Group 1:

Deficiencies in mineral nutrients that are part of carbon compounds. This first

group consists of nitro- gen and sulfur. Nitrogen availability in soils limits plant

productivity in most natural and agricultural ecosystems. By contrast, soils

generally contain sulfur in excess. Nonetheless, nitrogen and sulfur share the

property that their oxidation–reduction states range widely (see Chapter 12).

Some of the most energy-intensive reactions in life con- vert the highly

oxidized, inorganic forms absorbed from the soil into the highly reduced forms

found in organic compounds such as amino acids.

NITROGEN.

Nitrogen is the mineral element that plants require in greatest amounts. It

serves as a constituent of many plant cell components, including amino acids

and nucleic acids. Therefore, nitrogen deficiency rapidly inhibits plant growth.

If such a deficiency persists, most species show chlorosis (yellowing of the

leaves), especially in the older leaves near the base of the plant (for pictures

of nitro- gen deficiency and the other mineral deficiencies described in this

chapter, see Web Topic 5.1). Under severe nitrogen deficiency, these leaves

become completely yellow (or tan) and fall off the plant. Younger leaves may

not show these symptoms initially because nitrogen can be mobilized from

older leaves. Thus a nitrogen-deficient plant may have light green upper

leaves and yellow or tan lower leaves. When nitrogen deficiency develops

slowly, plants may have markedly slender and often woody stems. This wood-

iness may be due to a buildup of excess carbohydrates that cannot be used in

the synthesis of amino acids or other nitrogen compounds. Carbohydrates not

used in nitrogen metabolism may also be used in anthocyanin synthesis,

leading to accumulation of that pigment. This condition is revealed as a purple

coloration in leaves, petioles, and stems of some nitrogen-deficient plants,

such as tomato and certain varieties of corn.

SULFUR.

Sulfur is found in two amino acids and is a con- stituent of several coenzymes

and vitamins essential for metabolism. Many of the symptoms of sulfur

deficiency are similar to those of nitrogen deficiency, including chlorosis,

stunting of growth, and anthocyanin accumulation. This similarity is not

surprising, since sulfur and nitrogen are both constituents of proteins.

However, the chlorosis caused by sulfur deficiency generally arises initially in

mature and young leaves, rather than in the old leaves as in nitrogen

deficiency, because unlike nitrogen, sulfur is not easily remobilized to the

younger leaves in most species. Nonetheless, in many plant species sulfur

chlorosis may occur simultaneously in all leaves or even initially in the older

leaves.

Group 2:

Deficiencies in mineral nutrients that are impor- tant in energy storage or

structural integrity. This group consists of phosphorus, silicon, and boron.

Phosphorus and silicon are found at concentrations within plant tissue that

warrant their classification as macronutrients, whereas boron is much less

abundant and considered a micronutri- ent. These elements are usually

present in plants as ester linkages to a carbon molecule.

PHOSPHORUS.

Phosphorus (as phosphate, PO43–) is an inte- gral component of important

compounds of plant cells, including the sugar–phosphate intermediates of

respiration and photosynthesis, and the phospholipids that make up plant

membranes. It is also a component of nucleotides used in plant energy

metabolism (such as ATP) and in DNAand RNA. Characteristic symptoms of

phosphorus deficiency include stunted growth in young plants and a dark

green coloration of the leaves, which may be mal- formed and contain small

spots of dead tissue called necrotic spots (for a picture, see Web Topic 5.1). As

in nitrogen deficiency, some species may produce excess anthocyanins, giving

the leaves a slight purple col- oration. In contrast to nitrogen deficiency, the

purple col- oration of phosphorus deficiency is not associated with chlorosis. In

fact, the leaves may be a dark greenish purple. Additional symptoms of

phosphorus deficiency include the production of slender (but not woody)

stems and the death of older leaves. Maturation of the plant may also be

delayed.

SILICON.

Only members of the family Equisetaceae—called scouring rushes because at

one time their ash, rich in gritty silica, was used to scour pots—require silicon

to complete their life cycle. Nonetheless, many other species accumu- late

substantial amounts of silicon within their tissues and show enhanced growth

and fertility when supplied with adequate amounts of silicon (Epstein 1999).

Plants deficient in silicon are more susceptible to lodg- ing (falling over) and

fungal infection. Silicon is deposited primarily in the endoplasmic reticulum,

cell walls, and intercellular spaces as hydrated, amorphous silica (SiO2·nH2O).

