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Plasmolysis and turgor pressures


I am a high school student and I am a little confused in plasmolysis,

when we study plasmolysis, we say that at limiting plasmolysis, the turgor pressure OR pressure potential reduces to 0 what do we mean this by saying that turgor pressure becomes 0, like in gases if pressure becomes 0atm it simply means that there is no gas molecule left which can collide with the walls of container, but here water is still left in cell, but still we say that turgor pressure has become 0? why?

And if plasmolysis still continues we say that it has not become negative and starts contracting the plasma membrane and separates it from corners of cell wall {incipient plasmolysis} ? How can the water starts attracting the membrane and not colliding with it? what do we mean by saying negative turgor pressure or negative pressure potential? please explain in simple language and by giving as many examples as possible because its my first time I am studying this and it will become easier for me to then understand.


A pressure potential of 0 doesn't mean there isn't any water left in the cell, it just means that the existing water available in a cell is not able to exert any force on the cell wall. This is because in extremely hypertonic solutions (solutions with a higher solute concentration than the cytoplasm), enough water leaves the plant cell that there is not enough water to "fill" the entire volume created by the rigid cell wall. This leads to a pressure potential of 0, i.e. no force (since pressure is force/area) applied on the cell wall.

Now if there isn't enough water to fill the entire volume of the cell wall, which is rigid, the plasma membrane detaches and pulls away from the cell wall (plasmolysis) in order to be able to surround the remaining cytoplasm. It would be physically impossible for this not to happen (I would guess that a vacuum would end up forming because of the empty space that was once occupied by the water, creating enough negative pressure to physically pull apart the plasma membrane).

This brings us to the idea of a negative pressure potential. This can often be observed in vascular tissue, such as the cells of the xylem, where water is physically being pulled from the cell, creating a situation where, in simple terms, a "vacuum" of sorts is created due to the lack of water, which ends up "pulling" the water from xylem cells (called vessel elements) via the cohesion of water molecules. This "negative pressure" can also be called tension, where the inside of the cell actually exerts a "pulling" rather than a "pushing" force (here the "pulling" is what causes water to travel up the xylem against gravity).

Source: Campbell Biology 11th ed., Chapter 36: Resource Aquisition and Transport in Vascular Plants


Turgor pressure

It is also called hydrostatic pressure, and defined as the pressure measured by a fluid, measured at a certain point within itself when at equilibrium. [2] Generally, turgor pressure is caused by the osmotic flow of water and occurs in plants, fungi, and bacteria. The phenomenon is also observed in protists that have cell walls. [3] This system is not seen in animal cells, as the absence of a cell wall would cause the cell to lyse when under too much pressure. [4] The pressure exerted by the osmotic flow of water is called turgidity. It is caused by the osmotic flow of water through a selectively permeable membrane. Osmotic flow of water through a semipermeable membrane is when the water travels from an area with a low-solute concentration, to one with a higher-solute concentration. In plants, this entails the water moving from the low concentration solute outside the cell, into the cell's vacuole. [5]


Simultaneous measurement of turgor pressure and cell wall elasticity in growing pollen tubes

Plant growth and morphogenesis are tightly controlled processes of division and expansion of individual cells. To fully describe the factors that influence cell expansion, it is necessary to quantify the counteracting forces of turgor pressure and cell wall stiffness, which together determine whether and how a cell expands. Several methods have been developed to measure these parameters, but most of them provide only values for one or the other, and thus require complex models to derive the missing quantity. Furthermore, available methods for turgor measurement are either accurate but invasive, like the pressure probe or they lack accuracy, such as incipient plasmolysis or indentation-based methods that rely on information about the mechanical properties of the cell wall. Here, we describe a system that overcomes many of the above-mentioned disadvantages using growing pollen tubes of Lilium longiflorum as a model. By combining non-invasive microindentation and cell compression experiments, we separately measure turgor pressure and cell wall elasticity on the same pollen tube in parallel. Due to the modularity of the setup and the large range of the micro-positioning system, our method is not limited to pollen tubes but could be used to investigate the biomechanical properties of many other cell types or tissues.

