IB Biology SL Interaction and Interdependence Concepts

Enzymes are biological catalysts that increase reaction rate without being consumed.

They provide an alternative pathway with lower activation energy, so more substrate molecules can react at a given temperature. The enzyme is regenerated after products leave its active site.

For a catalyst claim, check:

• reaction rate increases
• activation energy decreases
• enzyme is not used up
• equilibrium position is unchanged

Adding catalase to hydrogen peroxide makes oxygen bubbles appear faster, but the catalase remains available for further reactions.

An enzyme changes kinetics, not the overall energy difference or equilibrium constant.

Metabolism is the complex network of interdependent and interacting chemical reactions occurring in a living organism; each step is catalysed by a specific enzyme.

Enzyme specificity requires many different enzymes, because each active site catalyses only a limited reaction. Linking enzyme-controlled steps lets the products of one reaction become substrates for another.

Cells control metabolic flux by changing enzyme synthesis, activity, location or access to substrate. Regulation at one key step can alter the output of an entire pathway while other pathways continue independently.

In a pathway A → B → C, one enzyme catalyses A → B and a different enzyme catalyses B → C; inhibiting the first step reduces both B formation and downstream C production.

Metabolism is not one reaction or only energy release: it includes all interacting anabolic and catabolic reactions and the controls acting through their enzymes.

Anabolic reactions build larger molecules from smaller units and require energy; catabolic reactions break down or oxidize molecules and often release usable energy.

Anabolism commonly joins monomers by condensation, forming covalent bonds and releasing water. Catabolism includes hydrolysis of macromolecules in digestion and oxidation of respiratory substrates.

Catabolic respiration can supply ATP and reducing power that drive anabolic protein or glycogen synthesis, linking the two parts of metabolism.

Energy input or release is a typical consequence, not the sole classification rule: identify whether the cellular pathway constructs or breaks/oxidizes material.

Most enzymes are globular proteins whose overall three-dimensional fold creates a small active-site pocket for substrate binding and catalysis.

Only a few amino-acid residues directly form the active site, but interactions among many residues elsewhere—hydrogen bonds, ionic attractions, hydrophobic effects and sometimes disulfide bonds—position those catalytic residues correctly.

The active site binds substrate to form an enzyme–substrate complex and presents chemical groups with the charge, polarity and geometry needed to stabilize the transition state and promote reaction.

Changing a residue far from the pocket can disrupt the protein fold and reposition an active-site residue, reducing catalysis even though that altered residue never contacts substrate.

The active site is only a small part of the enzyme, but it depends on the entire globular conformation; a matching outline alone is not enough for catalytic chemistry.

In induced-fit binding, initial substrate contact changes the conformation of both the enzyme active site and the substrate, producing a catalytically effective fit.

Enzyme side chains move to align catalytic groups, while the substrate can be bent, strained or have bonds polarized. These changes make the transition state easier to reach.

Sequence: initial recognition → enzyme–substrate complex → reciprocal conformational change → transition-state stabilization → products form and leave → enzyme returns to a reusable state.

Hexokinase closes around glucose and ATP, aligning them and excluding water; after phosphate transfer, the differently shaped products have weaker interactions and are released.

Induced fit is not a rigid lock-and-key event and does not mean the enzyme permanently changes. Specificity remains because only suitable substrates trigger productive interactions.

Enzyme catalysis requires random molecular motion to bring a substrate into a productive collision with an active site.

Higher kinetic energy increases motion and collision frequency up to the point where enzyme structure becomes unstable. A collision must also have suitable orientation and enough energy for binding and reaction.

Sometimes a large substrate is effectively immobilized, so enzyme molecules diffuse to exposed sites. In other systems the enzyme is immobilized in a membrane, and moving substrate molecules collide with its fixed active sites.

A membrane-embedded enzyme remains in one location while dissolved substrate diffuses through the membrane environment and collides with the active site.

Immobilized does not mean inactive, and faster motion alone cannot guarantee catalysis: molecular complementarity, orientation and enzyme conformation still matter.

