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Membrane transport is the passage of substances across a cell membrane. For the small solutes considered here, distinguish the available route from its driving force: a lipid bilayer, ion channel, or carrier protein determines how passage can occur, while differences in chemical potential and membrane potential determine which direction is energetically downhill. A large driving force cannot make an unavailable route conduct. See Alberts et al.: principles of membrane transport.

For an ideal dilute chemical solution at uniform temperature and pressure, with the same reference molar chemical potential on both sides, the molar electrochemical potential change for transferring a solute from compartment A to B isHere $c_{\mathrm{A}},c_{\mathrm{B}}$ are concentrations, $T$ is absolute temperature, $R$ is the molar gas constant, $z$ is signed ion charge number, $F$ is the Faraday constant, and $V_{\mathrm{B}}-V_{\mathrm{A}}$ is the electric potential difference. The natural logarithm contains a dimensionless ratio. The electrical term vanishes for an uncharged solute. More generally, use thermodynamic activities in place of the ideal concentration ratio. This combines the ideal-solution chemical potential difference with electrical energy per mole; see IUPAC Gold Book: electrochemical potential. For a biological cell, taking B inside and A outside makes the voltage term use the existing membrane potential convention.

A metabotropic receptor couples ligand recognition to intracellular signal transduction, which can regulate a separate ion channel, alter enzyme activity or change gene expression. In the usual neurotransmitter context, metabotropic receptors are G protein-coupled receptors: receptor activation is relayed by a G protein. There need not be a change in membrane potential at all. ^[ref]

Two routes should be distinguished. An activated G protein can regulate an ion channel locally at the cell membrane, without an obligatory diffusible second messenger. Alternatively, it can regulate an enzyme that changes the availability of a second messenger, such as cAMP or inositol trisphosphate. Downstream proteins then change channel opening, phosphorylation or other cellular activities. The receptor, G protein, second messenger and final target are distinct components; an activated G protein is a relay protein, rather than itself a small-molecule second messenger.^[ref]

Do not turn this useful chemical synapse classification into the claim that every receptor is a GPCR, or that every indirect response must pass through a G protein. For example, the insulin receptor is an enzyme-linked cell-surface receptor whose intracellular catalytic activity initiates protein phosphorylation. Intracellular receptors supply another category. “Metabotropic” commonly names the GPCR branch in neuroscience; the broader idea of biochemical coupling does not make all non-channel receptors structurally identical. ^[ref]

Separating recognition from execution allows signal amplification and branching. A persistently activated receptor can activate several relay proteins; a regulated enzyme can produce many second messenger molecules. As an explicitly invented count example, suppose one activated receptor activates four relay proteins during one interval, and each relay activates a distinct enzyme that produces fifteen second messenger molecules during the next interval. With sufficient substrates and no loss, this gives $4\times 15=60$ molecules. Those counts do not specify a physiological gain or response duration. A directly gated ion channel also passes many ions while open, so amplification is not an exclusive property of metabotropic receptors: always name the input and output being compared. ^[ref]

A particularly instructive electrophysiology experiment separated a chemical trigger from the ion channel carrying its eventual electric current. In 1987, Hirono, Ito and Sugiyama injected messenger RNA from rat brain into frog egg cells, then tested acquired responses to neurotensin and muscarinic acetylcholine stimulation. Under voltage clamp at $-60\mathrm{mV}$, neurotensin elicited transient, oscillatory inward electric currents after a delay of several tens of seconds. This delay refers to that response and preparation. Reversal potential measurements implicated increased permeability to chloride anions, rather than a pore specific to the applied ligand. Both neurotensin and acetylcholine responses were inhibited by pertussis toxin, which interferes with susceptible G proteins, and by intracellular EGTA, which binds free calcium. Injecting inositol trisphosphate mimicked the responses; a large prior dose of inositol trisphosphate reduced subsequent responses to either extracellular signal. These interventions implicate a shared intracellular relay and calcium-dependent channel opening.^[ref]

The informative comparison with the nicotinic acetylcholine receptor experiment is mechanistic: an extracellular ligand can produce an inward electric current either by directly gating the pore or by mobilizing an intracellular second messenger and stored calcium that activate another pore. Intracellular inositol trisphosphate bypasses reception, whereas EGTA tests the need for free calcium. However, neither inhibition nor mimicry alone identifies every molecular connection: a perturbation can affect several targets, and an injected mediator can activate a pathway without proving that it is the only natural route. The egg cell's endogenous machinery and the mixed messenger RNA preparation also limit extrapolation to an intact neuron. The experiment establishes functional coupling in its preparation, rather than the exact molecular composition or timing of every metabotropic receptor.

