Burst size of bacteriophage SP82 as a function of growth rate of its host Bacillus subtilis

1982 ◽  
Vol 28 (11) ◽  
pp. 1277-1280 ◽  
Author(s):  
Vera Webb ◽  
Eugene Leduc ◽  
George B. Spiegelman
Keyword(s):  
Growth Rate ◽  
Bacillus Subtilis ◽  
Cell Growth ◽  
Bacterial Growth ◽  
Growth Rates ◽  
Burst Size ◽  
Cell Growth Rate ◽  
Natural Logarithm ◽  
Bacterial Growth Rates

The burst size of bacteriophage SP82 in Bacillus subtilis has been measured under conditions of varying bacterial growth rates. The natural logarithm of the burst size was found to vary linearly with cell growth rate.

82 Methyl Donor Supplementation Alters Cytosine Methylation and Biological Processes of Cells Cultured in Divergent Glucose Media Reflecting Improvements in Mitochondrial Respiration and Cell Growth Rate

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 109-109
Author(s):  
Matthew S Crouse ◽  
Wellison Jarles Da Silva Diniz ◽  
Joel Caton ◽  
Carl R Dahlen ◽  
Lawrence P Reynolds ◽  
...  
Keyword(s):  
Growth Rate ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Vitamin B12 ◽  
Mitochondrial Respiration ◽  
Cytosine Methylation ◽  
Biological Processes ◽  
Cell Growth Rate ◽  
Metabolic Processes ◽  
Positive Regulation

Abstract We hypothesized that supplementation of one-carbon metabolites (OCM: methionine, folate, choline, and vitamin B12) to bovine embryonic tracheal fibroblasts in divergent glucose media would alter cytosine methylation, and alterations in cytosine methylation will reflect biological processes matching previously improved mitochondrial respiration, cell proliferation, and cell growth rate data. Cells were cultured with 1g/L glucose (Low) or 4.5g/L glucose (High). Control medium (CON) contained basal concentrations of folate (0.001g/L), choline (0.001g/L), vitamin B12 (4µg/L), and methionine (0.015g/L). The OCM were supplemented at 2.5 and 5 times (2.5X and 5X, respectively) the CON media, except methionine was limited to 2X across all supplemented treatments. Cells were passaged three times in their treatment media before DNA extraction. Reduced representation bisulfite sequencing was adopted to analyze and compare the genomic methylation patterns within and across treatments using edgeR. Biological processes (BP) were retrieved based on the nearest genes of differentially methylated cytosines (P < 0.01) for each comparison between treatments. In both Low and High treatments, greater OCM increased the proportion of hypomethylated vs. hypermethylated cytosines. Functional analyses pointed out positive regulation of BP related to energy metabolism, except for the contrasts within the High group. Among the BP, we can highlight positive regulation of: GTPase activity, catalytic activity, molecular function, protein modification processes, phosphorylation, protein phosphorylation, cellular protein metabolic processes, MAPK cascade, and metabolic processes. These data support previously reported results from this experiment that showed increased mitochondrial respiration, cell proliferation, and growth rates with increasing OCM levels. We interpret these data to imply that when energy and OCM requirements are met for growth and basal methylation levels, DNA methylation levels decrease which may allow for greater transcription. Thus, OCM can be utilized for other functions such as polyamine synthesis, nucleotide synthesis, energetic metabolites, and phosphatidylcholine synthesis. USDA is an equal opportunity provider and employer.

PGE2 inhibition & interferon-gamma restoration of type 1 T cell growth rate in atopic dermatitis

1993 ◽  
Vol 6 (1) ◽  
pp. 27
Author(s):  
Sai C. Chan ◽  
Shi-Hua Li ◽  
William R. Henderson ◽  
Jon M. Hanifin
Keyword(s):  
Growth Rate ◽  
Atopic Dermatitis ◽  
T Cell ◽  
Cell Growth ◽  
Interferon Gamma ◽  
Cell Growth Rate ◽  
T Cell Growth

scholarly journals Evolutionary Systems Biology integration of multi-level CTMC interaction models of biochemistry and cancer cell growth using Evolvix.

