ArticleMolecular and cellular biology2017
TOR Complex 2-Regulated Protein Kinase Fpk1 Stimulates Endocytosis via Inhibition of Ark1/Prk1-Related Protein Kinase Akl1 in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- The Yeast Gsk-3 Kinase Mck1 Is Necessary for Cell Wall Remodeling in Glucose-Starved and Cell Wall-Stressed Cells.International journal of molecular sciences · 2025Article
- Flipping the script: Advances in understanding how and why P4-ATPases flip lipid across membranes.Biochimica et biophysica acta. Molecular cell research · 2024Review
- The Ypk1 protein kinase signaling pathway is rewired and not essential for viability in Candida albicans.PLoS genetics · 2023Article
- Understanding the interplay of membrane trafficking, cell surface mechanics, and stem cell differentiation.Seminars in cell & developmental biology · 2023Review
- Article
- TOR complex 2 is a master regulator of plasma membrane homeostasis.The Biochemical journal · 2022Article
- The PH Domain and C-Terminal polyD Motif of Phafin2 Exhibit a Unique Concurrence in Animals.Membranes · 2022Article
- Environmental control of Pub1 (NEDD4 family E3 ligase) inLife science alliance · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- Investigation the global effect of rare earth gadolinium on the buddingFrontiers in microbiology · 2022Article
- Nickel induced cell impairments are negatively regulated by the Tor1 kinase in Schizosaccharomyces pombe.World journal of microbiology & biotechnology · 2021Article
- Phosphorylation of mRNA-Binding Proteins Puf1 and Puf2 by TORC2-Activated Protein Kinase Ypk1 Alleviates Their Repressive Effects.Membranes · 2021Article
- TOR complex 2 (TORC2) signaling and the ESCRT machinery cooperate in the protection of plasma membrane integrity in yeast.The Journal of biological chemistry · 2020Article
- Article
- An optogenetic system to control membrane phospholipid asymmetry through flippase activation in budding yeast.Scientific reports · 2020Article
- G protein α subunit suppresses sporangium formation through a serine/threonine protein kinase in Phytophthora sojae.PLoS pathogens · 2020Article
- TORC2 controls endocytosis through plasma membrane tension.The Journal of cell biology · 2019Article
- Rab5 GTPases are required for optimal TORC2 function.The Journal of cell biology · 2019Article
- Phosphorylation by the stress-activated MAPK Slt2 down-regulates the yeast TOR complex 2.Genes & development · 2018Article
- TOR complex 2-regulated protein kinase Ypk1 controls sterol distribution by inhibiting StARkin domain-containing proteins located at plasma membrane-endoplasmic reticulum contact sites.Molecular biology of the cell · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Depending on the stress, plasma membrane alterations activate or inhibit yeast target of rapamycin (TOR) complex 2, which, in turn, upregulates or downregulates the activity of its essential downstream effector, protein kinase Ypk1. Through phosphorylation of multiple substrates, Ypk1 controls many processes that restore homeostasis. One such substrate is protein kinase Fpk1, which is negatively regulated by Ypk1. Fpk1 phosphorylates and stimulates flippases that translocate aminoglycerophospholipids from the outer to the inner leaflet of the plasma membrane. Fpk1 has additional roles, but other substrates were uncharacterized. We show that Fpk1 phosphorylates and inhibits protein kinase Akl1, related to protein kinases Ark1 and Prk1, which modulate the dynamics of actin patch-mediated endocytosis. Akl1 has two Fpk1 phosphorylation sites (Ark1 and Prk1 have none) and is hypophosphorylated when Fpk1 is absent. Conversely, under conditions that inactivate TORC2-Ypk1 signaling, which alleviates Fpk1 inhibition, Akl1 is hyperphosphorylated. Monitoring phosphorylation of known Akl1 substrates (Sla1 and Ent2) confirmed that Akl1 is hyperactive when not phosphorylated by Fpk1. Fpk1-mediated negative regulation of Akl1 enhances endocytosis, because an Akl1 mutant immune to Fpk1 phosphorylation causes faster dissociation of Sla1 from actin patches, confers elevated resistance to doxorubicin (a toxic compound whose entry requires endocytosis), and impedes Lucifer yellow uptake (a marker of fluid phase endocytosis). Thus, TORC2-Ypk1, by regulating Fpk1-mediated phosphorylation of Akl1, adjusts the rate of endocytosis.
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