scholarly journals Exo70p mediates the secretion of specific exocytic vesicles at early stages of the cell cycle for polarized cell growth

2007 ◽  
Vol 176 (6) ◽  
pp. 771-777 ◽  
Author(s):  
Bing He ◽  
Fengong Xi ◽  
Jian Zhang ◽  
Daniel TerBush ◽  
Xiaoyu Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Plasma Membrane ◽  
Cell Growth ◽  
Daughter Cell ◽  
Protein Processing ◽  
Vesicle Formation ◽  
Secretory Vesicles ◽  
Early Stages ◽  
Polarized Cell Growth ◽  
Vesicle Secretion

In budding yeast, two classes of post-Golgi secretory vesicles carrying different sets of cargoes typified by Bgl2p and invertase are delivered to the plasma membrane for secretion. The exocyst is implicated in tethering these vesicles to the daughter cell membrane for exocytosis. In this study, we report that mutations in the exocyst component Exo70p predominantly block secretion of the Bgl2p vesicles. Furthermore, a defect in invertase vesicle trafficking caused by vps1Δ or pep12Δ in the exo70 mutant background is detrimental to the cell. The secretion defect in exo70 mutants was most pronounced during the early budding stage, which affected daughter cell growth. The selective secretion block does not occur at the vesicle formation or sorting stage because the exocytic vesicles are properly generated and protein processing is normal in the exo70 mutants. Our study suggests that Exo70p functions primarily at early stages of the cell cycle in Bgl2p vesicle secretion, which is critical for polarized cell growth.

scholarly journals Membrane association and functional regulation of Sec3 by phospholipids and Cdc42

2008 ◽  
Vol 180 (1) ◽  
pp. 145-158 ◽  
Author(s):  
Xiaoyu Zhang ◽  
Kelly Orlando ◽  
Bing He ◽  
Fengong Xi ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Yeast Cells ◽  
Membrane Association ◽  
Secretory Vesicles ◽  
Cell Morphogenesis ◽  
Guanosine Triphosphate ◽  
Polarized Cell Growth ◽  
N Terminus ◽  
Functional Regulation ◽  
Key Residues

The exocyst is an octameric protein complex implicated in tethering post-Golgi secretory vesicles at the plasma membrane in preparation for fusion. However, it is not clear how the exocyst is targeted to and physically associates with specific domains of the plasma membrane and how its functions are regulated at those regions. We demonstrate that the N terminus of the exocyst component Sec3 directly interacts with phosphatidylinositol 4,5-bisphosphate. In addition, we have identified key residues in Sec3 that are critical for its binding to the guanosine triphosphate–bound form of Cdc42. Genetic analyses indicate that the dual interactions of Sec3 with phospholipids and Cdc42 control its function in yeast cells. Disrupting these interactions not only blocks exocytosis and affects exocyst polarization but also leads to defects in cell morphogenesis. We propose that the interactions of Sec3 with phospholipids and Cdc42 play important roles in exocytosis and polarized cell growth.

scholarly journals A conserved signaling network monitors delivery of sphingolipids to the plasma membrane in budding yeast

2017 ◽  
Vol 28 (20) ◽  
pp. 2589-2599 ◽  
Author(s):  
Jesse Clarke ◽  
Noah Dephoure ◽  
Ira Horecka ◽  
Steven Gygi ◽  
Douglas Kellogg
Keyword(s):  
Cell Cycle ◽  
Plasma Membrane ◽  
Cell Growth ◽  
Membrane Trafficking ◽  
Ribosome Biogenesis ◽  
Essential Role ◽  
Budding Yeast ◽  
Control Cell ◽  
Signaling Network ◽  
Membrane Growth

In budding yeast, cell cycle progression and ribosome biogenesis are dependent on plasma membrane growth, which ensures that events of cell growth are coordinated with each other and with the cell cycle. However, the signals that link the cell cycle and ribosome biogenesis to membrane growth are poorly understood. Here we used proteome-wide mass spectrometry to systematically discover signals associated with membrane growth. The results suggest that membrane trafficking events required for membrane growth generate sphingolipid-dependent signals. A conserved signaling network appears to play an essential role in signaling by responding to delivery of sphingolipids to the plasma membrane. In addition, sphingolipid-dependent signals control phosphorylation of protein kinase C (Pkc1), which plays an essential role in the pathways that link the cell cycle and ribosome biogenesis to membrane growth. Together these discoveries provide new clues as to how growth-­dependent signals control cell growth and the cell cycle.

scholarly journals Polarized growth and organelle segregation in yeast

2003 ◽  
Vol 160 (6) ◽  
pp. 811-816 ◽  
Author(s):  
Anthony Bretscher
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Secretory Vesicles ◽  
Polarized Growth ◽  
Yeast Growth ◽  
Fate Determination ◽  
Organelle Segregation ◽  
Specific Receptors ◽  
Actin Cables ◽  
Specific Degradation

