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Dynamics and diversity in autophagy mechanisms: lessons from yeast

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TLDR
The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today.
Abstract
Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy.

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Selective regulation of autophagy by the Iml1-Npr2-Npr3 complex in the absence of nitrogen starvation.

TL;DR: Autophagy can be induced in response to more subtle changes in nutritional state, without severe nitrogen starvation, and the Iml1p-Npr2p- Npr3p complex selectively regulates this form of autophagy.
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Carotenoid deficiency triggers autophagy in the model green alga Chlamydomonas reinhardtii.

TL;DR: It is found that high light transiently activates autophagy in wild-type Chlamydomonas cells as part of an adaptation response to this stress, and a link between photo-oxidative damage, ROS accumulation and Autophagy activation in ChlamYdom onas cells with a reduced carotenoid content is revealed.
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Compromising mitochondrial function with the antiretroviral drug efavirenz induces cell survival-promoting autophagy

TL;DR: Clinical concentrations of EFV induce autophagy and, in particular, mitophagy in hepatic cells, which suggests that autophagic acts as an adaptive mechanism of cell survival, but exceeding a certain threshold of mitochondrial dysfunction is associated with an Autophagic overload or stress.
Journal ArticleDOI

Dynamics of Autophagosome Formation.

TL;DR: Environmental stress activates autophagy and leads to autophagosome formation at the endoplasmic reticulum.
Journal ArticleDOI

TRAPPIII is responsible for vesicular transport from early endosomes to Golgi, facilitating Atg9 cycling in autophagy.

TL;DR: It is shown that TRAPPIII functions at the Golgi complex to receive general retrograde vesicle traffic from early endosomes, which elucidates how general membrane traffic contributes to autophagy.
References
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Journal ArticleDOI

Autophagy fights disease through cellular self-digestion

TL;DR: Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health, and to play a role in cell death.
Journal ArticleDOI

TOR signaling in growth and metabolism.

TL;DR: The physiological consequences of mammalianTORC1 dysregulation suggest that inhibitors of mammalian TOR may be useful in the treatment of cancer, cardiovascular disease, autoimmunity, and metabolic disorders.
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p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy

TL;DR: It is demonstrated that the previously reported aggresome-like induced structures containing ubiquitinated proteins in cytosolic bodies are dependent on p62 for their formation and p62 is required both for the formation and the degradation of polyubiquitin-containing bodies by autophagy.
Journal ArticleDOI

Autophagy: process and function

TL;DR: In this review, the process of autophagy is summarized, and the role of autophileagy is discussed in a process-based manner.
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