Substrate specificity depends on the three-dimensional arrangement and chemistry of amino acids in the active site; denaturation disrupts that arrangement and lowers activity.

A suitable substrate forms complementary shape, charge, polarity and hydrogen-bond interactions. Temperature extremes or unsuitable pH can disrupt bonds maintaining tertiary structure, changing the active site's geometry.

Trace the relationship: amino-acid interactions maintain fold → fold positions active-site residues → substrate binds specifically → catalysis occurs. Denaturation breaks this chain without normally hydrolysing peptide bonds.

If heating moves a charged catalytic residue away from the substrate-binding position, fewer enzyme–substrate complexes form and the reaction rate falls even after the solution is cooled.

Denaturation is a structural loss, not simply temporary active-site occupancy. The protein may remain present and its peptide sequence intact while its function is lost.

Enzyme activity depends on temperature, pH, substrate concentration and enzyme concentration within an appropriate range.

Warming usually increases collisions until bonds in the protein are disrupted; pH changes alter ionization and active-site interactions. More substrate or enzyme increases rate only while another factor is not limiting.

Interpret a rate curve by locating:

• optimum region
• limiting factor
• denaturation or inhibition
• plateau from saturated active sites

Increasing substrate raises rate until every active site is occupied; further substrate then produces little additional increase.

The optimum is not a universal constant: it depends on the enzyme’s structure and cellular environment.

An enzyme reaction rate is measured from the change in substrate or product concentration per unit time.

Choose a signal proportional to concentration, keep conditions controlled and use the initial linear section before substrate depletion or product inhibition changes the rate.

A sound measurement includes:

• dependent signal and calibration
• controlled temperature and pH
• initial-rate interval
• repeats and uncertainty

A colorimeter can track product colour every ten seconds; the slope of absorbance against time estimates the initial rate.

A final product amount alone cannot distinguish a fast reaction from a slow reaction allowed to run longer.

Enzymes lower activation energy by providing an alternative reaction pathway that stabilizes the transition state; reactant and product energy levels remain unchanged.

Energy must be supplied to distort or break bonds in substrate before new product bonds can form. Bond formation then releases energy; the balance between starting and ending states determines the overall energy change.

On an energy profile, catalysed and uncatalysed curves begin and end at the same levels, but the catalysed curve has a lower peak. More molecules can reach that lower transition-state barrier at the same temperature.

Read the vertical gap from reactants to the peak as activation energy: the enzyme reduces this gap but does not alter the vertical difference between reactants and products.

An enzyme does not remove the barrier, add net energy or make an endergonic reaction exergonic. It changes rate, not the equilibrium position.

ATP—adenosine triphosphate—is a small soluble nucleotide that distributes energy between energy-releasing reactions and energy-requiring cell work.

ATP can move within the cell, release a manageable amount of energy rapidly by hydrolysis and transfer its terminal phosphate to coupled reactions. It is continuously regenerated rather than stored in large quantities.

Its adenine, ribose and three-phosphate structure supports reversible cycling with ADP. Respiration supplies energy to form ATP; ATP hydrolysis then drives transport, synthesis or movement near the point of use.

A membrane pump couples ATP hydrolysis to a conformational change that moves ions against an electrochemical gradient, while ADP and phosphate are returned to ATP-producing pathways.

ATP is an energy-transfer currency, not the original source of energy and not long-term energy storage. Energy comes from reactions such as respiration and is partly transferred through ATP.

Hydrolysis of adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and inorganic phosphate releases energy that can be coupled to cell work.

Energy from respiration is required to phosphorylate ADP + phosphate back to ATP. Rapid ATP ↔ ADP cycling links energy-yielding reactions to energy-requiring processes without requiring a large ATP store.

ATP supplies active transport across membranes, anabolic synthesis of macromolecules, movement of whole cells and movement of components such as chromosomes or motor proteins.

ATP hydrolysis powers a membrane pump; respiration then provides energy for ADP + Pi → ATP, allowing the same carrier system to support another round of transport.

