scholarly journals Macromolecular Crowding: a Hidden Link Between Cell Volume and Everything Else

2021 ◽  
Vol 55 (S1) ◽  
pp. 25-40
Keyword(s):  
Experimental Evidence ◽  
Cell Volume ◽  
Cell Density ◽  
Physiological Mechanism ◽  
Macromolecular Crowding ◽  
Cellular Responses ◽  
Macromolecular Complexes ◽  
Chemical Equilibria ◽  
General Overview ◽  
Volume Recovery

High density of intracellular macromolecules creates a special condition known as macromolecular crowding (MC). One well-established consequence of MC is that only a slight change in the concentration of macromolecules (e.g., proteins) results in a shift of chemical equilibria towards the formation of macromolecular complexes and oligomers. This suggests a physiological mechanism of converting cell density changes into cellular responses. In this review, we start by providing a general overview of MC; then we examine the available experimental evidence that MC may act as a direct signaling factor in several types of cellular activities: mechano- and osmosensing, cell volume recovery in anisosmotic solutions, and apoptotic shrinkage. The latter phenomenon is analyzed in particular detail, as persistent shrinkage is known both to cause apoptosis and to occur during apoptosis resulting from other stimuli. We point to specific apoptotic reactions that involve formation of macromolecular complexes and, therefore, may provide a link between shrinkage and downstream responses.

scholarly journals The ionic basis of the hypo-osmotic depolarization in neurons from the opisthobranch mollusc Elysia chlorotica

1992 ◽  
Vol 163 (1) ◽  
pp. 169-186
Author(s):  
R. H. Quinn ◽  
S. K. Pierce
Keyword(s):  
Cell Volume ◽  
Time Course ◽  
The Other ◽  
Resting Potential ◽  
Ion Concentrations ◽  
Elysia Chlorotica ◽  
Apparent Relationship ◽  
Volume Recovery ◽  
Original Potential ◽  
Ionic Basis

The resting potential of identified cells (Parker cells) in the abdominal ganglion of Elysia chlorotica (Gould) depolarizes by about 30 mV in response to a 50% reduction in osmolality and returns to the original potential in 20 min. Cell volume recovery requires approximately 2 h. Thus, recovery of the resting potential is not dependent on recovery of cell volume. The hypo-osmotic depolarization persists following inhibition of the electrogenic Na+/K(+)-ATPase with ouabain, and the levels of extracellular K+ and Cl- have little effect on the magnitude of the depolarization, while decreasing extracellular Na+ concentration produces a depolarization of only 10 mV. This suggests that the hypo-osmotic depolarization in Parker cells results mostly from increased relative permeability to Na+. Following transfer from 920 to 460 mosmol kg-1, Na+, Cl- and proline betaine leave the cells while intracellular K+ is conserved. Loss of intracellular Na+ and conservation of intracellular K+ are dependent on active transport by the Na+/K(+)-ATPase. Na+ and proline betaine leave the cells with a time course that is much longer than that of the hypo-osmotic depolarization. Unlike the other solutes, most of the reduction in intracellular Cl- concentration occurs coincidentally with the hypo-osmotic depolarization. However, unlike the hypo-osmotic depolarization, bulk loss of Cl- does not require the reduction in osmolality, only the reduction in extracellular ion concentrations. There is no apparent relationship between membrane depolarization and the regulation of intracellular osmolytes in Elysia neurons following hypo-osmotic stress.