Even G protein-dependent channel regulation need not involve a lengthy second messenger cascade. Pfaffinger and colleagues reported in 1985 that acetylcholine-evoked potassium channel activation in embryonic chick atrial cells required intracellular GTP, a guanine-containing nucleotide, and was abolished by pertussis-toxin pretreatment. Changes in cyclic nucleotides, including cAMP, did not account for the channel response. The report discusses intrinsic activation delays of roughly $30$–$100\mathrm{ms}$, illustrating relatively rapid metabotropic receptor action. These observations support a G protein coupling step without cyclic-nucleotide second messengers; they do not by themselves exclude every possible intermediary or prove the specific subunit-channel interaction.^[ref]

A small timing model makes the extra steps visible without inventing an experimental trace. Let $u(t)$ jump from zero to one at $t=0$ and remain on. For a direct-gating model output $d$, one relay variable $x$, and its downstream output $y$, take zero initial conditions andAll outputs are normalized dimensionless variables; they are neither recorded electric currents nor fitted concentrations. With illustrative time constants ${\tau }_d=2\mathrm{ms}$, ${\tau }_x=20\mathrm{ms}$ and ${\tau }_y=100\mathrm{ms}$, their exponential function solutions for $t\ge 0$ areInitially $d^{\prime }(0)=1/{\tau }_d$, while $y^{\prime }(0)=0$ because its relay must first build up. Both outputs eventually approach one. Equal normalized final values do not imply equal biological amplitudes or absence of signal amplification; normalization deliberately removes that question.

The model's useful feature is the delayed buildup created by sequential relaxation, not its arbitrary numbers. Actual kinetics also depend on ligand delivery, relay deactivation, neurotransmitter clearance and the final target. A local G protein route can act promptly, while an ionotropic receptor can remain active during continued exposure or feed a longer-lasting intracellular response. The beauty of metabotropic receptor coupling is its flexibility: the same recognition event can adjust electrical responsiveness and other cellular tasks through different targets. To classify an observed response, combine timing with molecular identity and controlled perturbations.

A multicellular organism has a body of multiple biological cells whose growth and activities are integrated into the life of the whole organism. Extensive cell differentiation is common in complex examples, but specialized biological cells are not a prerequisite for every simple form. Ask how the body develops, how its parts cooperate and how it produces descendants, rather than counting attached biological cells alone. The boundary with a biological colony depends on the degree of integration and the criteria being investigated; there is no universal cell-count threshold. See the Queller and Strassmann account cited under unicellular organism.

Specialization makes the whole capable of combinations that one general-purpose biological cell cannot achieve in the same way. In an animal, a neuron transmits signals while a red blood cell carries oxygen; each still requires a working cell membrane and metabolism. A mature mammalian red blood cell lacks a cell nucleus and mitochondria, illustrating how a useful part need not retain the equipment of a self-reproducing organism. See Clark, Douglas and Choi, Biology 2e, 40.2: red blood cell specialization. Cell differentiation generally involves different gene expression, rather than a different inherited genome for each function. Biological development must coordinate growth, position, interactions and specialization: increasing the number of biological cells is only one component. See Alberts et al., Molecular Biology of the Cell, chapter 21 (2002): construction of multicellular bodies.