Keywords: Biomechanics Cell compression Cell wall elasticity Force sensor Microindentation Pollen tube Turgor pressure Young's modulus.


Plasmolysis: Meaning and Importance | Plant Physiology

Shrinkage of the protoplast of a cell from its cell wall under the influence of a hypertonic solution is called plasmolysis. Hypertonic solution causes exosmosis or withdrawal of water from cytoplasm and then the central vacuole of cell.

The size of cytoplasm as well as central vacuole and hence protoplast becomes reduced. The pressure on the wall is simultaneously reduced and the elastic wall contracts causing a reduction in cell size.

This is first stage of plasmolysis called limiting plasmolysis. At limiting plasmolysis, the pressure potential (Ѱp) is zero and the osmotic concentration of cell interior is just equivalent to that of external solution (isotonic). The cell is called flaccid.

The extra hypertonic external solution continues to withdraw water from the central vacuole by exosmosis. Central vacuole shrinks further causing a similar shrinkage of pro­toplast from the cell wall. Pressure potential becomes negative.

Initially the protoplast with­draws itself from the comers. This stage is known as incipient plasmolysis. The hypertonic solution now enters the cell in between the protoplast and the cell wall. Due to continued exosmosis, protoplast shrinks further and withdraws from the cell wall except one or a few points. It is known as evident plasmolysis.

The swelling up of a plasmolysed protoplast under the influence of hypotonic solution or water is called de-plasmolysis. It is due to endosmosis. De-plasmolysis is possible only immediately after plasmolysis otherwise the cell protoplast becomes permanently damaged.

During de-plasmolysis water diffuses into protoplast. It enters the central vacuole and cyto­plasm. Consequently, the protoplast swells up. It first comes in contact with cell wall and then starts building a pressure on cell wall. This pressure is called turgor pressure. It makes the cell turgid.

Importance of Plasmolysis:

1. Plasmolysis proves that the cell membrane is semipermeable.

2. It shows that the cell wall is elastic as well as permeable.

3. Osmotic pressure of a cell can be measured by plasmolysis. It will be roughly equivalent to the osmotic pressure of a solution which will be strong enough to cause only incipient plasmolysis.

4. Plasmolysis can be shown only by living cells. It can, therefore, determine whether a cell is living or dead.

5. By salting tennis lawns, the weeds can be killed due to permanent plasmolysis and consequent death of their cells.

6. Plants are not allowed to grow in the cracks of the walls by the method of salting.

7. Salting of pickles, meat and fish and sweetening of the jams and jellies with sugar, kill the spores of fungi and bacteria.

8. Excessive concentration of chemical fertilizers at one place in the soil should be avoided otherwise the plants will die down.

Dead cells are fully permeable. It can be observed by cutting beet root into thin slices and washing them thoroughly under tap water till no more colour diffuses out. The slices are placed in water. No coloured sap comes out of them. Heat them. A reddish sap begins to come out of the slices. Heating has killed the cell membranes and made them permeable so that the sap diffuses out.


How to Calculate Turgor Pressure

Many things are taken into consideration when measuring the turgor pressure of a cell. It is known that a fully turgid cell has a turgor pressure value equal to that of the cell and that a flaccid cell has a value at or near to zero. Cellular mechanisms taken into consideration for the calculation of turgor pressure include the protoplast, solute concentration, transpiration rate of the plant, and the cell wall’s tension.

Some standard units used to measure turgor pressure are bars, MPa, and Newtons per square meter. The widely used methods to measure turgor pressure: equation of water potential, pressure-bomb technique, atomic force microscopy, pressure prove, and micro-manipulation probe.


Plasmolysis

The plant cell wall can either shrink or become turgid in response to the movement of water. It is the surrounding isotonic, hypotonic and hypertonic solution outside the cell that decides the direction in which water flows.