Cell volume, K transport, and cell density in human erythrocytes

1987 ◽  
Vol 252 (3) ◽  
pp. C269-C276 ◽  
Author(s):  
C. Brugnara ◽  
D. C. Tosteson
Keyword(s):  
Cell Volume ◽  
Cell Density ◽  
Human Erythrocytes ◽  
Ph Optimum ◽  
Cation Content ◽  
Original Volume ◽  
Dense Fraction ◽  
Normal Human ◽  
K Transport ◽  
Hypotonic Swelling

We report here studies on the regulation of cell volume and K transport in human erythrocytes separated according to density. When cell volume was increased (isosmotic swelling, nystatin technique), erythrocytes of the least dense but not of the densest fraction shrunk back toward their original volume. This process was due to a ouabain (0.1 mM) and bumetanide (0.01 mM) (OB)-resistant K loss. OB-resistant K+ efflux from the least dense fraction was stimulated by hypotonic swelling and had a bell-shaped dependence on pH (pH optimum 6.75–7.0). These pH and volume effects were not evident in the densest fraction. The swelling-induced K+ efflux from the least dense fraction was inhibited when chloride was substituted by nitrate, thiocyanate, and acetate, whereas it was stimulated by bromide. Increasing cell Mg2+ content also markedly inhibited K+ efflux from isosmotically swollen cells. N-ethylmaleimide (NEM, 1 mM) greatly increased OB-resistant K+ efflux from the least dense fraction but not from the densest fraction. These data reveal the presence, in the lease dense fraction of normal human erythrocytes, of a pathway for K+ transport that is dependent on volume, pH, and chloride, is inhibited by internal Mg2+, and possibly plays a role in determining the erythrocyte water and cation content.

Ca2+-sensitive, small-conductance potassium channels contribute to cell volume recovery in human cholangiocarcinoma cells

2000 ◽  
Vol 118 (4) ◽  
pp. A932
Author(s):  
Thorsten Schlenker ◽  
Yu Wang ◽  
Wolfgang Stremmel ◽  
J. Gregory Fitz ◽  
Richard M. Roman
Keyword(s):  
Potassium Channels ◽  
Cell Volume ◽  
Volume Recovery ◽  
Small Conductance

scholarly journals Decreased Effective Macromolecular Crowding in Escherichia coli Adapted to Hyperosmotic Stress

2019 ◽  
Vol 201 (10) ◽  
Author(s):  
Boqun Liu ◽  
Zarief Hasrat ◽  
Bert Poolman ◽  
Arnold J. Boersma
Keyword(s):  
Escherichia Coli ◽  
Osmotic Stress ◽  
Cell Volume ◽  
Volume Fraction ◽  
Macromolecular Crowding ◽  
Metabolic Energy ◽  
Content Type ◽  
Energy Limitation ◽  
General Response ◽  
In Cells

ABSTRACT Escherichia coli adapts to changing environmental osmolality to survive and maintain growth. It has been shown that the diffusion of green fluorescent protein (GFP) in cells adapted to osmotic upshifts is higher than expected from the increase in biopolymer volume fraction. To better understand the physicochemical state of the cytoplasm in adapted cells, we now follow the macromolecular crowding during adaptation with fluorescence resonance energy transfer (FRET)-based sensors. We apply an osmotic upshift and find that after an initial increase, the apparent crowding decreases over the course of hours to arrive at a value lower than that before the osmotic upshift. Crowding relates to cell volume until cell division ensues, after which a transition in the biochemical organization occurs. Analysis of single cells by microfluidics shows that changes in cell volume, elongation, and division are most likely not the cause for the transition in organization. We further show that the decrease in apparent crowding upon adaptation is similar to the apparent crowding in energy-depleted cells. Based on our findings in combination with literature data, we suggest that adapted cells have indeed an altered biochemical organization of the cytoplasm, possibly due to different effective particle size distributions and concomitant nanoscale heterogeneity. This could potentially be a general response to accommodate higher biopolymer fractions yet retaining crowding homeostasis, and it could apply to other species or conditions as well. IMPORTANCE Bacteria adapt to ever-changing environmental conditions such as osmotic stress and energy limitation. It is not well understood how biomolecules reorganize themselves inside Escherichia coli under these conditions. An altered biochemical organization would affect macromolecular crowding, which could influence reaction rates and diffusion of macromolecules. In cells adapted to osmotic upshift, protein diffusion is indeed faster than expected on the basis of the biopolymer volume fraction. We now probe the effects of macromolecular crowding in cells adapted to osmotic stress or depleted in metabolic energy with a genetically encoded fluorescence-based probe. We find that the effective macromolecular crowding in adapted and energy-depleted cells is lower than in unstressed cells, indicating major alterations in the biochemical organization of the cytoplasm.