A motivating experiment: select for a property of groups. Ratcliff, Denison, Borrello and Travisano's 2012 study began with Saccharomyces cerevisiae growing as unicellular organisms. Daily transfer favored rapidly settling material. Their initial protocol allowed a $10\mathrm{mL}$ culture to settle for $45\min$, discarded the upper $9.9\mathrm{mL}$, and transferred the bottom $100\mu \mathrm{L}$ into fresh medium. After seven days, they instead sampled $1.5\mathrm{mL}$ and centrifuged it at $100$ times gravitational acceleration for $10\mathrm{s}$, again transferring the bottom $100\mu \mathrm{L}$. Faster settling made it more likely that a lineage would seed tomorrow's culture; the procedure selected a physical outcome without specifying how it must arise. These protocol details are explicitly recounted in Gulli, Herron and Ratcliff, Evolution of altruistic cooperation among nascent multicellular organisms (2019): original settling protocol.

The primary 2012 paper reports snowflake yeast dominating all ten initial replicate populations by 60 transfers. To distinguish the joining of previously separate biological cells from clonal development, the researchers enzymatically separated clusters and followed individual biological cells for $16\mathrm{h}$: attached descendants rebuilt clusters, with no such joining observed. Staining localized attachments at bud scars. Time-lapse observations also showed clusters releasing smaller multicellular offspring, called propagules; small clusters grew before they reproduced. See Ratcliff et al., Experimental evolution of multicellularity (2012), figures 1–3: emergence, development and reproduction.

The experimental comparisons ask different questions. Competition with the unicellular organism ancestor showed a reported $34\%$ advantage under settling selection. Without settling selection, the estimated $10\%$ disadvantage had a one-sided $P=0.06$, so it was suggestive rather than decisive evidence of a cost. Separately, three populations derived from one evolved isolate retained the cluster form through 35 transfers without settling selection. That persistence tests stability, not whether clusters always outperform single biological cells. See Ratcliff et al. (2012), figure 2 and the cluster-formation results cited above.

A 2015 follow-up added a causal test: deleting the gene ACE2 in the unicellular organism ancestor produced snowflake yeast, while supplying functional ACE2 to one evolved isolate restored separation into single biological cells. Sequence changes altering the encoded protein were found in ACE2 in five of ten examined lineages; the study did not identify that same sequence-change mechanism in every lineage. The deletion and restoration comparisons support a mechanism beyond the observation that clusters settle quickly. See Ratcliff, Fankhauser, Rogers, Greig and Travisano, Origins of multicellular evolvability in snowflake yeast (2015), figure 1.

What follows, and what does not. The evidence supports inherited cluster formation, clonal development and a reproducing collective whose properties can respond to natural selection. Calling these simple multicellular organisms recognizes those demonstrated properties; it does not turn every clump into an animal or establish animal-like cell differentiation. This laboratory route also does not reconstruct the actual ancestry of animals or show that complex developmental integration must follow. The interesting achievement is narrower and testable: a change in how descendants remain connected creates a new scale at which growth and reproductive success can be measured.

For the toy figure, let $p$ be the fraction of tracked units of type C before transfer and let $s_C,s_U$ be the respective probabilities of transfer for C and U. Assume equally weighted units and equal multiplication between transfers. When overall transfer probability is nonzero, conditioning on transfer givesWith $p=1/5$, $s_C=4/5$ and $s_U=1/10$, the numerator is $4/25$ and the denominator $6/25$, giving $p_{\mathrm{after}}=2/3$. If both types have the same nonzero transfer probability, the fraction stays $1/5$. This is conditional probability, not a model of the full experimental life cycle: real cluster sizes, growth and fragmentation affect which quantity a frequency measures. In particular, a fraction of clusters is not automatically a fraction of biological cells.

The Nernst equilibrium potential is the inside-minus-outside membrane potential at which one ion species has equal electrochemical potential on both sides of a cell membrane. At uniform temperature $T$, using the same reference chemical potential on both sides, $z\ne 0$ is the signed ion charge number, $R$ the molar gas constant, $F$ the Faraday constant, and $a$ the dimensionless thermodynamic activity of that ion. For an ideal dilute chemical solution, the activity ratio becomes the concentration ratio. See Purves et al.: the forces that create membrane potentials and the Nernst equation.

