Peroxisome homeostasis in

Leão, Adriana N; Kiel, Jan A.K.W.

doi:10.1016/s1567-1356(03)00070-9

Cited by 35 publications

(30 citation statements)

References 53 publications

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“…Consistent with experimental data for autophagy in Leishmania species, 5,6 the analysis presented here shows that trypanosomatids have the core protein complement necessary to implement autophagy and related processes; no key component is apparently absent in these organisms. Clearly the autophagy of glycosomes, analogous to pexophagy, for which experimental evidence is accumulating, is viable from a genomic viewpoint.…”

Section: Discussionsupporting

confidence: 89%

“…1), and new peroxisomes with a different enzymic content synthesized. 6,7 Peroxisomes seem to provide the cells the capability of efficiently changing a set of enzymes necessary under specific conditions, and thus to quickly adapt to a new situation. Peroxisomal degradation can occur by either macro-or microautophagy, called respectively macro-and micropexophagy.…”

Section: Introductionmentioning

confidence: 99%

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Autophagy and Related processes in Trypanosomatids: Insights from Genomic and Bioinformatic Analyses

Herman

Gillies²,

Michels³

et al. 2006

Autophagy

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Autophagy and Related processes in Trypanosomatids: Insights from Genomic and Bioinformatic Analyses

Herman

Gillies²,

Michels³

et al. 2006

Autophagy

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“…For example, peroxisomes (induced by growth on methanol or fatty acids) can be eliminated by either macro-or microautophagy (pexophagy) upon modification of the carbon source (Leao and Kiel, 2003). Moreover, while bulk degradation of mitochondria following nutrient starvation (or TORC1 inactivation) occurs via a selective macroautophagic process (i.e.…”

Section: Mitophagy and Pexophagymentioning

confidence: 99%

Cell growth control: little eukaryotes make big contributions

2006

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The story of rapamycin is a pharmaceutical fairytale. Discovered as an antifungal activity in a soil sample collected on Easter Island, this macrocyclic lactone and its derivatives are now billion dollar drugs, used in, and being evaluated for, a number of clinical applications. Taking advantage of its antifungal property, the molecular Target Of Rapamycin, TOR, was first described in the budding yeast Saccharomyces cerevisiae. TORs encode large, Ser/Thr protein kinases that reside in two distinct, structurally and functionally conserved, multi-protein complexes. In yeast, these complexes coordinate many different aspects of cell growth. TOR complex 1, TORC1, promotes protein synthesis and other anabolic processes, while inhibiting macroautophagy and other catabolic and stress-response processes. TORC2 primarily regulates cell polarity, although additional readouts of this complex are beginning to be characterized. TORC1 appears to be activated by nutrient cues and inhibited by stresses and rapamycin; however, detailed mechanisms are not known. In contrast, TORC2 is insensitive to rapamycin and physiological regulators of this complex have yet to be defined. Given the unsurpassed resources available to yeast researchers, this simple eukaryote continues to contribute to our understanding of eukaryotic cell growth in general and TOR function in particular

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“…34 A number of genes involved in autophagy and/or the cvt pathway, including Atg1, Atg11 and Atg17, have been implicated in regulation of pexophagy in H. polymorpha and in Saccharomyces cerevisiae, suggesting that there is overlap between the three pathways. 28,[33][34][35] In addition to activation of the autophagy machinery, a key determinant of pexophagy appears to be localized on the peroxisome membrane. Pex14, which is conserved from yeast to humans, has been shown to be a prime target for macropexophagy in H. polymorpha.…”

Section: Macroautophagy In Yeast Is a Multistep Process That Is Regulmentioning

confidence: 99%

Macroautophagy versus mitochondrial autophagy: a question of fate?

Kundu

Thompson²

2005

Cell Death Differ

106

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Autophagy is a catabolic process that allows recycling of cytoplasmic components (including organelles) into basic components, offering a bioenergetically efficient alternative to de novo synthesis. In yeast, autophagy functions primarily as an adaptive mechanism allowing survival in the response to changes in the availability of nutrients in the environment. Over the past decade, genetic screens performed in yeast have elucidated many of the molecular components involved in this adaptive response. [1][2][3] More recently, the roles of homologous genes are being explored in multicellular organisms and in cells derived from these organisms. 4 These studies have demonstrated that while autophagy is often induced as part of an adaptive response, induction of autophagy may also lead to cell death. During Drosophila larval development, for example, starvation-induced autophagy occurs in the larval fat body and is required for maintaining circulating nutrient levels and survival of the larvae under unfavorable nutritional conditions; 5 by contrast, programmed autophagy results in cell death and is the primary means of removing certain larval organs during metamorphosis. 6 On a cellular level, autophagy is observed prior to apoptosis in growth factor-deprived neuronal cultures. 7,8 In cells lacking critical proapoptotic proteins, the adaptive process of autophagy aimed at maintaining bioenergetic homeostasis can be unmasked in response to growthfactor withdrawal. 9 In contrast, cell death in response to a variety of chemicals has been suggested to result from autophagic destruction of the cell and to be suppressed by inhibition of autophagy. 10 The factors that determine whether induction of autophagy contributes to cell survival or cell death are not well-elucidated; however, two key issues may be the rate of autophagic degradation and the specificity of the engulfed components. Although autophagy is generally considered a nonspecific process, there are instances where the mitochondria (and other organelles) appear to be specifically targeted. Here, we focus on the signals and pathways involved in regulating the induction of autophagy and mitochondrial autophagy in yeast and how these processes are relevant to survival and death of mammalian cells.In general terms, 'autophagy' refers to any intracellular process that involves the degradation of cytosolic components by the lysosome. There are at least three distinct autophagic pathways: macroautophagy, microautophagy and chaperone-mediated autophagy. Macroautophagy is a multistep process by which portions of cytoplasm and/or organelles are sequestered in a double or multimembrane structure ('autophagosome') and delivered to the lysosome for degradation (Figure 1). Upon fusion of the autophagosome with the lysosome, it becomes an autophagolysosome or autophagic vacuole. Although macroautophagy is generally considered a nonspecific process there are instances in which organelles, such as mitochondria and peroxisomes, appear to be preferentially sequestered. These process...

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Peroxisome homeostasis in

Cited by 35 publications

References 53 publications

Autophagy and Related processes in Trypanosomatids: Insights from Genomic and Bioinformatic Analyses

Autophagy and Related processes in Trypanosomatids: Insights from Genomic and Bioinformatic Analyses

Cell growth control: little eukaryotes make big contributions

Macroautophagy versus mitochondrial autophagy: a question of fate?

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