1, and concomitant with reduced caspase activation and ER stress marker induction. TRAPPC13 depletion reduces Rab1a and Rab1b activity, impairs autophagy and leads to increased infectivity to the pathogenic bacterium
MeSH term(s)	A549 Cells ; ADP-Ribosylation Factor 1/metabolism ; Anti-Bacterial Agents/pharmacology ; Antigens, Neoplasm/drug effects ; Antigens, Neoplasm/metabolism ; Autophagy/physiology ; Brefeldin A/pharmacology ; Dysentery, Bacillary/drug therapy ; Dysentery, Bacillary/metabolism ; Gene Knockdown Techniques ; Golgi Apparatus/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; HEK293 Cells ; HT29 Cells ; HeLa Cells ; Humans ; Shigella flexneri/drug effects ; Vesicular Transport Proteins/antagonists & inhibitors ; Vesicular Transport Proteins/drug effects ; Vesicular Transport Proteins/metabolism
Chemical Substances	Anti-Bacterial Agents ; Antigens, Neoplasm ; GBF1 protein, human ; Guanine Nucleotide Exchange Factors ; TRAPPC1 protein, human ; Vesicular Transport Proteins ; Brefeldin A (20350-15-6) ; ADP-Ribosylation Factor 1 (EC 3.6.5.2)
Language	English
Publishing date	2017-05-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.199521
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