If the concentration of the external solution is more than that of the cytoplasm, that is, if it has more solutes, it is said to be hypertonic. If a plant cell is placed in a hypertonic solution, water moves out of the cell cytoplasm and then the vacuole due to osmosis. The cell membrane shrinks away from the cell wall. This phenomenon is called plasmolysis, while the cell is said to be plasmolysed.

This movement of water takes place from a cell which has a higher water potential to an area outside the cell that has a lower water potential. However, plasmolysis is a reversible process.

If the concentration of the external solution is lower than that of the cytoplasm, it is said to be hypotonic. When plasmolysed cells are placed in a hypotonic solution, that is, a solution with less solutes and higher water potential water moves from the solution into the cell due to osmosis. This causes the cytoplasm to build a pressure against the cell wall. This pressure is called turgor pressure, which enables the plant to be erect. This turgor pressure exerted by the protoplast against the cell wall due to the entry of water is called pressure potential, Ψp. Since plant cells have a rigid cell wall, the cell does not rupture despite the turgor pressure.

If the concentration of the external solution is the same as that of the cell cytoplasm, the solution is said to be isotonic. Now if the cell is placed in an isotonic solution, there is no net flow of water either from inside or outside the cell. When the flow of water from and into the cell is in equilibrium, the cell is said to be in a flaccid state. Flaccid cells are found in a wilted plant that has not been watered for a long time.

Summary

The plant cell wall can either shrink or become turgid in response to the movement of water. It is the surrounding isotonic, hypotonic and hypertonic solution outside the cell that decides the direction in which water flows.

If the concentration of the external solution is more than that of the cytoplasm, that is, if it has more solutes, it is said to be hypertonic. If a plant cell is placed in a hypertonic solution, water moves out of the cell cytoplasm and then the vacuole due to osmosis. The cell membrane shrinks away from the cell wall. This phenomenon is called plasmolysis, while the cell is said to be plasmolysed.

This movement of water takes place from a cell which has a higher water potential to an area outside the cell that has a lower water potential. However, plasmolysis is a reversible process.

If the concentration of the external solution is lower than that of the cytoplasm, it is said to be hypotonic. When plasmolysed cells are placed in a hypotonic solution, that is, a solution with less solutes and higher water potential water moves from the solution into the cell due to osmosis. This causes the cytoplasm to build a pressure against the cell wall. This pressure is called turgor pressure, which enables the plant to be erect. This turgor pressure exerted by the protoplast against the cell wall due to the entry of water is called pressure potential, Ψp. Since plant cells have a rigid cell wall, the cell does not rupture despite the turgor pressure.

If the concentration of the external solution is the same as that of the cell cytoplasm, the solution is said to be isotonic. Now if the cell is placed in an isotonic solution, there is no net flow of water either from inside or outside the cell. When the flow of water from and into the cell is in equilibrium, the cell is said to be in a flaccid state. Flaccid cells are found in a wilted plant that has not been watered for a long time.


Carbohydrates and Their Derivatives Including Tannins, Cellulose, and Related Lignings

3.10.1.1.2 Functions of the peptidoglycan layer

The primary function of the peptidoglycan layer is to prevent lysis of the bacterial cell through turgor pressure , which arises owing to the higher osmotic pressure inside the cell than in the outside medium. The high internal osmotic pressure would cause water to enter the cell until the turgor pressure is matched by the elastic stretch of the peptidoglycan layer. The internal turgor pressure has been estimated at 0.5 mPa (5 atm) for Gram-negative bacteria and as much as 3 MPa (30 atm) for Gram-positive bacteria. 1 The peptidoglycan layer must therefore be very strong and rigid.

During growth and cell division, changes in cell shape take place, hence the bacterial cell must possess a system for continuously breaking down and rebuilding the peptidoglycan layer. Consequently, there are a number of bacteriolytic enzymes which have been discovered which can break down peptidoglycan, which will be discussed in Section 3.10.2.6 . The regulation of the peptidoglycan layer is therefore tightly coupled to cell division, cell growth, and the maintenance of cell shape.