ATP hydrolysis releases sufficient energy for many cell tasks, but a numerical kilojoule value is not required. ATP is recycled rather than used once.

Cell respiration is an enzyme-controlled system that transfers energy released from carbon compounds into ATP; glucose and fatty acids are major substrates, although other organic compounds can also be used.

Word equations: glucose + oxygen → carbon dioxide + water; glucose → lactate. In both cases energy released is transferred to ATP, but mitochondrial aerobic stages produce far more.

Cell respiration is chemical energy transfer inside cells; gas exchange is movement of oxygen and carbon dioxide across a surface. Mitochondria are required for aerobic but not human anaerobic respiration.

Cell-respiration rate can be measured as substrate use or product formation per unit time, with results normalized when organisms differ in mass or number.

In a respirometer, soda lime absorbs carbon dioxide, so a pressure or gas-volume decrease reflects oxygen uptake. Keep temperature constant in a water bath and use a control without respiring material to correct for non-biological pressure changes.

Use the calibrated capillary displacement to find oxygen-volume change, subtract the control change, divide by elapsed time, then divide by sample mass if samples are being compared.

A respirometer measures oxygen uptake only when carbon dioxide is appropriately absorbed and the system is sealed. Temperature, pressure, mass, activity and acclimation time must be controlled.

Photosynthesis captures light energy and stores it as chemical energy in organic molecules.

Pigments absorb photons and excite electrons; electron transfer creates ATP and reduced NADP, which then drive carbon fixation. The process depends on light, pigments, membranes, water, carbon dioxide and suitable conditions.

Trace the energy conversion:

• photon absorbed by pigment
• electron transfer and proton gradient
• ATP and reduced NADP formed
• carbon compounds synthesized

A leaf exposed to light can use ATP and reduced NADP from the thylakoid reactions to build carbohydrate in the stroma.

Light provides energy but is not itself converted directly into glucose molecules.

The overall photosynthesis equation shows carbon dioxide and water converted to carbohydrate using light energy: 6CO₂ + 6H₂O → C₆H₁₂O₆ + 6O₂. Carbon dioxide supplies the carbon skeleton and is reduced using hydrogen derived from water. Oxygen is released when water is split by photolysis in the light-dependent reactions, not directly from CO₂. Glucose represents a carbohydrate product; the products can be used to make starch, sucrose and other organic compounds.

• Word equation: carbon dioxide + water → glucose + oxygen, using light energy.
• Symbol equation: 6CO₂ + 6H₂O → C₆H₁₂O₆ + 6O₂.
• O₂ comes from photolysis of H₂O.
• Plants, algae and cyanobacteria perform oxygenic photosynthesis.

Photosynthetic pigments can be separated and identified because they differ in solubility in the mobile solvent and attraction to the stationary phase.

Extract pigments, place a small concentrated spot on paper or a thin-layer plate, keep the spot above the solvent, allow the solvent front to rise, then mark the solvent front immediately and observe the separated bands.

If a pigment travels 4.2 cm while the solvent front travels 6.0 cm, Rf = 4.2 ÷ 6.0 = 0.70. Identify a pigment using both its colour and an Rf reference obtained with the same solvent and stationary phase.

Rf has no unit and normally lies between 0 and 1. It depends on the solvent and stationary phase, so an Rf from different conditions is not a secure identification; band distance alone is not pigment abundance.

An absorption spectrum shows the proportion of each wavelength absorbed by a pigment; an action spectrum shows the measured rate or effectiveness of photosynthesis at each wavelength.

Only photons with suitable energies are absorbed and excite electrons in pigment molecules. Chlorophylls and accessory pigments absorb different wavelength ranges, so their combined absorption helps explain the action spectrum.

Plot wavelength in nanometres, with the corresponding light colours, on the horizontal axis. For an action spectrum, calculate photosynthesis rate from oxygen production or carbon-dioxide consumption at each wavelength and plot rate on the vertical axis.