It also forms complexes with polyphenols and thus serves as an alternative to

lignin in the reinforcement of cell walls. In addition, silicon can ameliorate the

toxicity of many heavy metals.

BORON.

Although the precise function of boron in plant metabolism is unclear,

evidence suggests that it plays roles in cell elongation, nucleic acid synthesis,

hormone responses, and membrane function (Shelp 1993). Boron- deficient

plants may exhibit a wide variety of symptoms, depending on the species and

the age of the plant.

Mineral Nutrition 73

A characteristic symptom is black necrosis of the young leaves and terminal

buds. The necrosis of the young leaves occurs primarily at the base of the leaf

blade. Stems may be unusually stiff and brittle. Apical dominance may also be

lost, causing the plant to become highly branched; how- ever, the terminal

apices of the branches soon become necrotic because of inhibition of cell

division. Structures such as the fruit, fleshy roots, and tubers may exhibit

necro- sis or abnormalities related to the breakdown of internal tissues.

Group 3:

Deficiencies in mineral nutrients that remain in ionic form. This group includes

some of the most familiar mineral elements: The macronutrients potassium,

calcium, and magnesium, and the micronutrients chlorine, manganese, and

sodium. They may be found in solution in the cytosol or vacuoles, or they may

be bound electrostati- cally or as ligands to larger carbon-containing

compounds.

POTASSIUM.

Potassium, present within plants as the cation K+, plays an important role in

regulation of the osmotic potential of plant cells (see Chapters 3 and 6). It also

acti- vates many enzymes involved in respiration and photo- synthesis. The

first observable symptom of potassium defi- ciency is mottled or marginal

chlorosis, which then develops into necrosis primarily at the leaf tips, at the

mar- gins, and between veins. In many monocots, these necrotic lesions may

initially form at the leaf tips and margins and then extend toward the leaf

base. Because potassium can be mobilized to the younger leaves, these

symptoms appear initially on the more mature leaves toward the base of the

plant. The leaves may also curl and crinkle. The stems of potassium-deficient

plants may be slender and weak, with abnormally short internodal regions. In

potassium-deficient corn, the roots may have an increased susceptibility to

root-rotting fungi present in the soil, and this susceptibility, together with

effects on the stem, results in an increased tendency for the plant to be easily

bent to the ground (lodging).

CALCIUM.

Calcium ions (Ca2+) are used in the synthesis of new cell walls, particularly

the middle lamellae that sepa- rate newly divided cells. Calcium is also used in

the mitotic spindle during cell division. It is required for the normal functioning

of plant membranes and has been implicated as a second messenger for

various plant responses to both environmental and hormonal signals (Sanders

et al. 1999). In its function as a second messenger, calcium may bind to

calmodulin, a protein found in the cytosol of plant cells. The calmodulin–

calcium complex regulates many meta- bolic processes. Characteristic

symptoms of calcium deficiency include necrosis of young meristematic

regions, such as the tips of roots or young leaves, where cell division and wall

forma- tion are most rapid. Necrosis in slowly growing plants may

be preceded by a general chlorosis and downward hook- ing of the young

leaves. Young leaves may also appear deformed. The root system of a

calcium-deficient plant may appear brownish, short, and highly branched.

Severe stunting may result if the meristematic regions of the plant die

prematurely.

MAGNESIUM.

In plant cells, magnesium ions (Mg2+) have a specific role in the activation of

enzymes involved in respi- ration, photosynthesis, and the synthesis of

DNAand RNA. Magnesium is also a part of the ring structure of the chloro-

phyll molecule (see Figure 7.6A). Acharacteristic symptom of magnesium

deficiency is chlorosis between the leaf veins, occurring first in the older

leaves because of the mobility of this element. This pattern of chlorosis results

because the chlorophyll in the vascular bundles remains unaffected for longer

periods than the chlorophyll in the cells between the bundles does. If the

deficiency is extensive, the leaves may become yellow or white. An additional

symptom of mag- nesium deficiency may be premature leaf abscission.

CHLORINE.

The element chlorine is found in plants as the chloride ion (Cl–). It is required

for the water-splitting reac- tion of photosynthesis through which oxygen is

produced (see Chapter 7) (Clarke and Eaton-Rye 2000). In addition, chlorine

may be required for cell division in both leaves and roots (Harling et al. 1997).

Plants deficient in chlorine develop wilting of the leaf tips followed by general

leaf chlorosis and necrosis. The leaves may also exhibit reduced growth.