The short derivation is to set the outside-to-inside electrochemical potential change from membrane transport to zero: $RT\ln (a_{\mathrm{inside}}/a_{\mathrm{outside}})+zFV=0$, and solve for $V$. An open pathway carrying only this species by passive transport then has this reversal potential. A balance of several nonzero ion electric currents does not establish this equilibrium condition for each species.

A neuron is a specialized biological cell that receives, integrates and transmits signals. Its shape separates places where inputs arrive from places where outputs reach other biological cells: this functional asymmetry is neuronal polarity. Understanding a neuron therefore means connecting its anatomy to changes in membrane potential, rather than treating it as a wire that merely forwards every input.

In a common multipolar neuron, branching dendrites receive inputs at synapses; the soma contains the cell nucleus and most major organelles; the axon carries signals to distant or nearby targets; and axon terminals form output contacts. All these regions belong to one biological cell enclosed by a continuous cell membrane. An axon can branch, allowing one neuron to influence several receiving biological cells.^[ref]

At an input chemical synapse, a neurotransmitter acts on a receptor, changing an electric current directly or through signal transduction.^[ref] A resulting synaptic potential contributes to synaptic integration in the dendrites and soma. In many spiking neurons, sufficiently strong depolarization recruits voltage-gated ion channels in the axon initial segment, initiating an action potential that propagates along the axon. At an output chemical synapse, calcium entry through voltage-gated ion channels promotes synaptic vesicle exocytosis, releasing neurotransmitter. An action potential is thus regenerated electrically along a cell membrane; it is not a packet of neurotransmitter travelling from the dendrites to the axon terminals.^[ref]

The compartments are specializations, not exclusive jobs. Inputs can contact the soma or axon as well as dendrites; dendrites can support active voltage-gated ion channels. Paired recordings from a pyramidal neuron's soma and dendrite or axon established that an action potential can begin in the axon and propagate back into the dendrites. The usual output direction therefore does not make every electrical signal strictly one-way.^[ref] An electrical synapse, which directly couples cytoplasms through gap junctions, also differs from the sending-and-receiving arrangement of a chemical synapse.^[ref]

Nor does every neuron have the upper diagram's shape. A bipolar neuron has two main processes, one dendrite and one axon; a multipolar neuron has several dendrites; and a pseudounipolar neuron has a single process from the soma that divides into peripheral and central branches. In the last arrangement, sensory signals can travel past the soma rather than obligatorily through it. These shape categories do not specify every neuron's receptor, connectivity or firing behavior.^[ref] Some neurons in the retina communicate through graded changes in membrane potential without generating action potentials.^[ref]

Why timing changes the computation. Synaptic integration can combine inputs at different locations, called spatial summation, and inputs arriving at different times, called temporal summation. A minimal example uses the leaky integrate-and-fire model with the illustrative parameters already given there: resting and reset membrane potential $-65\mathrm{mV}$, firing threshold $-50\mathrm{mV}$, electrical resistance $R=100\mathrm{M\Omega }$, capacitance $C=200\mathrm{pF}$, time constant $\tau =RC=20\mathrm{ms}$ and neuronal refractory period $2\mathrm{ms}$. These are chosen model values, not measured properties of a particular neuron. Before firing, a constant inward electric current $I$ starting from rest givesThe exponential function expresses the competition between charging the cell membrane's capacitance and leakage through its electrical resistance.^[ref]

Two $100\mathrm{pA}$ inputs, each lasting $40\mathrm{ms}$, produce different outputs depending on their timing. Either input alone reaches only $-56.3534\mathrm{mV}$. Applied together, they give $I=200\mathrm{pA}$ and reach threshold after $20\ln 4\mathrm{ms}\approx 27.7259\mathrm{ms}$, producing one action potential event during the pulse. If instead the second input begins $20\mathrm{ms}$ after the first ends, the earlier depolarization has partly decayed: the second pulse peaks at approximately $-55.9229\mathrm{mV}$ and neither pulse produces an action potential. The two-input protocols deliver the same total electric charge, $8\mathrm{pC}$, yet only the coincident protocol fires. Counting total input alone misses this timing dependence.

