Essential and distinct roles of phosphatidylinositol 4-kinases, Pik1p and Stt4p, in yeast autophagy

Kurokawa, Yuna; Konishi, Rikako; Yoshida, Akane; Tomioku, Kanna; Futagami, Taiki; Tamaki, Hiroyuki; Tanabe, Kenji; Fujita, Akikazu

doi:10.1016/j.bbalip.2019.05.004

Cited by 10 publications

(18 citation statements)

References 66 publications

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“…This model is inspired by the effects of nutrient starvation in both yeast and mammalian cells. In both cases, nutrient starvation triggers a reduction of Golgi PI(4)P levels due to PI4KB release from the Golgi combined with import of the PI(4)P phosphatase SAC1 at the Golgi [57,73], and this is linked to induction of autophagy at MERCs, which requires the activity of PI4KB in Golgi-derived vesicles [56,166]. The transfer of PI4KB-containing vesicles from the Golgi to MERCs involves NM2A [56,167,168], which is tightly associated with APOLs [8].…”

Section: Discussionmentioning

confidence: 99%

“…For example, (a) the PI(4)P-binding protein GOLPH3 binds to the NM2A-interacting myosin MYO18A [47][48][49][50], (b) ASAP1 interacts with the GOLPH3-binder ADP-ribosylation factor 1 and with NM2A [51][52][53][54], (c) the NM2A heavy chain MYH9 directly binds to anionic phospholipids [55], and (d) together with autophagy-related protein 9 (ATG9) and arfaptin 2, PI4KB and PI(4)P initiate autophagy in NM2A-driven vesicles derived from the trans-Golgi [56]. Given the requirement of PIK1 and ATG9 for autophagy initiation also in S. cerevisiae [57], Golgi PI (4)P-mediated autophagy is probably an evolutionary ancient process.…”

Section: Key Role Of Pi(4)p In Cellular Physiologymentioning

confidence: 99%

“…Although from the model this last effect could be expected to reduce PI4KB activity due to a lower level of PI4KB-stimulating APOL3 at the Golgi, no major difference in cellular PI(4)P level was observed [8]. I propose that interferon signalling induces PI4KB delocalization from the Golgi to the ER, like occurs following nutrient depletion for both PI4KB and PIK1/FRQ1 together with the reverse shuttling of the PI(4)P phosphatase suppressor of actin 1 (SAC1) from the ER to the Golgi [57,73]. Indeed, interferon signalling and energy deprivation share the characteristic of triggering autophagy [74,75], and several interferon-inducible Golgi GTPases drive the movement of Golgi membranes, with proteins such as APOL2, to MERCs [76][77][78].…”

Section: Relevance Of the Model To Kidney Diseasementioning

confidence: 99%

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The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

Pays

2020

The FEBS Journal

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The discovery that apolipoprotein L1 (APOL1) is the trypanolytic factor of human serum raised interest about the function of APOLs, especially following the unexpected finding that in addition to their protective action against sleeping sickness, APOL1 C-terminal variants also cause kidney disease. Based on the analysis of the structure and trypanolytic activity of APOL1, it was proposed that APOLs could function as ion channels of intracellular membranes and be involved in mechanisms triggering programmed cell death. In this review, the recent finding that APOL1 and APOL3 inversely control the synthesis of phosphatidylinositol-4-phosphate (PI(4)P) by the Golgi PI(4)-kinase IIIB (PI4KB) is commented. APOL3 promotes Ca 2+-dependent activation of PI4KB, but due to their increased interaction with APOL3, APOL1 C-terminal variants can inactivate APOL3, leading to reduction of Golgi PI(4)P synthesis. The impact of APOLs on several pathological processes that depend on Golgi PI(4)P levels is discussed. I propose that through their effect on PI4KB activity, APOLs control not only actomyosin activities related to vesicular trafficking, but also the generation and elongation of autophagosomes induced by inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Key Role Of Pi(4)p In Cellular Physiologymentioning

confidence: 99%

Section: Relevance Of the Model To Kidney Diseasementioning

confidence: 99%

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The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

Pays

2020

The FEBS Journal

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“…PIK3C3 is further phosphorylated on Thr159, which reduces its binding to BECN1 and results in autophagy inhibition. This Pik1 Sac1 [189,191,192,198]…”

Section: Phosphoregulation During Phagophore Nucleation: the Ptdins3k Complex I And Ptdins3pmentioning

confidence: 99%

Phosphoregulation of the autophagy machinery by kinases and phosphatases

et al. 2021

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Eukaryotic cells use post-translational modifications to diversify and dynamically coordinate the function and properties of protein networks within various cellular processes. For example, the process of autophagy strongly depends on the balanced action of kinases and phosphatases. Highly conserved from the budding yeast Saccharomyces cerevisiae to humans, autophagy is a tightly regulated self-degradation process that is crucial for survival, stress adaptation, maintenance of cellular and organismal homeostasis, and cell differentiation and development. Many studies have emphasized the importance of kinases and phosphatases in the regulation of autophagy and identified many of the core autophagy proteins as their direct targets. In this review, we summarize the current knowledge on kinases and phosphatases acting on the core autophagy machinery and discuss the relevance of phosphoregulation for the overall process of autophagy.

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“…Both phospholipases D (PLD) and the PI4 Kinase enzymes colocalize at autophagic structures in mammalian cells, even though their exact functions in autophagy are still to be determined [ 112 , 140 ]. Furthermore, the lipid PI4P is unevenly distributed in both leaflets of phagophore membranes from yeast and mammals, suggesting that the action of PI4K is tightly regulated in space [ 141 ]. Another example is the PHOSPHATIDYLINOSITOL SYNTHASE (PIS1) enzyme, which was shown to accumulate at the site of phagophore nucleation on ER subdomains of mammalian cells, and to colocalize with components of the initiation machinery [ 123 ].…”

Section: Membrane Lipids Are Fundamental Actors Of Autophagy Activity Induction and Regulation Upon Stressmentioning

confidence: 99%

How Lipids Contribute to Autophagosome Biogenesis, a Critical Process in Plant Responses to Stresses

Gomez

Lupette

Chambaud

et al. 2021

Cells

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Throughout their life cycle, plants face a tremendous number of environmental and developmental stresses. To respond to these different constraints, they have developed a set of refined intracellular systems including autophagy. This pathway, highly conserved among eukaryotes, is induced by a wide range of biotic and abiotic stresses upon which it mediates the degradation and recycling of cytoplasmic material. Central to autophagy is the formation of highly specialized double membrane vesicles called autophagosomes which select, engulf, and traffic cargo to the lytic vacuole for degradation. The biogenesis of these structures requires a series of membrane remodeling events during which both the quantity and quality of lipids are critical to sustain autophagy activity. This review highlights our knowledge, and raises current questions, regarding the mechanism of autophagy, and its induction and regulation upon environmental stresses with a particular focus on the fundamental contribution of lipids. How autophagy regulates metabolism and the recycling of resources, including lipids, to promote plant acclimation and resistance to stresses is further discussed.

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Essential and distinct roles of phosphatidylinositol 4-kinases, Pik1p and Stt4p, in yeast autophagy

Cited by 10 publications

References 66 publications

The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

Phosphoregulation of the autophagy machinery by kinases and phosphatases

How Lipids Contribute to Autophagosome Biogenesis, a Critical Process in Plant Responses to Stresses

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