Eventually, the leaves may take on a bronzelike color (“bronzing”). Roots of

chlorine-deficient plants may appear stunted and thickened near the root tips.

Chloride ions are very soluble and generally available in soils because

seawater is swept into the air by wind and is delivered to soil when it rains.

Therefore, chlorine defi- ciency is unknown in plants grown in native or

agricultural habitats. Most plants generally absorb chlorine at levels much

higher than those required for normal functioning.

MANGANESE.

Manganese ions (Mn2+) activate several enzymes in plant cells. In particular,

decarboxylases and dehydrogenases involved in the tricarboxylic acid (Krebs)

cycle are specifically activated by manganese. The best- defined function of

manganese is in the photosynthetic reaction through which oxygen is

produced from water (Marschner 1995). The major symptom of manganese

defi- ciency is intervenous chlorosis associated with the devel- opment of

small necrotic spots. This chlorosis may occur on younger or older leaves,

depending on plant species and growth rate.

SODIUM.

Most species utilizing the C4 and CAM pathways of carbon fixation (see

Chapter 8) require sodium ions (Na+). In these plants, sodium appears vital

for regenerat- ing phosphoenolpyruvate, the substrate for the first

carboxylation in the C4 and CAM pathways (Johnstone et al. 1988). Under

sodium deficiency, these plants exhibit chloro- sis and necrosis, or even fail to

form flowers. Many C3 species also benefit from exposure to low levels of

sodium ions. Sodium stimulates growth through enhanced cell expansion, and

it can partly substitute for potassium as an osmotically active solute.

Group 4:

Deficiencies in mineral nutrients that are involved in redox reactions. This

group of five micronu- trients includes the metals iron, zinc, copper, nickel,

and molybdenum. All of these can undergo reversible oxidations and

reductions (e.g., Fe2+ ~ Fe3+) and have important roles in electron transfer

and energy transformation. They are usu- ally found in association with larger

molecules such as cytochromes, chlorophyll, and proteins (usually enzymes).

IRON.

Iron has an important role as a component of enzymes involved in the

transfer of electrons (redox reac- tions), such as cytochromes. In this role, it is

reversibly oxi- dized from Fe2+ to Fe3+ during electron transfer. As in mag-

nesium deficiency, a characteristic symptom of iron deficiency is intervenous

chlorosis. In contrast to magne- sium deficiency symptoms, these symptoms

appear ini- tially on the younger leaves because iron cannot be readily

mobilized from older leaves. Under conditions of extreme or prolonged

deficiency, the veins may also become chlorotic, causing the whole leaf to

turn white. The leaves become chlorotic because iron is required for the

synthesis of some of the chlorophyll–protein complexes in the chloroplast. The

low mobility of iron is probably due to its precipitation in the older leaves as

insoluble oxides or phosphates or to the formation of complexes with phyto-

ferritin, an iron-binding protein found in the leaf and other plant parts (Oh et

al. 1996). The precipitation of iron dimin- ishes subsequent mobilization of the

metal into the phloem for long-distance translocation.

ZINC. Many enzymes require zinc ions (Zn2+) for their activity, and zinc may

be required for chlorophyll biosyn- thesis in some plants. Zinc deficiency is

characterized by a reduction in internodal growth, and as a result plants dis-

play a rosette habit of growth in which the leaves form a circular cluster

radiating at or close to the ground. The leaves may also be small and

distorted, with leaf margins having a puckered appearance. These symptoms

may result from loss of the capacity to produce sufficient amounts of the

auxin indoleacetic acid. In some species (corn, sorghum, beans), the older

leaves may become inter- venously chlorotic and then develop white necrotic

spots. This chlorosis may be an expression of a zinc requirement for

chlorophyll biosynthesis.

COPPER.

Like iron, copper is associated with enzymes involved in redox reactions being

reversibly oxidized from

Cu+ to Cu2+. An example of such an enzyme is plasto- cyanin, which is

involved in electron transfer during the light reactions of photosynthesis

(Haehnel 1984). The ini- tial symptom of copper deficiency is the production of

dark green leaves, which may contain necrotic spots. The necrotic spots

appear first at the tips of the young leaves and then extend toward the leaf

base along the margins. The leaves may also be twisted or malformed. Under

extreme copper deficiency, leaves may abscise prematurely.