This example makes a neuron a detector of sufficiently clustered input, not a perfect logical gate: different parameters change the result. Actual dendrites introduce location-dependent filtering and active responses, and an inhibitory postsynaptic potential or shunting inhibition can change whether another input succeeds. The single-compartment leaky integrate-and-fire model omits these mechanisms.^[ref] Across connected neurons, branching axons distribute outputs while converging synapses combine inputs; spike trains can support temporal coding and rate coding, and synaptic plasticity changes the influence of an input. Connectivity and cellular dynamics together determine the computation.^[ref][ref]

Testing the connection between structure and function. Whole-cell recording connects anatomy to a measured membrane potential. In a published mouse protocol, a two-photon microscope guides solution-filled glass pipettes to neurons; an amplifier and bath reference electrode complete the electrical recording apparatus. A high-resistance seal forms against the cell membrane, then brief suction opens the membrane patch beneath the tip. In current clamp, the amplifier supplies a chosen electric current and records the resulting membrane potential, unlike voltage clamp, which controls voltage and measures electric current. The investigators used $500\mathrm{ms}$ current steps of several amplitudes to characterize excitability and firing, and negative current pulses to estimate input electrical resistance.^[ref]

The observable is a voltage trace, including graded responses and action potentials. Comparing injected electric current with that trace tests how input becomes output; it does not identify every underlying ion channel. The protocol checks access electrical resistance, which can distort voltage and action potential measurements, and includes intervals without stimulation to record spontaneous activity. In a teaching replication, repeated zero-input trials and monitoring baseline drift would provide further controls; these are recommended comparisons, not additional results attributed to the paper. A recording at the soma also cannot establish the local voltage everywhere in a branching dendrite, and this anesthetized preparation does not establish behavior in every awake neuron.^[ref]

A complementary experiment used simultaneous whole-cell recordings from the soma and an apical dendrite or axon of the same pyramidal neuron in a brain slice. The relative onset times of action potentials, together with sodium currents in excised dendrite membrane patches, supported axonal initiation followed by active propagation into dendrites. Pairing sites within one neuron is a useful comparison because it avoids confusing differences between cells with differences between compartments. Instrument timing and comparable recording quality would be essential controls when reproducing the inference. Only the published abstract was accessible here, so no unverified timing values, drug controls or channel distributions are supplied.^[ref]

An organism is an individual living system, made of one biological cell or an integrated assembly of biological cells. An Escherichia coli cell is an entire organism; a neuron is normally a specialized part of an animal. Metabolism, regulated exchange through cell membranes, and inherited information connect these very different scales. See OpenStax Biology 2e, 1.2: living systems and levels of organization.

Keep two questions separate: how many biological cells make the organism, and how those biological cells are organized. A yeast and an Escherichia coli are both unicellular organisms, but the yeast is a eukaryote and the Escherichia coli a prokaryote. A plant and an animal are multicellular organisms with eukaryotic cellular organization. Neither distinction ranks organisms as better or worse: natural selection acts on reproduction in particular environments.

Osmosis is net movement of water across a boundary whose permeability differs for water and relevant solutes. The direction depends on the chemical potential of water, including both dissolved material and pressure. A cell wall can let water reach the cell membrane, yet oppose expansion through turgor pressure. Zero net movement does not mean individual water molecules have stopped crossing.

Model a spatially uniform cell membrane as a capacitor of membrane capacitance $C_m$ in parallel with membrane electrical resistance $R_m$ and a fixed leak reversal potential $E_L$. Exclude active ion channels, seal leak current and pipette capacitance. For electric current $I$ injected into the biological cell, electric charge conservation yieldsStarting at $V(0)=E_L$ and applying constant $I$ gives the ordinary differential equation solutionThe steady state rise is $I{R}_m$; the time constant is $R_m{C}_m$. With $I=50\mathrm{pA}$, $R_m=200\mathrm{M\Omega }$, $C_m=50\mathrm{pF}$ and $E_L=-70\mathrm{mV}$, the rise is $10\mathrm{mV}$ and ${\tau }_m=10\mathrm{ms}$. At one time constant the rise is $10(1-e^{-1})\mathrm{mV}\approx 6.321\mathrm{mV}$. The figure's uncompensated pipette voltage adds $I{R}_s=1\mathrm{mV}$ for $R_s=20\mathrm{M\Omega }$. The membrane voltage is continuous at step onset in this model, while the pipette voltage immediately acquires that access drop.

