Bidirectional regulation between TORC1 and autophagy in<i>Saccharomyces cerevisiae</i>

Shin, Chun-Shik; Huh, Won-Ki

doi:10.4161/auto.7.8.15696

Cited by 23 publications

(18 citation statements)

References 43 publications

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“…Indeed, we find that all concentrations tested of rapamycin in the range of 20 -200 ng/ml are equally effective at inducing autophagy ( Fig. 2A), a key downstream consequence of lowered TORC1 activity (14,28,29), and at inhibiting proliferation ( Fig. 2B) in wild-type cells.…”

Section: Ego Complex Is Selectively Required For Recovery Frommentioning

confidence: 98%

Recovery from Rapamycin

Evans

Burgess

Gray

2014

Journal of Biological Chemistry

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Background:The EGO complex activates yeast TORC1 and is somehow required for recovery from rapamycin, a potent inhibitor of TORC1. Results: Rapamycin-insensitive activity of TORC1 partly depends on the EGO complex and supports residual cell proliferation that dilutes the metabolically stable drug among progeny cells. Conclusion: TORC1 activity is required to dilute rapamycin. Significance: Rapamycin only partly inhibits yeast TORC1.

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Section: Ego Complex Is Selectively Required For Recovery Frommentioning

confidence: 98%

Recovery from Rapamycin

Evans

Burgess

Gray

2014

Journal of Biological Chemistry

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“…Furthermore, reactivation of mTOR during sustained nutrient starvation is required to allow re-formation and recycling of lysosomes following the massive delivery of autophagic membrane and cargo. This recovery of mTOR activity and lysosomal integrity is dependent on autophagic degradation and efflux, suggesting that nutrients derived from the autolysosome are able to promote mTOR activation (Rong et al, 2011;Shin and Huh, 2011;Yu et al, 2010). Nutrient efflux from autolysosomes also appears to promote TOR signaling required for secretory activity in senescent cells (Narita et al, 2011).…”

Section: Autophagy and The Cell Growth Machinerymentioning

confidence: 99%

Autophagy and cell growth – the yin and yang of nutrient responses

Neufeld

2012

Journal of Cell Science

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SummaryAs a response to nutrient deprivation and other cell stresses, autophagy is often induced in the context of reduced or arrested cell growth. A plethora of signaling molecules and pathways have been shown to have opposing effects on cell growth and autophagy, and results of recent functional screens on a genomic scale support the idea that these processes might represent mutually exclusive cell fates. Understanding the ways in which autophagy and cell growth relate to one another is becoming increasingly important, as new roles for autophagy in tumorigenesis and other growth-related phenomena are uncovered. This Commentary highlights recent findings that link autophagy and cell growth, and explores the mechanisms underlying these connections and their implications for cell physiology and survival. Autophagy and cell growth can inhibit one another through a variety of direct and indirect mechanisms, and can be independently regulated by common signaling pathways. The central role of the mammalian target of rapamycin (mTOR) pathway in regulating both autophagy and cell growth exemplifies one such mechanism. In addition, mTOR-independent signaling and other more direct connections between autophagy and cell growth will also be discussed.This article is part of a Minifocus on Autophagy. For further reading, please see related articles: 'Ubiquitin-like proteins and autophagy at a glance' by Tomer Shpilka et al. (J. Cell Sci. 125, 2343-2348 and 'Autophagy and cancer -issues we need to digest' by Emma Liu and Kevin Ryan (J. Cell Sci. 125, 2349-2358).

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“…Because PKA is known to inhibit the initiation of autophagy (11), these results point toward feedback regulation. A bidirectional regulation between TOR and autophagy was shown recently (31). Inhibition of TOR lifts the repression of autophagy, and recycled amino acids reactivate TOR, which in turns attenuates autophagy.…”

Section: Filteau Et Almentioning

confidence: 99%

Systematic identification of signal integration by protein kinase A

Filteau

Diss

Torres-Quiroz

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Cellular processes and homeostasis control in eukaryotic cells is achieved by the action of regulatory proteins such as protein kinase A (PKA). Although the outbound signals from PKA directed to processes such as metabolism, growth, and aging have been well charted, what regulates this conserved regulator remains to be systematically identified to understand how it coordinates biological processes. Using a yeast PKA reporter assay, we identified genes that influence PKA activity by measuring proteinprotein interactions between the regulatory and the two catalytic subunits of the PKA complex in 3,726 yeast genetic-deletion backgrounds grown on two carbon sources. Overall, nearly 500 genes were found to be connected directly or indirectly to PKA regulation, including 80 core regulators, denoting a wide diversity of signals regulating PKA, within and beyond the described upstream linear pathways. PKA regulators span multiple processes, including the antagonistic autophagy and methionine biosynthesis pathways. Our results converge toward mechanisms of PKA posttranslational regulation by lysine acetylation, which is conserved between yeast and humans and that, we show, regulates protein complex formation in mammals and carbohydrate storage and aging in yeast. Taken together, these results show that the extent of PKA input matches with its output, because this kinase receives information from upstream and downstream processes, and highlight how biological processes are interconnected and coordinated by PKA.Ras/cAMP/PKA pathway | acetylation | methionine | autophagy | TOR

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Bidirectional regulation between TORC1 and autophagy inSaccharomyces cerevisiae

Cited by 23 publications

References 43 publications

Recovery from Rapamycin

Recovery from Rapamycin

Autophagy and cell growth – the yin and yang of nutrient responses

Systematic identification of signal integration by protein kinase A

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