In yeast, growth and organelle segregation requires formin-dependent assembly of polarized actin cables. These tracks are used by myosin Vs to deliver secretory vesicles for cell growth, organelles for their segregation, and mRNA for fate determination. Several specific receptors have been identified that interact with the cargo-binding tails of the myosin Vs. A recent study implicates specific degradation in the bud of the vacuolar receptor, Vac17, as a mechanism for cell cycle–regulated segregation of this organelle.

scholarly journals Conserved Ark1-related kinases control TORC2 signaling

2019 ◽  
Author(s):  
Maria Alcaide-Gavilán ◽  
Selene Banuelos ◽  
Rafael Lucena ◽  
Douglas R. Kellogg
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Plasma Membrane ◽  
Cell Growth ◽  
Cell Size ◽  
Cell Cycle Progression ◽  
Coordinated Control ◽  
Cycle Progression ◽  
Membrane Growth ◽  
Slow Growing

AbstractIn all orders of life, cell cycle progression is dependent upon cell growth, and the extent of growth required for cell cycle progression is proportional to growth rate. Thus, cells growing rapidly in rich nutrients are substantially larger than slow growing cells. In budding yeast, a conserved signaling network surrounding Tor complex 2 (TORC2) controls growth rate and cell size in response to nutrient availability. Here, a search for new components of the TORC2 network identified a pair of redundant kinase paralogs called Ark1 and Prk1. Previous studies found that Ark/Prk play roles in endocytosis. Here, we show that Ark/Prk are embedded in the TORC2 network, where they appear to influence TORC2 signaling independently of their roles in endocytosis. We also show that reduced endocytosis leads to increased cell size, which indicates that cell size homeostasis requires coordinated control of plasma membrane growth and endocytosis. The discovery that Ark/Prk are embedded in the TORC2 network suggests a model in which TORC2-dependent signals control both plasma membrane growth and endocytosis, which would ensure that the rates of each process are matched to each other and to the availability of nutrients so that cells achieve and maintain an appropriate size.

scholarly journals Exo-endocytic trafficking and the septin-based diffusion barrier are required for the maintenance of Cdc42p polarization during budding yeast asymmetric growth

2011 ◽  
Vol 22 (5) ◽  
pp. 624-633 ◽  
Author(s):  
Kelly Orlando ◽  
Xiaoli Sun ◽  
Jian Zhang ◽  
Tu Lu ◽  
Lauren Yokomizo ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cell Growth ◽  
Membrane Trafficking ◽  
Daughter Cell ◽  
Lateral Diffusion ◽  
Cell Cortex ◽  
Actin Organization ◽  
Cell Plasma ◽  
Biochemical Fractionation ◽  
Asymmetric Growth

Cdc42p plays a central role in asymmetric cell growth in yeast by controlling actin organization and vesicular trafficking. However, how Cdc42p is maintained specifically at the daughter cell plasma membrane during asymmetric cell growth is unclear. We have analyzed Cdc42p localization in yeast mutants defective in various stages of membrane trafficking by fluorescence microscopy and biochemical fractionation. We found that two separate exocytic pathways mediate Cdc42p delivery to the daughter cell. Defects in one of these pathways result in Cdc42p being rerouted through the other. In particular, the pathway involving trafficking through endosomes may couple Cdc42p endocytosis from, and subsequent redelivery to, the plasma membrane to maintain Cdc42p polarization at the daughter cell. Although the endo-exocytotic coupling is necessary for Cdc42p polarization, it is not sufficient to prevent the lateral diffusion of Cdc42p along the cell cortex. A barrier function conferred by septins is required to counteract the dispersal of Cdc42p and maintain its localization in the daughter cell but has no effect on the initial polarization of Cdc42p at the presumptive budding site before symmetry breaking. Collectively, membrane trafficking and septins function synergistically to maintain the dynamic polarization of Cdc42p during asymmetric growth in yeast.

scholarly journals A conserved signaling network monitors delivery of sphingolipids to the plasma membrane in budding yeast

2017 ◽  
Author(s):  
Jesse Clarke ◽  
Noah Dephoure ◽  
Ira Horecka ◽  
Steven Gygi ◽  
Douglas Kellogg
Keyword(s):  
Cell Cycle ◽  
Plasma Membrane ◽  
Cell Growth ◽  
Membrane Trafficking ◽  
Ribosome Biogenesis ◽  
Essential Role ◽  
Budding Yeast ◽  
Control Cell ◽  
Signaling Network ◽  
Membrane Growth

AbstractIn budding yeast, cell cycle progression and ribosome biogenesis are dependent upon plasma membrane growth, which ensures that events of cell growth are coordinated with each other and with the cell cycle. However, the signals that link the cell cycle and ribosome biogenesis to membrane growth are poorly understood. Here, we used proteome-wide mass spectrometry to systematically discover signals associated with membrane growth. The results suggest that membrane trafficking events required for membrane growth generate sphingolipid-dependent signals. A conserved signaling network plays an essential role in signaling by responding to delivery of sphingolipids to the plasma membrane. In addition, sphingolipid-dependent signals control phosphorylation of protein kinase C (Pkc1), which plays an essential role in the pathways that link the cell cycle and ribosome biogenesis to membrane growth. Together, these discoveries provide new clues to how growth-dependent signals control cell growth and the cell cycle.

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