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| Open AccessTelomere-to-mitochondria signalling by ZBP1 mediates replicative crisis
Dysfunctional telomeres activate innate immune responses through mitochondrial TERRA–ZBP1 complexes to eliminate cells that are destined for neoplastic transformation.
- Joe Nassour
- , Lucia Gutierrez Aguiar
- & Jan Karlseder
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Letter |
PKG1-modified TSC2 regulates mTORC1 activity to counter adverse cardiac stress
Phosphorylation of one of two adjacent serine residues in TSC2 is both required and sufficient for PKG1-mediated cardiac protection against pressure overload in mice; these serine residues provide a genetic tool for the bidirectional regulation of stress-stimulated mTORC1 activity.
- Mark J. Ranek
- , Kristen M. Kokkonen-Simon
- & David A. Kass
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Letter |
Autophagic cell death restricts chromosomal instability during replicative crisis
Cell death during replicative crisis involves autophagy induced by telomere dysfunction.
- Joe Nassour
- , Robert Radford
- & Jan Karlseder
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Letter |
Autophagy maintains tumour growth through circulating arginine
Mice with whole-body or liver-specific deletion of Atg7 release circulating arginase I and have reduced levels of serum arginine, which impairs the growth of allografted arginine-auxotrophic tumours.
- Laura Poillet-Perez
- , Xiaoqi Xie
- & Eileen White
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Letter |
Polyglutamine tracts regulate beclin 1-dependent autophagy
The polyglutamine domain in ataxin 3, which is expanded in spinocerebellar ataxia type 3, allows normal ataxin 3 to interact with and deubiquitinate beclin 1 and thereby to promote autophagy.
- Avraham Ashkenazi
- , Carla F. Bento
- & David C. Rubinsztein
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Article |
Autophagy maintains the metabolism and function of young and old stem cells
Loss of autophagy increases the accumulation of mitochondria and the respiration status of haematopoietic stem cells, which perturbs their self-renewal and regeneration activities, and promotes cellular aging.
- Theodore T. Ho
- , Matthew R. Warr
- & Emmanuelle Passegué
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Letter |
Microenvironmental autophagy promotes tumour growth
During early-stage tumour growth in Drosphila, tumour cells acquire necessary nutrients by triggering autophagy in surrounding cells in the tumour microenvironment.
- Nadja S. Katheder
- , Rojyar Khezri
- & Tor Erik Rusten
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Letter |
Receptor usage dictates HIV-1 restriction by human TRIM5α in dendritic cell subsets
Human TRIM5α restricts HIV-1 infection of Langerhans cells through Langerin-dependent autophagy pathway.
- Carla M. S. Ribeiro
- , Ramin Sarrami-Forooshani
- & Teunis B. H. Geijtenbeek
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Letter |
Autophagy mediates degradation of nuclear lamina
In response to cancer-associated stress, autophagy machinery mediates degradation of nuclear lamina components in mammals, suggesting that cells might degrade nuclear components to prevent tumorigenesis.
- Zhixun Dou
- , Caiyue Xu
- & Shelley L. Berger
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Letter |
Receptor-mediated selective autophagy degrades the endoplasmic reticulum and the nucleus
In yeast, the novel protein Atg40 is enriched in the cortical and cytoplasmic endoplasmic reticulum (ER), and loads these ER subdomains into autophagosomes to facilitate ER autophagy; Atg39 localizes to the perinuclear ER and induces autophagic sequestration of part of the nucleus, thus ensuring cell survival under nitrogen-deprived conditions.
- Keisuke Mochida
- , Yu Oikawa
- & Hitoshi Nakatogawa
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Letter |
ATG14 promotes membrane tethering and fusion of autophagosomes to endolysosomes
The essential autophagy mediator ATG14 promotes vesicle fusion by forming homo-oligomers, which bind to a component of the SNARE membrane fusion complex and stabilize this complex on autophagosomes.
- Jiajie Diao
- , Rong Liu
- & Qing Zhong
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Letter |
Quantitative proteomics identifies NCOA4 as the cargo receptor mediating ferritinophagy
Through a quantitative proteomics analysis, a cohort of proteins is identified that associate with autophagosomes, among them a new cargo receptor called NCOA4 that, in response to iron deprivation, targets ferritin to autophagosomes and thereby releases iron.
- Joseph D. Mancias
- , Xiaoxu Wang
- & Alec C. Kimmelman
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Article |
A Crohn’s disease variant in Atg16l1 enhances its degradation by caspase 3
The Crohn’s disease risk-conferring T300A variant in the autophagy protein ATG16L1 increases its sensitivity to caspase-3-mediated cleavage; this decreases the induction of autophagy in response to metabolic stress or pathogen infection, leading to increased secretion of inflammatory cytokines.
- Aditya Murthy
- , Yun Li
- & Menno van Lookeren Campagne
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Article |
Functional interaction between autophagy and ciliogenesis
The primary cilium is a microtubule-based organelle that functions in sensory and signal transduction; here the authors show that the primary cilium is required for activation of starvation-induced autophagy and that basal autophagy negatively regulates ciliogenesis.
- Olatz Pampliega
- , Idil Orhon
- & Ana Maria Cuervo
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Letter |
Autophagy promotes primary ciliogenesis by removing OFD1 from centriolar satellites
The primary cilium is a microtubule-based organelle that functions in sensory and signal transduction; the authors demonstrate here that autophagic degradation of the oral-facial-digital syndrome 1 (OFD1) protein at centriolar satellites promotes primary cilium biogenesis, and that autophagy modulation might provide a novel means of ciliopathy treatment.
- Zaiming Tang
- , Mary Grace Lin
- & Qing Zhong
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Letter |
Autophagosomes form at ER–mitochondria contact sites
This study shows that autophagosomes form at sites of contact between the endoplasmic reticulum and mitochondria, and that formation requires the SNARE protein syntaxin 17.
- Maho Hamasaki
- , Nobumichi Furuta
- & Tamotsu Yoshimori
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Article |
Identification of a candidate therapeutic autophagy-inducing peptide
A cell-permeable peptide is constructed that is derived from a region of an essential autophagy protein called beclin 1; the peptide is a potent inducer of autophagy in mammalian cells and in vivo in mice, and is effective in the clearance of several viruses.
- Sanae Shoji-Kawata
- , Rhea Sumpter
- & Beth Levine
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News & Views |
Mitochondrial damage control
Defects in mitochondria are implicated in Parkinson's disease. Study of a quality-control pathway involving the proteins PINK1 and Parkin provides further clues about the mechanism involved.
- Asa Abeliovich