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Termination of autophagy and reformation of lysosomes regulated by mTOR (2010)

L. Yu ; C. K. McPhee ; L. Zheng ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 465(7300): 942-6. doi: 10.1038/nature09076.

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Publication Date: 2010-06-08

Description: Autophagy is an evolutionarily conserved process by which cytoplasmic proteins and organelles are catabolized. During starvation, the protein TOR (target of rapamycin), a nutrient-responsive kinase, is inhibited, and this induces autophagy. In autophagy, double-membrane autophagosomes envelop and sequester intracellular components and then fuse with lysosomes to form autolysosomes, which degrade their contents to regenerate nutrients. Current models of autophagy terminate with the degradation of the autophagosome cargo in autolysosomes, but the regulation of autophagy in response to nutrients and the subsequent fate of the autolysosome are poorly understood. Here we show that mTOR signalling in rat kidney cells is inhibited during initiation of autophagy, but reactivated by prolonged starvation. Reactivation of mTOR is autophagy-dependent and requires the degradation of autolysosomal products. Increased mTOR activity attenuates autophagy and generates proto-lysosomal tubules and vesicles that extrude from autolysosomes and ultimately mature into functional lysosomes, thereby restoring the full complement of lysosomes in the cell-a process we identify in multiple animal species. Thus, an evolutionarily conserved cycle in autophagy governs nutrient sensing and lysosome homeostasis during starvation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920749/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920749/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- McPhee, Christina K -- Zheng, Lixin -- Mardones, Gonzalo A -- Rong, Yueguang -- Peng, Junya -- Mi, Na -- Zhao, Ying -- Liu, Zhihua -- Wan, Fengyi -- Hailey, Dale W -- Oorschot, Viola -- Klumperman, Judith -- Baehrecke, Eric H -- Lenardo, Michael J -- 2010CB833704/CB/NCI NIH HHS/ -- GM079431/GM/NIGMS NIH HHS/ -- R01 GM079431/GM/NIGMS NIH HHS/ -- Z01 AI000718-13/Intramural NIH HHS/ -- Z01 AI000718-14/Intramural NIH HHS/ -- ZIA AI000718-15/Intramural NIH HHS/ -- England -- Nature. 2010 Jun 17;465(7300):942-6. doi: 10.1038/nature09076. Epub 2010 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20526321" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Autophagy/*physiology ; Cell Line ; Cercopithecus aethiops ; HeLa Cells ; Homeostasis/physiology ; Humans ; Intracellular Signaling Peptides and Proteins/*metabolism ; Lysosomes/*metabolism/ultrastructure ; *Nutritional Physiological Phenomena ; Protein-Serine-Threonine Kinases/*metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases ; Vero Cells

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Activation of autophagy during cell death requires the engulfment receptor Draper (2010)

C. K. McPhee ; M. A. Logan ; M. R. Freeman ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 465(7301): 1093-6. doi: 10.1038/nature09127.

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Publication Date: 2010-06-26

Description: Autophagy degrades cytoplasmic components that are required for cell survival in response to starvation. Autophagy has also been associated with cell death, but it is unclear how this is distinguished from autophagy during cell survival. Drosophila salivary glands undergo programmed cell death that requires autophagy genes, and engulfment of salivary gland cells by phagocytes does not appear to occur. Here we show that Draper (Drpr), the Drosophila melanogaster orthologue of the Caenorhabditis elegans engulfment receptor CED-1, is required for autophagy during cell death. Null mutations in, and salivary gland-specific knockdown of, drpr inhibit salivary gland degradation. Knockdown of drpr prevents the induction of autophagy in dying salivary glands, and expression of the Atg1 autophagy regulator in drpr mutants suppresses the failure in degradation of salivary glands. Surprisingly, drpr is required in the same dying salivary gland cells in which it regulates autophagy induction, but drpr knockdown does not prevent starvation-induced autophagy in the fat body, which is associated with survival. In addition, components of the conserved engulfment pathway are required for clearance of dying salivary glands. To our knowledge, this is the first example of an engulfment factor that is required for self-clearance of cells. Further, Drpr is the first factor that distinguishes autophagy that is associated with cell death from autophagy associated with cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892814/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892814/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McPhee, Christina K -- Logan, Mary A -- Freeman, Marc R -- Baehrecke, Eric H -- DK32520/DK/NIDDK NIH HHS/ -- GM079431/GM/NIGMS NIH HHS/ -- NS053538/NS/NINDS NIH HHS/ -- R01 GM079431/GM/NIGMS NIH HHS/ -- R01 GM079431-04/GM/NIGMS NIH HHS/ -- R01 GM079431-05/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jun 24;465(7301):1093-6. doi: 10.1038/nature09127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577216" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Animals, Genetically Modified ; Autophagy/genetics/*physiology ; Caspases/metabolism ; Cell Death/physiology ; Cell Survival ; Drosophila Proteins/deficiency/genetics/*metabolism ; Drosophila melanogaster/*cytology/enzymology/genetics/*metabolism ; Fat Body/cytology ; Food Deprivation ; Genes, Insect/genetics ; Membrane Proteins/deficiency/genetics/*metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Salivary Glands/cytology/metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8 (2004)