2017 ◽  
Author(s):  
Jocelyn R Meyer ◽  
Elaine Alarid ◽  
Laurence Loewe
Keyword(s):  
Growth Rate ◽  
Cell Growth ◽  
Cancer Cell ◽  
Growth Rates ◽  
Population Variation ◽  
Mass Action ◽  
Model Description ◽  
Estrogen Metabolism ◽  
Cancer Cell Growth ◽  
Multi Level

While biochemistry evidently affects the growth rate of cells, many biochemists routinely ignore population variation, just like population geneticists usually ignore causal details of biochemistry that underpin a change in growth rate caused by a mutation. A true EvoSysBio integration requires an explicit mechanism for how molecular reaction rates affect the reproduction rates that determine the fitness of an organism. Here we simulate a very simple and completely explicit Continuous-Time Markov Chain (CTMC) model of cancer cells whose growth rate is affected by the biochemical equilibrium between two molecular complexes. Approximately 70% of breast cancers are of a type that overexpress Estrogen Receptor-alpha (ERα). Cell growth in this type of cancer is inhibited by hormonal therapies that antagonize ERα function as a transcription factor. ERα is encoded by the ESR1 gene, which itself is a target of ERα mediated transcription. When activated by estrogen, ERα binds to the ESR1 promoter, repressing new synthesis of ERα protein. Estrogen binding also induces pathways that lead to degradation of ERα protein. This negative feedback loop is finely tuned to natural levels of estrogen and results in natural levels of growth. In breast cancer, the system is thrown off its natural course such that increased levels of ERα induce levels of cell growth that can lead to cancer. Thus, both genetic changes to the ESR1 promoter, ERα protein degradation, and biochemical changes in estrogen metabolism can effectively cause changes in cell growth rates, which can be seen as the ‘fitness’ of a cancer cell. Predicting cancer cell growth in this system raises a conceptual multi-level simulation problem, because the molecular aspects of this model need to compute the biochemistry in a way that influences growth rates at the cellular level, without resetting growth at each cell division. We present progress towards addressing this simulation challenge in pure mass-action models, which we implemented using the Evolvix model description language. We found that such models can be constructed in more than one way. We explored some candidate model properties that could aid efforts to develop abstractions for more efficiently simulating the common multi-level modeling problems behind many important biological questions. These efforts are ongoing and aim to find efficient ways of encoding and exploring such models in silico. In particular, we are investigating how architecting a new compiler for a general-purpose programming language for biology could improve the efficiency of analyzing the dynamic multi-level simulation scenarios that characterize many questions in EvoSysBio. Progress can be followed at http://evolvix.org.

scholarly journals ANTAGONISM BY DIBUTYRYL ADENOSINE CYCLIC 3',5'-MONOPHOSPHATE AND TESTOSTERONE OF CELL ROUNDING REACTIONS

1973 ◽  
Vol 59 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Brian Storrie
Keyword(s):  
Growth Rate ◽  
Protein Synthesis ◽  
Cell Growth ◽  
Concanavalin A ◽  
Divalent Cations ◽  
Cell Growth Rate ◽  
Dibutyryl Camp ◽  
Cell Rounding ◽  
Drug Removal ◽  
Kinetics Of

In an attempt to understand further the mechanism of the morphological and functional "reverse transformation" of CHO-K1 cells induced by dibutyryl adenosine cyclic 3',5'-monophosphate (cAMP) and testosterone, the kinetics of variation in the susceptibility of cells to rounding after the addition or deletion of dibutyryl cAMP and testosterone have been investigated. Changes in susceptibility to cell rounding upon removal of divalent cations or pulse exposure to concanavalin A were complete within 0.5–1 h after addition or deletion of drug. In comparison, the gross conversion of CHO-K1 cells from epithelial- to fibroblast-like morphology after drug treatment or the converse change after drug removal required 8 or 4 h, respectively. The effects on cell rounding are not caused by an effect of dibutyryl cAMP upon cell growth rate. Inhibitor experiments indicate that the changes investigated do not require continued RNA or protein synthesis and are not prevented by agents which depolymerize microtubules.

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