Checking the units is instructive: electrical resistance times capacitance has units $\Omega \mathrm{F}=\mathrm{s}$, and electric current times electrical resistance has units of voltage. Unlike the passive voltage clamp transient under patch-clamp series resistance, this ideal current clamp membrane time constant is set by $R_m{C}_m$, not $R_s{C}_m$. Strong current steps can recruit voltage-gated ion channels; the passive model then fails and cannot generate an action potential. Small pulses of both signs, stable access and repeated baseline measurements help test whether the passive approximation is appropriate.

Patch clamp connects an electrode to a small area of cell membrane through a solution-filled patch pipette. A gigaohm seal around the rim makes tiny electric currents through ion channels distinguishable from seal leak current. The beautiful change of scale is from a population's average response to individual opening and closing events in single-channel recording.

Separate two questions. The configuration determines which cell membrane is accessible: an intact patch in cell-attached recording, an excised inside-out patch or outside-out patch, or intracellular access in whole-cell recording. The recording mode determines what is commanded and what is observed: voltage clamp commands an electric potential difference and measures electric current; current clamp commands electric current and measures membrane potential. Whole-cell recording supports both modes. A patch can contain several ion channels; a small recording area does not establish that only one is present.

The 1976 article Single-channel currents recorded from membrane of denervated frog muscle fibres describes an extracellular fire-polished pipette with a $3$–$5\mu \mathrm{m}$ opening and $2$–$5\mathrm{M\Omega }$ electrical resistance. It contained saline and a channel-activating compound. Two separate intracellular electrodes supplied local voltage clamp of the muscle fibre; the patch amplifier measured local electric current. Cooling to $6$–$8{}^{\circ }\mathrm{C}$ and hyperpolarization helped resolve elementary events. Figure 2 shows step-like pulses with a $200\mathrm{Hz}$ filter at $-120\mathrm{mV}$ and $8{}^{\circ }\mathrm{C}$. Discrete amplitudes and overlapping events supported individual ion channel openings rather than a smoothly varying population response. This was neither whole-cell recording through the patch pipette nor current clamp. The specialized conditions improved visibility but limit generalization to warmer preparations; filtering can conceal brief openings.^[ref]

For a new single-channel recording experiment, useful controls include a matched recording without the activating compound, controlled membrane potential, repeated seal tests, and an explicitly stated filter frequency response. These are proposed controls, not claims that every one was performed in that 1976 figure. Changing membrane potential tests the single-channel current-voltage relation; changing the recording filter tests whether a short pulse's apparent amplitude is an instrument artifact. A flat baseline establishes neither an absence of ion channels nor an absence of very brief events.

Peptidoglycan is a mesh of linked sugar chains cross-linked by short chains of amino acids in the cell walls of most bacteria. Its absence from the cell walls of archaea helps distinguish envelope chemistry without confusing either cell wall with a cell membrane. See OpenStax Microbiology, 3.3: cell walls and peptidoglycan.

Phospholipids are lipids containing a phosphate group as part of their structure linked by covalent bonds. The familiar membrane-forming phospholipids are amphiphilic: a hydrophilic head region with chemical polarity coexists with a hydrophobic, largely nonpolar hydrocarbon region. These descriptions refer to different parts of the same molecule, not to two separate substances. See IUPAC Gold Book: phospholipids and IUPAC Gold Book: amphiphilic.

A typical two-chain glycerophospholipid provides a useful example: a glycerol scaffold carries two fatty acid-derived acyl groups through ester linkages, plus a phosphate-containing head region. Phosphatidylcholine is one example. This scaffold describes an important subclass, rather than all phospholipids: sphingomyelin has a different backbone, and even glycerophospholipids need not all have two acyl groups. See IUPAC–IUB, Nomenclature of Lipids (1976), Lip-1.5 and Lip-2.1–2.6.

