Sequestration Revisited: Integrating Traditional Electron Microscopy, De Novo Assembly and New Results

Kovács, Attila; Pálfia, Zsolt; Réz, Gábor; Vellai, Tibor; Kovács, János

doi:10.4161/auto.4590

Cited by 65 publications

(63 citation statements)

References 27 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Formation of the autophagosome is described as de novo to distinguish it from what happens in the secretory pathway because these double-membrane vesicles do not form by budding from a preexisting organelle (Noda et al 2002;Kovacs et al 2007). The process of autophagosome biogenesis is perhaps the least understood part of macroautophagy, and many aspects remain to be fully elucidated.…”

Section: Nonselective Macroautophagymentioning

confidence: 99%

Autophagic Processes in Yeast: Mechanism, Machinery and Regulation

2013

View full text Add to dashboard Cite

Autophagy refers to a group of processes that involve degradation of cytoplasmic components including cytosol, macromolecular complexes, and organelles, within the vacuole or the lysosome of higher eukaryotes. The various types of autophagy have attracted increasing attention for at least two reasons. First, autophagy provides a compelling example of dynamic rearrangements of subcellular membranes involving issues of protein trafficking and organelle identity, and thus it is fascinating for researchers interested in questions pertinent to basic cell biology. Second, autophagy plays a central role in normal development and cell homeostasis, and, as a result, autophagic dysfunctions are associated with a range of illnesses including cancer, diabetes, myopathies, some types of neurodegeneration, and liver and heart diseases. That said, this review focuses on autophagy in yeast. Many aspects of autophagy are conserved from yeast to human; in particular, this applies to the gene products mediating these pathways as well as some of the signaling cascades regulating it, so that the information we relate is relevant to higher eukaryotes. Indeed, as with many cellular pathways, the initial molecular insights were made possible due to genetic studies in Saccharomyces cerevisiae and other fungi. TABLE OF CONTENTS Abstract 341Introduction 342

show abstract

Section: Nonselective Macroautophagymentioning

confidence: 99%

Autophagic Processes in Yeast: Mechanism, Machinery and Regulation

2013

View full text Add to dashboard Cite

show abstract

“…Until recently, the dogma was that the phagophore and autophagosome formed de novo, meaning that the sequestering membrane does not form in "one step" from a pre-existing organelle already containing its cargo as occurs throughout the secretory pathway [45,46]. Regardless of the specific mechanism, autophagosome formation is thought to occur by the expansion of the phagophore, that is, a sheet of membrane that would correspond to the size of a complete autophagosome does not separate from the endomembrane system and simply curl up to form an autophagosome.…”

Section: Origin Of the Phagophorementioning

confidence: 99%

The machinery of macroautophagy

et al. 2013

View full text Add to dashboard Cite

Autophagy is a primarily degradative pathway that takes place in all eukaryotic cells. It is used for recycling cytoplasm to generate macromolecular building blocks and energy under stress conditions, to remove superfluous and damaged organelles to adapt to changing nutrient conditions and to maintain cellular homeostasis. In addition, autophagy plays a critical role in cytoprotection by preventing the accumulation of toxic proteins and through its action in various aspects of immunity including the elimination of invasive microbes and its participation in antigen presentation. The most prevalent form of autophagy is macroautophagy, and during this process, the cell forms a double-membrane sequestering compartment termed the phagophore, which matures into an autophagosome. Following delivery to the vacuole or lysosome, the cargo is degraded and the resulting macromolecules are released back into the cytosol for reuse. The past two decades have resulted in a tremendous increase with regard to the molecular studies of autophagy being carried out in yeast and other eukaryotes. Part of the surge in interest in this topic is due to the connection of autophagy with a wide range of human pathophysiologies including cancer, myopathies, diabetes and neurodegenerative disease. However, there are still many aspects of autophagy that remain unclear, including the process of phagophore formation, the regulatory mechanisms that control its induction and the function of most of the autophagy-related proteins. In this review, we focus on macroautophagy, briefly describing the discovery of this process in mammalian cells, discussing the current views concerning the donor membrane that forms the phagophore, and characterizing the autophagy machinery including the available structural information.

show abstract

“…4 During autophagy, subcellular membrane structures are formed to sequester cargo into lysosomes for breakdown by acid hydrolases. 5,6 Autophagy is activated upon nutrient deprivation and reduced insulin/IGF-1 or TOR signaling, 7,8 raising the possibility that autophagy-mediated renewal of cytosolic materials is a prerequisite of normal cell growth.…”

Section: Autophagy Genes Are Required For Normal Cell Sizementioning

confidence: 99%

Regulation of cell growth by autophagy

et al. 2008

Self Cite

View full text Add to dashboard Cite

Cell growth-the primary determinant of cell size-has an intimate relationship with proliferation; cells divide only after they reach a critical size. Despite its developmental and medical significance, little is known about cellular pathways that mediate the growth of cells. Accumulating evidence demonstrates a role for autophagy-a mechanism of eukaryotic cells to digest their own constituents during development or starvation-in cell size control. Increasing autophagic activity by prolonged starvation, rapamycin treatment inhibiting TOR (target of rapamycin) signaling, or genetic intervention, causes cellular atrophy in worms, flies and mammalian cell cultures. In contrast, we have shown that in the nematode Caenorhabditis elegans mutational inactivation of two autophagy genes, unc-51/Atg1 and bec-1/Atg6, confers reduced cell size. We argue that physiological levels of autophagy are required for normal cell size, whereas both insufficient and excessive levels of autophagy lead to retarded cell growth. Furthermore, we discuss data suggesting that the insulin/IGF-1 (insulin-like growth factor receptor-1) and TGF-β (transforming growth factor-beta) signaling systems acting as major growth regulatory pathways converge on autophagy genes to control cell size. Thus, autophagy may act as a central regulatory mechanism of cell growth.

show abstract

Sequestration Revisited: Integrating Traditional Electron Microscopy, De Novo Assembly and New Results

Cited by 65 publications

References 27 publications

Autophagic Processes in Yeast: Mechanism, Machinery and Regulation

Autophagic Processes in Yeast: Mechanism, Machinery and Regulation

The machinery of macroautophagy

Regulation of cell growth by autophagy

Contact Info

Product

Resources

About