NICKEL. Urease is the only known nickel-containing enzyme in higher plants,

although nitrogen-fixing microor- ganisms require nickel for the enzyme that

reprocesses some of the hydrogen gas generated during fixation (hydrogen

uptake hydrogenase) (see Chapter 12). Nickel- deficient plants accumulate

urea in their leaves and, con- sequently, show leaf tip necrosis. Plants grown

in soil sel- dom, if ever, show signs of nickel deficiency because the amounts

of nickel required are minuscule.

MOLYBDENUM. Molybdenum ions (Mo4+ through Mo6+) are components of

several enzymes, including nitrate reductase and nitrogenase. Nitrate

reductase catalyzes the reduction of nitrate to nitrite during its assimilation by

the plant cell; nitrogenase converts nitrogen gas to ammonia in nitrogen-fixing

microorganisms (see Chapter 12). The first indication of a molybdenum

deficiency is general chloro- sis between veins and necrosis of the older

leaves. In some plants, such as cauliflower or broccoli, the leaves may not

become necrotic but instead may appear twisted and sub- sequently die

(whiptail disease). Flower formation may be prevented, or the flowers may

abscise prematurely. Because molybdenum is involved with both nitrate

assimilation and nitrogen fixation, a molybdenum defi- ciency may bring about

a nitrogen deficiency if the nitrogen source is primarily nitrate or if the plant

depends on sym- biotic nitrogen fixation. Although plants require only small

amounts of molybdenum, some soils supply inadequate levels. Small additions

of molybdenum to such soils can greatly enhance crop or forage growth at

negligible cost.

CELL CYCLE REGULATION

The cell division cycle, or cell cycle, is the process by which cells reproduce

themselves and their genetic material, the nuclear DNA. The four phases of

the cell cycle are desig- nated G1, S, G2, and M (Figure 1.26A).

Each Phase of the Cell Cycle Has a Specific Set of Biochemical and Cellular

Activities Nuclear DNA is prepared for replication in G1 by the assembly of a

prereplication complex at the origins of repli- cation along the chromatin.

DNAis replicated during the S phase, and G2 cells prepare for mitosis. The

whole architecture of the cell is altered as cells enter mitosis: The nuclear

envelope breaks down, chromatin con- denses to form recognizable

chromosomes, the mitotic spindle forms, and the replicated chromosomes

attach to the spindle fibers. The transition from metaphase to anaphase of

mitosis marks a major transition point when

the two chromatids of each replicated chromosome, which were held together

at their kinetochores, are separated and the daughter chromosomes are

pulled to opposite poles by spindle fibers. At a key regulatory point early in G1

of the cell cycle, the cell becomes committed to the initiation of DNA

synthesis. In yeasts, this point is called START. Once a cell has passed START,

it is irre- versibly committed to initiating DNAsynthesis and completing the cell

cycle through mitosis and cytokinesis. After the cell has completed mitosis, it

may initiate another complete cycle (G1 through mitosis), or it may leave the

cell cycle and differen- tiate. This choice is made at the critical G1 point,

before the cell begins to replicate its DNA. DNAreplication and mitosis are

linked in mammalian cells. Often mammalian cells that have stopped dividing

can be stimulated to reenter the cell cycle by a variety of hormones and

growth factors. When they do so, they reen- ter the cell cycle at the critical

point in early G1. In contrast, plant cells can leave the cell division cycle either

before or after replicating their DNA(i.e., during G1 or G2). As a con-

sequence, whereas most animal cells are diploid (having two sets of

chromosomes), plant cells frequently are tetraploid (having four sets of

chromosomes), or even poly- ploid (having many sets of chromosomes), after

going through additional cycles of nuclear DNAreplication with- out mitosis.

The Cell Cycle Is Regulated by Protein Kinases The mechanism regulating the

progression of cells through their division cycle is highly conserved in

evolution, and plants have retained the basic components of this mecha- nism

(Renaudin et al. 1996). The key enzymes that control the transitions between

the different states of the cell cycle, and the entry of nondividing cells into the

cell cycle, are the cyclin-dependent protein kinases, or CDKs (Figure 1.26B).