Polar does not mean negatively charged overall. At near-neutral pH, phosphatidylcholine is zwitterionic: its phosphate region carries negative electric charge and its choline region positive electric charge, with zero net electric charge for the molecule. Counting those opposite charges gives $(-1)+(+1)=0$; it does not remove their local interactions with water. See Lodish et al., Molecular Cell Biology: membrane lipids.

In a lipid bilayer, two membrane leaflets orient their hydrophilic heads toward the water on either side and their hydrophobic chains toward the shared interior. The hydrophobic effect helps explain this organization through the free energy of the water and lipids together. It is not a special repulsive chemical bond between chains and water. Which organization is favored also depends on molecular geometry, temperature, concentration, and the surrounding chemical solution; a phospholipid label alone does not guarantee a lipid bilayer. See Alberts et al., Molecular Biology of the Cell: the lipid bilayer.

This organization supplies a flexible barrier for compartments. A fluid lipid bilayer allows lipids to undergo diffusion within each membrane leaflet; barrier function therefore coexists with motion of molecules, as in the fluid mosaic model. It is not completely impermeable: small nonpolar molecules such as molecular oxygen and carbon dioxide cross much more readily than ions. In a cell membrane, ion channels and other membrane transport proteins provide selective routes; the existing membrane transport article explains their driving forces. See Alberts et al.: principles of membrane transport.

In 1925, E. Gorter and F. Grendel extracted lipids from red blood cells and compared the surface area of a one-molecule-thick film on water with the estimated total surface area of the red blood cells. Their table gave ratios near two, supporting a two-layer covering; they also proposed heads facing the aqueous surroundings on both sides. The inference depends on recovering the relevant lipids, estimating the red blood cell surface area correctly, and comparing compatible packing in the film and the cell membrane. It was indirect evidence, not an image of the lipid bilayer. The paper itself notes possible losses during evaporation. See Gorter and Grendel, On Bimolecular Layers of Lipoids on the Chromocytes of the Blood, Journal of Experimental Medicine 41 (1925), 439–443.

Plants are eukaryotes. A typical photosynthetic leaf cell has a cell nucleus, mitochondria, chloroplasts, and a cell wall outside its cell membrane. A root cell need not have chloroplasts; the plant's parts specialize for different functions. Plants perform cellular respiration as well as photosynthesis. See OpenStax Biology 2e, 4.3: plant cell organization.

A plant cell wall provides reinforcement outside the cell membrane, with cellulose as a major structural component. It is a composite rather than a solid sheet of pure cellulose. Wall construction varies with the kind and developmental state of the biological cell.

Plasmolysis is withdrawal of the membrane-bounded contents from parts of a cell wall after water loss. A sufficiently concentrated external hypertonic solution, with solutes effectively excluded by the cell membrane over the observation time, can cause this. The cell wall remains; the enclosed material contracts. Plasmolysis is therefore distinct from osmotic lysis, which breaks the cellular boundary during excessive swelling. A return to a less concentrated surrounding chemical solution can reverse plasmolysis if the biological cell remains functional.^[ref]

A prokaryote is an organism whose biological cells lack a membrane-bounded cell nucleus. The DNA of its chromosomes occupies a nucleoid within the cytoplasm. Bacteria and archaea have this cellular organization. Both contain ribosomes that perform biological translation and a selective cell membrane; neither is a bag of unorganized chemicals. See OpenStax Biology 2e, 4.2: prokaryotic organization.

The word prokaryotic describes organization, not a single exclusive clade. Grouping bacteria and archaea by the absence of a cell nucleus is useful for comparing biological cells, but does not establish that they share a more recent ancestor with one another than either does with eukaryotes. See three-domain system and two-domain system for the different ancestry models.

Prokaryotic does not mean membrane-free. Cyanobacteria contain internal thylakoid membranes for oxygenic photosynthesis, despite lacking chloroplasts and a cell nucleus. Many prokaryotes have circular chromosomes, but circular shape and a single chromosome are not defining requirements. See OpenStax Biology 2e, 22.2: bacterial and archaeal structures.