Release from Density Dependent Growth Inhibition by Proteolytic Enzymes

Nature ◽  
1970 ◽  
Vol 227 (5260) ◽  
pp. 843-845 ◽  
Author(s):  
B. M. SEFTON ◽  
H. RUBIN
Nature ◽  
1974 ◽  
Vol 250 (5469) ◽  
pp. 739-741 ◽  
Author(s):  
IIH-NAN CHOU ◽  
PAUL H. BLACK ◽  
RICHARD O. ROBLIN

2019 ◽  
Vol 49 (4) ◽  
pp. 590-604.e9 ◽  
Author(s):  
Takuya Ooki ◽  
Naoko Murata-Kamiya ◽  
Atsushi Takahashi-Kanemitsu ◽  
Weida Wu ◽  
Masanori Hatakeyama

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0165358 ◽  
Author(s):  
Núria Rovira-Graells ◽  
Sara Aguilera-Simón ◽  
Elisabet Tintó-Font ◽  
Alfred Cortés

1974 ◽  
Vol 249 (11) ◽  
pp. 3483-3488
Author(s):  
Nancy Lewis Baenziger ◽  
Christa H. Jacobi ◽  
Robert E. Thach

2021 ◽  
Author(s):  
Sabrin Hilau ◽  
Sophia Katz ◽  
Tanya Wasserman ◽  
Ruth Hershberg ◽  
Yonatan Savir

Although closely related genetically, bacterial strains belonging to the same species show significant variability in their growth and death dynamics. However, our understanding of the underlying processes that lead to this variability is still lacking. Here, we measured the growth and death dynamics of 11 strains of E. coli originating from different hosts and developed a mathematical model that captures their growth and death dynamics. Our model considers two environmental factors that determine growth dynamics: resource utilization efficiency and density-dependent growth inhibition. Here we show that both factors are required to capture the measured dynamics. Interestingly, our model results indicate that the main process that determines the major differences between the strains is the critical density at which they slow down their growth, rather than maximal growth rate or death rate. Finally, we found that bacterial growth and death dynamics can be reduced to only two dimensions and described by death rates and density-dependent growth inhibition alone.


1984 ◽  
Vol 4 (8) ◽  
pp. 1572-1576
Author(s):  
S Powers ◽  
P B Fisher ◽  
R Pollack

We have measured in a defined serum-free medium the platelet-derived growth factor (PDGF) and insulin requirements of normal Swiss 3T3 cells, simian virus 40-transformed 3T3 cells, and partial revertants of simian virus 40-transformed 3T3 cells. Swiss 3T3 cells displayed strong requirements for both PDGF and insulin. Both of these requirements were significantly diminished in simian virus 40-transformed 3T3 cells. Analysis of the PDGF and insulin requirements of the revertants indicated that the loss of either of these two growth factor requirements was not necessarily linked to the other; rather, the growth factor requirements were specifically associated with other parameters of transformation. The reacquisition of a PDGF requirement cosegregated with reversion to density-dependent growth inhibition, whereas reacquisition of a normal insulin requirement cosegregated with reversion to a normal growth dependence on calf serum. Anchorage dependence was dissociable from both growth factor requirements. The relationship between the PDGF requirement and density-dependent growth inhibition was further analyzed in normal 3T3 cells by measuring the PDGF requirement at different cell densities. At high cell densities, the requirement for PDGF became significantly greater. We suggest that at least in part the ability of transformed cells to grow to high saturation densities results from their loss of a requirement for PDGF.


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