Protein kinases are enzymes that phosphorylate proteins using ATP. Most

multicellular eukaryotes use several pro- tein kinases that are active in

different phases of the cell cycle. All depend on regulatory subunits called

cyclins for their activities. The regulated activity of CDKs is essential for the

transitions from G1 to S and from G2 to M, and for the entry of nondividing

cells into the cell cycle. CDK activity can be regulated in various ways, but two

of the most important mechanisms are (1) cyclin synthe- sis and destruction

and (2) the phosphorylation and dephosphorylation of key amino acid residues

within the CDK protein. CDKs are inactive unless they are associated

Plant Cells 23

Nuclear envelope

Vesicles

Microtubule

Nucleus

FIGURE 1.25 Electron micrograph of a cell plate forming in a maple seedling

(10,000×). (© E. H. Newcomb and B. A. Palevitz/Biological Photo Service.)

with a cyclin. Most cyclins turn over rapidly. They are syn- thesized and then

actively degraded (using ATP) at specific points in the cell cycle. Cyclins are

degraded in the cytosol by a large proteolytic complex called the proteasome.

Before being degraded by the proteasome, the cyclins are marked for

destruction by the attachment of a small pro- tein called ubiquitin, a process

that requires ATP. Ubiquiti- nation is a general mechanism for tagging cellular

proteins destined for turnover (see Chapter 14). The transition from G1 to S

requires a set of cyclins (known as G1 cyclins) different from those required in

the transition from G2 to mitosis, where mitotic cyclins acti- vate the CDKs

(see Figure 1.26B). CDKs possess two tyro- sine phosphorylation sites: One

causes activation of the enzyme; the other causes inactivation. Specific

kinases carry out both the stimulatory and the inhibitory phos- phorylations.

Similarly, protein phosphatases can remove phosphate from CDKs, either

stimulating or inhibiting their activity, depending on the position of the

phosphate. The addition or removal of phosphate groups from CDKs is highly

reg- ulated and an important mechanism for the control of cell cycle

progression (see Figure 1.26B). Cyclin inhibitors play an important role in

regulating the cell cycle in animals, and probably in plants as well, although

little is known about plant cyclin inhibitors. Finally, as we will see later in the

book, certain plant hormones are able to regulate the cell cycle by regulating

the synthesis of key enzymes in the regulatory pathway.

FIGURE 1.26 (A) Diagram of the cell cycle. (B) Diagram of the regulation of the

cell cycle by cyclin-dependent protein kinase (CDK). During G1, CDK is in its

inactive form. CDK becomes activated by binding to G1 cyclin (CG1) and by

being phosphorylated (P) at the activation site. The activated CDK–cyclin

complex allows the transition to the S phase. At the end of the S phase, the

G1 cyclin is degraded and the CDK is dephosphorylated, resulting in an

inactive CDK. The cell enters G2. During G2, the inactive CDK binds to the

mitotic cyclin (CM), or M cyclin. At the same time, the CDK–cyclin complex

becomes phosphorylated at both its activation and its inhibitory sites. The

CDK–cyclin complex is still inactive because the inhibitory site is phosphory-

lated. The inactive complex becomes activated when the phosphate is

removed from the inhibitory site by a protein phosphatase. The activated CDK

then stimulates the transi- tion from G2 to mitosis. At the end of mitosis, the

mitotic cyclin is degraded and the remaining phosphate at the acti- vation site

is removed by the phosphatase, and the cell enters G1 again.

Potensial air sel

Pengukuran potensial air sel dipergunakan untuk mengetahui status energi air

sel. Hal ini sangat penting untuk mempelajari fisiologi tumbuhan karena dapat

digunakan

29

untuk (1) menentukan arah dan gerakan air yaitu air akan mengalir dari

tempat berpotensial air tinggi ke tempat yang lebih rendah (mengikuti

gradien konsentrasi), (2) memonitor status air tumbuhan. Sehingga potensial

air dapat dijadikan alat diagnostik keadaan air sel atau jaringan. Makin rendah

potensial air sel atau jaringan makin tinggi kemampuannya menyerap air.

Sebaliknya makin tinggi potensial airnya makin besar kemampuannya untuk

memberikan air ke sel atau jaringan yang lebih kering. Potensial air dapat

digunakan untuk menentukan sel atau jaringan yang defisit air, cekaman air

dan sebagainya.

Potensial air sering disebut potensial kimia air diberikan tanda Psi (Ψ), dan

dengan satuan Psi, bar, atm atau mega Pascal (MPa). Kesetaraan dari satuan

tersebut adalah 1 Mpa=10 atm (1 atm=760 mm Hg= 14,7 lbs sq in-1)=10

bar=147 Psi. Potensial air diberikan tanda nilai negative karena banyaknya

zat terlarut dalam sel, dan dihitung dengan membandingkannya dengan

potensial kimia air murni yang diukur pada temperature dan tekanan yang

sama. Satuan tersebut adalah satuan tekanan karena sel tumbuhan

mendapat tekanan dari dinding sel dan tekanan mudah diukur. Rumus

potensial air

Perhitungan potensial air harus memperhitungkan faktor yang mempengaruhi

difusi dan faktor lainnya.