L. Yu ; A. Alva ; H. Su ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 304(5676): 1500-2. doi: 10.1126/science.1096645.

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Publication Date: 2004-05-08

Description: Caspases play a central role in apoptosis, a well-studied pathway of programmed cell death. Other programs of death potentially involving necrosis and autophagy may exist, but their relation to apoptosis and mechanisms of regulation remains unclear. We define a new molecular pathway in which activation of the receptor-interacting protein (a serine-threonine kinase) and Jun amino-terminal kinase induced cell death with the morphology of autophagy. Autophagic death required the genes ATG7 and beclin 1 and was induced by caspase-8 inhibition. Clinical therapies involving caspase inhibitors may arrest apoptosis but also have the unanticipated effect of promoting autophagic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- Alva, Ajjai -- Su, Helen -- Dutt, Parmesh -- Freundt, Eric -- Welsh, Sarah -- Baehrecke, Eric H -- Lenardo, Michael J -- GM59136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1500-2. Epub 2004 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131264" target="_blank"〉PubMed〈/a〉

Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Apoptosis Regulatory Proteins ; *Autophagy ; Caspase 8 ; *Caspase Inhibitors ; Caspases/genetics/*metabolism ; *Cell Death ; Cell Line ; Cells, Cultured ; Humans ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 7 ; MAP Kinase Signaling System ; Membrane Proteins ; Mice ; Mitogen-Activated Protein Kinase Kinases/genetics/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Proteins/genetics/*metabolism ; RNA Interference ; Receptor-Interacting Protein Serine-Threonine Kinases

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Tuberculosis: Autophagy is not the answer (2015)

S. M. Behar ; E. H. Baehrecke

Nature Publishing Group (NPG)

In: Nature. 528(7583): 482-3. doi: 10.1038/nature16324.

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Publication Date: 2015-12-10

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Behar, Samuel M -- Baehrecke, Eric H -- R01 AI098637/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):482-3. doi: 10.1038/nature16324. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Physiological Systems, and Eric H. Baehrecke is in the Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649822" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Female ; Male ; Microtubule-Associated Proteins/*metabolism ; *Mycobacterium tuberculosis ; Neutrophils/*immunology ; Tuberculosis/*immunology/*pathology

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

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CDDis celebrates 1000 publications of essential research (2014)

E H Baehrecke

Springer Nature

In: Cell Death & Disease

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Publication Date: 2014-01-31

Description: CDDis celebrates 1000 publications of essential research Cell Death and Disease 5, e1042 (January 2014). doi:10.1038/cddis.2014.19 Author: E H Baehrecke

Electronic ISSN: 2041-4889

Topics: Biology , Medicine

Published by Springer Nature

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6

Electronic Resource

Cell surface exposure of phosphatidylserine during apoptosis is phylogenetically conserved (1998)

van den Eijnde, S. M. ; Boshart, L. ; Baehrecke, E. H. ; [et al.]

Springer

Apoptosis 3 (1998), S. 9-16

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ISSN: 1573-675X

Keywords: Chick ; development ; Drosphila ; mouse ; phagocytosis ; plasma membrane

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract Exposure of the aminophospholipid phosphatidylserine at the outer leaflet of the plasma membrane by apoptotic cells can trigger phagocytic removal of these dying cells. This functionality of phosphatidylserine exposure in the process of phagocytosis is indicated by in vitro studies of mammalian and insect phagocytes. We have studied the in vivo distribution of cell-surface exposed phosphatidylserine by injecting biotinylated Annexin V, a Ca 2+ -dependent phosphatidyl-serine binding protein, into viable mouse and chick embryos and Drosophila pupae. The apparent binding of Annexin V to cells with a morphology which is characteristicof apoptosis and which was present in regions of developmental cell death indicates that phosphatidylserine exposure by apoptotic cells is a phylogenetically conserved mechanism.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1009650917818

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Electronic Resource

Foraging behavior of Campoletis sonorensis in response to Heliothis virescens and cotton plants (1990)

Baehrecke, E. H. ; Vinson, S. B. ; Williams, H. J.