Experimental evidence of an electronic transition in CeP under pressure using Ce L3 XAS

2017 ◽  
Vol 19 (27) ◽  
pp. 17526-17530 ◽  
Author(s):  
B. Joseph ◽  
R. Torchio ◽  
C. Benndorf ◽  
T. Irifune ◽  
T. Shinmei ◽  
...  
Keyword(s):  
Experimental Evidence ◽  
Cell Volume ◽  
Electronic Transition ◽  
Unit Cell Volume ◽  
Unit Cell ◽  
Compelling Evidence ◽  
Induced Changes

A direct compelling evidence of an electronic transition associated with the isostructural unit-cell volume discontinuity in CeP under pressure is provided using Ce L3-XAS. A DAC with a combination of a mini and a partially perforated anvils made of nanodiamonds permitted us to track the pressure induced changes in the 4f state of Ce in CeP.

Extracellular ATP stimulates volume decrease inNecturus red blood cells

1999 ◽  
Vol 277 (3) ◽  
pp. C480-C491 ◽  
Author(s):  
Douglas B. Light ◽  
Tracy L. Capes ◽  
Rachel T. Gronau ◽  
Matthew R. Adler
Keyword(s):  
Cell Volume ◽  
Osmotic Fragility ◽  
Inhibitory Effect ◽  
Ringer Solution ◽  
Extracellular Atp ◽  
Whole Cell ◽  
A 23187 ◽  
Volume Recovery ◽  
Hypotonic Swelling ◽  
Volume Decrease

This study examined whether extracellular ATP stimulates regulatory volume decrease (RVD) in Necturus maculosus (mudpuppy) red blood cells (RBCs). The hemolytic index (a measure of osmotic fragility) decreased with extracellular ATP (50 μM). In contrast, the ATP scavenger hexokinase (2.5 U/ml, 1 mM glucose) increased osmotic fragility. In addition, the ATP-dependent K+ channel antagonist glibenclamide (100 μM) increased the hemolytic index, and this inhibition was reversed with ATP (50 μM). We also measured cell volume recovery in response to hypotonic shock electronically with a Coulter counter. Extracellular ATP (50 μM) enhanced cell volume decrease in a hypotonic (0.5×) Ringer solution. In contrast, hexokinase (2.5 U/ml) and apyrase (an ATP diphosphohydrolase, 2.5 U/ml) inhibited cell volume recovery. The inhibitory effect of hexokinase was reversed with the Ca2+ ionophore A-23187 (1 μM); it also was reversed with the cationophore gramicidin (5 μM in a choline-Ringer solution), indicating that ATP was linked to K+ efflux. In addition, glibenclamide (100 μM) and gadolinium (10 μM) inhibited cell volume decrease, and the effect of these agents was reversed with ATP (50 μM) and A-23187 (1 μM). Using the whole cell patch-clamp technique, we found that ATP (50 μM) stimulated a whole cell current under isosmotic conditions. In addition, apyrase (2.5 U/ml), glibenclamide (100 μM), and gadolinium (10 μM) inhibited whole cell currents that were activated during hypotonic swelling. The inhibitory effect of apyrase was reversed with the nonhydrolyzable analog adenosine 5′- O-(3-thiotriphosphate) (50 μM), and the effect of glibenclamide or gadolinium was reversed with ATP (50 μM). Finally, anionic whole cell currents were activated with hypotonic swelling when ATP was the only significant charge carrier, suggesting that increases in cell volume led to ATP efflux through a conductive pathway. Taken together, these results indicate that extracellular ATP stimulated cell volume decrease via a Ca2+-dependent step that led to K+ efflux.

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