. Ψair =Ψp + Ψs+Ψm+ Ψg

Ψair = potensial air

Ψp= potensial tekanan

Ψs= potensial larutan

Ψm= potensial matriks

Ψg= potensial gravitasi

1. Potensial larutan atau potensial osmotik (:Ψs) Potensial ini disebabkan

karena adanya senyawa-senyawa terlarut dalam sel. Larutan ini mengurangi

energi bebas air sehingga nilainya selalu negatif. Semakin kental larutan

semakin negatif potensial larutannya. Potensial larutan dapat dihitung dengan

rumus Van’t Hoff yaitu Ψs=-mi RT yang mana m adalah molalitas (mol/1000g

pelarut), i adalah konstante ionisasi biasanya 1,0, R adalah konstante gas

0,00831 liter x MPa/mol deg dan T adalah temperatur Calvin (oC+273o).

2. Tekanan atau potensial tekanan (Ψp). Tekanan yang disebabkan oleh

kekuatan protoplasma menekan dinding sel. Tekanan ini mempunyai nilai

positif tetapi ada juga yang negatif misalnya pada xilem. Tekanan ini dapat

diukur dengan osmometer.

3. Potensial matriks (Ψm). Potensial ini berasal dari ikatan air dan koloid

dalam sel, permukaan bermuatan. Nilainya adalah negatif karena ikatan ini

mengurangi kemampuan air untuk bergerak. Pada volume besar air, potensial

matrik sangat kecil sehingga dapat diabaikan. Nilai potensial matriks yang

sangat kecil ini kadang sangat penting dalam tanah tertutama bila

dihubungkan dengan hubungan akar dan tanah.

4. Potensial gravitasi (Ψg).Potensial akibat gaya tarik bumi yang biasanya

diabaikan karena nilainya sangat kecil kecuali pada ujung pohon–pohon tinggi.

35

Karena Ψm dan Ψg nilainya sangat kecil dan dapat diabaikan maka rumus

disederhanakan menjadi

Ψair =Ψp + Ψs Ψp walaupun nilainya positif tetapi sangat kecil dan dapat

Diabaikan sehingga rumus menjadi lebih sederhana lagi

Ψair = Ψs sehingga Ψair= -miRT

Contoh soal : Berapakah potensial air pada larutan sukrosa 1m pada

temperatur 30 oC?

Ψair= - (1)(1)(0,00831)(303) mol/l airxlMPa/mol Kx K

= -2,518 Mpa

Berapakah Ψair bila temperatur 0 oC?

Ψair= -(1)(1)(0,00831)(273)

= -0,2,269 MPa

Faktor-faktor yang mempengaruhi potensial air sel

Pada perpindahan air dari tempat yang tinggi ke yang rendah potensial

airnya, pergerakan air akan berhenti jika potensial air kedua tempat sama.

Potensial air tergantung pada beberapa faktor yaitu

1. Temperatur: Kandungan energi air akan mempengaruhi potensial kimia air

dalam suatu sistem. Salah satu faktor yang berpengaruh adalah temperatur.

Potensial air dalam suatu sistem dipengaruhi oleh temperatur dalam sistem

tersebut. Temperatur terutama berpengaruh terhadap solute dan imbiban.

Karena Ψair = Ψs maka pengaruh temperatur terhadap solute secara mutlak

mempengaruhi Ψair sel atau jaringan. Temperatur meningkat sejalan dengan

kenaikan potensial kimia air sel.

2. Solute dan imbiban. Air yang yang berikatan dengan protoplasma dan

dinding sel dengan sejumlah energi atau kekuatan tertentu sehingga dapat

mengurangi kecenderungan untuk lari. Ikatan antara air dengan ion dan

molekul larutan menurunkan tekanan uap air dalam larutan Penurunan

tekanan uap air sejalan dengan total jumlah partikel dalam larutan. Sehingga

kalau digambarkan 36 dengan grafik semakin banyak imbiban dalam larutan

semakin rendah potensial airnya.

3. Tekanan atau tegangan. Air dalam sel yang sedang tumbuh biasanya lebih

tinggi tekanannya dibandingkan dengan dalam beker.