Although the primary role of peptidoglycan is structural, in both Gram-positive and Gram-negative bacteria the peptidoglycan layer is associated with other cellular structures. The thick Gram-positive peptidoglycan layer is associated with teichoic acids, strongly anionic polyol phosphates, which have been implicated in the sequestration of metal cations. 12 In Gram-negative bacteria, the peptidoglycan layer is associated with lipoproteins of the outer membrane. 1 Hence there are also nonstructural roles for the peptidoglycan layer.


THE EFFECTS OF TURGOR PRESSURE ON PUNCTURE AND VISCOELASTIC PROPERTIES OF TOMATO TISSUE

Current affiliation: ORTECH International, Food, Pharmaceutical and Consumer Products Group, 2395 Speakman Drive, Mississauga, Ontario, Canada L5K 1B3.

Department of Food Science University of Guelph Guelph, Ontario, Canada N1G 2W1

Department of Food Science University of Guelph Guelph, Ontario, Canada N1G 2W1

To whom correspondence should be addressed.Search for more papers by this author

Department of Food Science University of Guelph Guelph, Ontario, Canada N1G 2W1

Current affiliation: ORTECH International, Food, Pharmaceutical and Consumer Products Group, 2395 Speakman Drive, Mississauga, Ontario, Canada L5K 1B3.

Department of Food Science University of Guelph Guelph, Ontario, Canada N1G 2W1

Department of Food Science University of Guelph Guelph, Ontario, Canada N1G 2W1

To whom correspondence should be addressed.Search for more papers by this author

ABSTRACT

The effects of turgor pressure on puncture and viscoelastic properties of mature-green tomato pericarp were examined using tissue discs soaked in a range of osmotica (0.0–0.6 M mannitol) for at least 36 h at 4C. Turgor pressure was estimated from the osmotic potential of soaking solutions that induced incipient plasmolysis. Based on volume changes, the osmotic potential and turgor pressure of fresh tissue were estimated to be −0.56 ± 0.08 MPa and 0.20 MPa, respectively. However, puncture and viscoelastic properties corresponded to a turgor pressure of 0.15 MPa. The discrepancy between calculated and actual turgor pressures was attributed to the presence of apoplastic solutes. The data from this study revealed a general increase in cell wall stress, strain and elasticity with increasing turgor. With increases in turgor above that of untreated tissue both wall extensibility and elasticity became limiting and thus cell wall stiffness increased. Conversely, a decrease in turgor below that of untreated tissue led to an increase in viscoelasticity. Increases in bioyield and pseudoplastic bioyield strains with a variation in turgor from that of untreated tissue were consistent with cell debonding as a dominant mechanism of tomato tissue bioyielding. The reduced failure force, deformation and firmness with increasing turgor were consistent with cell rupture as a predominant mechanism of failure of mature-green tomato pericarp tissue.


Significance of plasmolysis spaces as markers for periseptal annuli and adhesion sites

During hyperosmotic shock, the protoplast and stretched-out peptidoglycan layer first shrink together until the turgor pressure in the cell is relieved. Being non-compressible, the outer and inner membranes must fold their superfluous surfaces. While the protoplast contracts further, the inner membrane rearranges into plasmolysis spaces visible by phase-contrast microscopy. Two opposing theories predict a similar positioning of spaces in dividing cells and filaments: the 'periseptal annulus model', based on adhesion zones, involved in the predetermination of the division site and a 'restricted, random model', based on physical properties of the protoplast. Strong osmotic shock causes retraction of the inner membrane over almost the entire surface forming the so-called 'Bayer bridges'. These tubular adhesion sites are preserved by chemical fixation, and can be destroyed by cryofixation and freeze-substitution of unfixed cells. Both the regular positioning of the plasmolysis spaces and the occurrence of tubular adhesion sites can be explained on the basis of physical properties of the membrane which necessitate rearrangements by membrane flow during shrinkage of the protoplast.


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