Springer

Entomologia experimentalis et applicata 55 (1990), S. 47-57

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ISSN: 1570-7458

Keywords: Campoletis sonorensis ; parasitoid ; Hymenoptera ; Ichneumonidae ; Heliothis virescens ; cotton ; potential host community location ; host location

Source: Springer Online Journal Archives 1860-2000

Topics: Biology

Description / Table of Contents: Résumé Les comportements d'évaluation de l'effectif d'hôtes potentiels et de la position des hôtes par C. sonorensis (Hyméno.: Iccheumonidae) ont été quantifiés pour déterminer les séquences significatives des événements comportementaux. La localisation de la colonie potentielle d'hôtes est apparue comme une séquence régulière des événements comportementaux. Une fois que le parasitoïde a localisé une colonie potentielle, on a constaté que la recherche au hasard des hôtes se poursuit jusqu'à ce qu'il ait la démonstration qu'il s'agit d'une plante attaquée. La localisation par le parasitoïde d'un hôte certain a consitué une autre séquence régulière des événements comportementaux terminant la localisation de l'hôte. L'influence de pieds de coton intacts, de pieds abîmés mécaniquement et de pieds occupés par des chenilles du 3ème stade de l'hôte et de plantes dont les chenilles ont été retirées juste avant l'expérience a été déterminée en modifiant la composition du complexe hôte/plante. Des femelles naïves de C. sonorensis ont montré en présence de pieds de coton intacts apparemment toutes les séquences comportementales de vol impliquées dans la localisation d'une colonie potentielle d'hôtes. Une fois que le parasitoïde a atteint la colonie potentielle d'hôtes, la présence de dégâts de l'hôte n'a pas modifié le temps passé sur la plante, mais a modifié le temps consacré à la prospection.

Notes: Abstract Wind tunnel flight behavior of inexperienced female Campoletis sonorensis (Cameron) (Hymenoptera; Ichneumonidae) in response to its larval host Heliothis virescens (F.) (Lepidoptera: Noctuidae) feeding on the host plant cotton (Gossypium hirsutum L.) is described. The flight behavioral sequence was determined by quantification of frequencies of observed behaviors and probabilities of first-order behavioral transitions. Comparison of inexperienced C. sonorensis flights to undamaged and damaged cotton indicated that stimuli from undamaged plants alone are adequate to elicit the complete flight behavioral sequence observed in response to H. virescens feeding on cotton. Parasitoid foraging behavior was also analyzed after landing on the stimulus. This behavior appeared to be random in its initial stages, but became sequential after location of evidence of a host. Analysis of foraging on undamaged and 3 treatments of damaged cotton resulted in the determination that parasitoids tend to remain on damaged plants longer than undamaged plants although no significant difference was detected. C. sonorensis spent a greater percentage of their time foraging on host damaged plants than on undamaged plants.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00188227

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Electronic Resource

Electroantennogram responses ofCampoletis sonorensis (hymenoptera: Ichneumonidae) to chemicals in cotton (Gossypium hirsutum L.) (1989)

Baehrecke, E. H. ; Williams, H. J. ; Vinson, S. B.

Springer

Journal of chemical ecology 15 (1989), S. 37-45

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ISSN: 1573-1561

Keywords: Campoletis sonorensis ; parasitoid ; Hymenoptera ; Ichneumonidae ; cotton ; Gossypium hirsutum ; host habitat location ; green leaf chemical ; monoterpene ; sesquiterpene ; electroantennogram ; olfaction ; volatile

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Chemistry and Pharmacology

Notes: Abstract Combined gas chromatography-electroantennogram (GC-EAG) recording ofCampoletis sonorensis (Cameron) responses to cotton plant volatile chemicals was performed.C. sonorensis antennal olfactory receptors respond differentially to green leaf, mono-, and sesquiterpene chemicals that have been identified previously in cotton. EAG depolarizations to green leaf chemicals were greater than to terpenes.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF02027772

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