scholarly journals Measuring Single-Cell Phenotypic Growth Heterogeneity Using a Microfluidic Cell Volume Sensor

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Wenyang Jing ◽  
Brendan Camellato ◽  
Ian J. Roney ◽  
Mads Kaern ◽  
Michel Godin
1993 ◽  
Vol 265 (2) ◽  
pp. C447-C452 ◽  
Author(s):  
J. C. Parker

Urea equilibrates rapidly across the red blood cells of mammals. It was speculated that urea might affect the cell volume sensor by virtue of its properties as a protein perturbant. At concentrations of 0.1-0.6 M, urea caused a decrease in the set points for shrinkage-induced Na-H exchange, swelling-induced K-Cl cotransport, and swelling-induced Ca-Na exchange of dog red blood cells. Okadaic acid opposed the action of urea on all three pathways. The effects were reversible and not due to cyanate. Formamide and acetamide had actions similar to urea but not as potent. Equimolar concentrations of methanol had no effect. The coordinated influence of urea on three separate volume-activated transporters suggests that it acts on a mutual regulatory system that senses and transduces volume stimuli.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Priyanka Rana ◽  
Manabu Kurokawa ◽  
Michael Model

1999 ◽  
Vol 93 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Louise Allansson ◽  
Siamak Khatibi ◽  
Tomas Gustavsson ◽  
Fredrik Blomstrand ◽  
Torsten Olsson ◽  
...  

2020 ◽  
Author(s):  
Francisco Diaz-Pascual ◽  
Knut Drescher

<p>Bacterial cells are often exposed to stress by changes in their environment. During the last decades the response of isolated cells to stress has been investigated in great detail. By contrast, little is known about the emergent multicellular level responses to stress, such as antibiotic exposure. Studying responses at the community level is key to understand the structure and function of the most common bacterial state: the multicellular communities termed biofilms. Here, by analysing <em>Vibrio cholerae</em> biofilms exposed to all different classes of antibiotics with single-cell resolution, we found that inhibition of protein synthesis cause striking changes in cell volume and biofilm architecture. The observed changes in cell volume are a single-cell level response driven by metabolic effects of the translational inhibition. The multicellular-level responses result from changes in matrix composition, matrix-cell dissociation and mechanical properties of the biofilms. We observed that these antibiotic-induced changes in biofilm architecture have strong consequences on the ecological dynamics of biofilms by making biofilms prone to invasion by bacteriophages and other bacterial cells. These mechanistic and ecological consequences of the emergent group-level architectural response to antibiotics are important to fully understand the ecological succession of biofilms and the implications of antibiotic therapy.</p>


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