scholarly journals Cell density-dependent linoleic acid toxicity to Saccharomyces cerevisiae

2011 ◽  
Vol 11 (5) ◽  
pp. 408-417 ◽  
Author(s):  
Túlio César Ferreira ◽  
Lídia Maria Pepe de Moraes ◽  
Élida Geralda Campos
2008 ◽  
Vol 74 (18) ◽  
pp. 5674-5685 ◽  
Author(s):  
S. Horowitz Brown ◽  
R. Zarnowski ◽  
W. C. Sharpee ◽  
N. P. Keller

ABSTRACT Aspergillus flavus differentiates to produce asexual dispersing spores (conidia) or overwintering survival structures called sclerotia. Results described here show that these two processes are oppositely regulated by density-dependent mechanisms and that increasing the cell density (from 101 to 107 cells/plate) results in the lowest numbers of sclerotial and the highest numbers of conidial. Extract from spent medium of low-cell-density cultures induced a high-sclerotium-number phenotype, whereas high-cell-density extract increased conidiation. Density-dependent development is also modified by changes in lipid availability. Exogenous linoleic acid increased sclerotial production at intermediate cell densities (104 and 105 cells/plate), whereas oleic and linolenic acids inhibited sclerotium formation. Deletion of Aflox encoding a lipoxygenase (LOX) greatly diminished density-dependent development of both sclerotia and conidia, resulting in an overall increase in the number of sclerotia and a decrease in the number of conidia at high cell densities (>105 cells/plate). Aflox mutants showed decreased linoleic acid LOX activity. Taken together, these results suggest that there is a quorum-sensing mechanism in which a factor(s) produced in dense cultures, perhaps a LOX-derived metabolite, activates conidium formation, while a factor(s) produced in low-density cultures stimulates sclerotium formation.


2019 ◽  
Vol 19 (5) ◽  
Author(s):  
Michela Winters ◽  
Nils Arneborg ◽  
Rudi Appels ◽  
Kate Howell

ABSTRACTQuorum sensing is a well-described mechanism of intercellular signalling among bacteria, which involves cell-density-dependent chemical signal molecules. The concentration of these quorum-sensing molecules increases in proportion to cell density until a threshold value is exceeded, which triggers a community-wide response. In this review, we propose that intercellular signalling mechanisms can be associated with a corresponding ecological interaction type based on similarities between how the interaction affects the signal receiver and producer. Thus, we do not confine quorum sensing, a specific form of intercellular signalling, to only cooperative behaviours. Instead, we define it as cell-density-dependent responses that occur at a critical concentration of signal molecules and through a specific signalling pathway. For fungal species, the medically important yeast Candida albicans has a well-described quorum sensing system, while this system is not well described in Saccharomyces cerevisiae, which is involved in food and beverage fermentations. The more precise definition for quorum sensing proposed in this review is based on the studies suggesting that S. cerevisiae may undergo intercellular signalling through quorum sensing. Through this lens, we conclude that there is a lack of evidence to support a specific signalling mechanism and a critical signal concentration of these behaviours in S. cerevisiae, and, thus, these features require further investigation.


2021 ◽  
Author(s):  
Trina Roy ◽  
Sinchan Ghosh ◽  
Bapi Saha ◽  
Sabyasachi Bhattacharya

Abstract Cell proliferation often experiences a density-dependent intrinsic proliferation rate (IPR) and negative feedback from growth-inhibiting molecules in culture media. The lack of flexible models with explanatory parameters fails to capture such a proliferation mechanism. We propose an extended logistic growth law with the density-dependent IPR and additional negative feedback. The extended parameters of the proposed model can be interpreted as density-dependent cell-cell cooperation and negative feedback on cell proliferation. Moreover, we incorporate further density regulation for flexibility in the model through environmental resistance on cells. The proposed growth law has similarities with the strong Allee model and harvesting phenomenon. We also develop the stochastic analog of the deterministic model by representing possible heterogeneity in growth-inhibiting molecules and environmental perturbation of the culture setup as correlated multiplicative and additive noises. The model provides a maximum sustainable stable cell density (MSSCD) and a new fitness measure for proliferative cells. The proposed model shows superiority to the logistic law after fitting to real cell culture datasets. We illustrate both MSSCD and the new cell fitness for a range of parameters. The cell density distributions reveal the chance of overproliferation, underproliferation, or decay for different parameter sets under the deterministic and stochastic setups.


2020 ◽  
Vol 45 (12) ◽  
pp. 795-800
Author(s):  
Takato Hara ◽  
Misato Saeki ◽  
Yuichi Negishi ◽  
Toshiyuki Kaji ◽  
Chika Yamamoto

2016 ◽  
Vol 229 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Erika Galgoczi ◽  
Florence Jeney ◽  
Annamaria Gazdag ◽  
Annamaria Erdei ◽  
Monika Katko ◽  
...  

During the course of Graves’ orbitopathy (GO), orbital fibroblasts are exposed to factors that lead to proliferation and extracellular matrix (ECM) overproduction. Increased levels of tissue plasminogen activator inhibitor type 1 (PAI-1 (SERPINE1)) might promote the accumulation of ECM components. PAI-1 expression is regulated by cell density and various cytokines and growth factors including transforming growth factorβ(TGF-β). We examined the effects of increasing cell densities and TGF-β on orbital fibroblasts obtained from GO patients and controls. Responses were evaluated by the measurement of proliferation, PAI-1 expression, and ECM production. There was an inverse correlation between cell density and the per cell production of PAI-1. GO orbital, normal orbital, and dermal fibroblasts behaved similarly in this respect. Proliferation rate also declined with increasing cell densities. Hyaluronan (HA) production was constant throughout the cell densities tested in all cell lines. In both GO and normal orbital fibroblasts, but not in dermal fibroblasts, TGF-β stimulated PAI-1 production in a cell density-dependent manner, reaching up to a five-fold increase above baseline. This has been accompanied by increased HA secretion and pericellular HA levels at high cell densities. Increasing cell density is a negative regulator of proliferation and PAI-1 secretion both in normal and GO orbital fibroblasts; these negative regulatory effects are partially reversed in the presence of TGF-β. Cell density-dependent regulation of PAI-1 expression in the orbit, together with the local cytokine environment, may have a regulatory role in the turnover of the orbital ECM and may contribute to the expansion of orbital soft tissue in GO.


2005 ◽  
Vol 56 (1) ◽  
pp. 189-203 ◽  
Author(s):  
Timothy D. Minogue ◽  
Aurelien L. Carlier ◽  
Maria D. Koutsoudis ◽  
Susanne B. Von Bodman

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