If oxygen production is greatest in blue and red light and lowest in green light, the action spectrum has blue and red peaks that broadly match pigment absorption; accessory pigments can make the curves differ.

Absorption and photosynthesis rate are different dependent variables. Do not label an action-spectrum y-axis as absorbance, and compare rates only when intensity and other limiting factors are controlled.

At any moment, the limiting factor is the condition in shortest effective supply relative to photosynthetic demand; increasing it raises rate until another factor becomes limiting.

State a testable hypothesis, vary one independent variable—carbon-dioxide concentration, light intensity or temperature—and measure photosynthesis rate as the dependent variable. Control the other two, plant material, time and measurement conditions; repeat measurements.

Vary light with lamp distance or a light meter, CO₂ with known hydrogencarbonate concentrations or gas control, and temperature with a thermostatically controlled water bath. Measure an initial oxygen-production or CO₂-consumption rate.

A rate rising with light intensity and then reaching a plateau supports the hypothesis that light was initially limiting; at the plateau, CO₂ concentration, temperature or biochemical capacity may limit instead.

A hypothesis is provisional and needs repeated testing. A plateau does not mean photosynthesis has stopped, and moving a lamp can also change temperature unless heat is controlled.

Carbon-dioxide enrichment experiments test how higher atmospheric CO₂ may alter photosynthesis and plant growth, but responses depend on other limiting factors.

Compare enriched and ambient-CO₂ treatments with replication. Record photosynthetic rate and longer-term growth or biomass while monitoring controlled variables such as light, temperature, water, nutrients and plant age.

A crop may show greater CO₂ uptake under enrichment when light and nutrients are sufficient, but little additional biomass under shade or nutrient limitation. This conditional response improves predictions of future growth.

Higher CO₂ does not guarantee a proportional or permanent rise in photosynthesis or yield. Greenhouse results cannot be transferred to natural ecosystems without considering enclosure effects and field interactions.

A neuron is a specialized cell of the nervous system that conducts electrical impulses along elongated nerve fibres.

The cell body contains cytoplasm and the nucleus. Multiple shorter dendrites usually conduct impulses toward the cell body, while one long axon conducts impulses away toward other neurons or effector cells.

Identify the nucleus and cytoplasm in the cell body, then distinguish the long single axon from the multiple shorter dendrites. Fibre length and branching vary with neuron function.

A motor neuron's long axon can carry an impulse from the central nervous system to a distant muscle, while its dendrites receive inputs from other neurons.

An axon and dendrites are cellular projections, not separate cells. Neuron shape varies, so use fibre number, length and direction of impulse rather than assuming every drawing has the same layout.

The resting potential is the negative voltage across a resting neuron's polarized plasma membrane, maintained by sodium and potassium ion gradients.

ATP supplies energy to the sodium–potassium pump, which moves Na⁺ out and K⁺ in opposite directions against their gradients. The membrane is more permeable to K⁺ at rest, so more positive charge diffuses out than enters and the inside remains negative relative to outside.

ATP-driven pumping establishes and maintains high Na⁺ outside and high K⁺ inside; selective leak channels create unequal ion movement; separated charge produces membrane polarization and a measurable membrane potential.

If ATP production stops, the pump can no longer maintain the gradients. Existing gradients may persist briefly, but continued leakage gradually erodes the negative resting potential.

The pump maintains the gradients over time; it does not directly create each action potential. A concentration gradient and a voltage gradient both influence ion movement.

An action potential is a brief, threshold-triggered reversal of membrane potential that propagates along an axon.

Voltage-gated sodium channels open rapidly during depolarization, then inactivate while potassium channels open to repolarize the membrane. Refractory periods prevent immediate re-firing in the same segment. The threshold is a condition, not a fixed promise: if it is not reached, the full action potential does not start.

Trace the phases:

• threshold
• Na⁺ influx and depolarization
• K⁺ efflux and repolarization
• hyperpolarization and recovery

A stimulus below threshold produces no full impulse, while a threshold stimulus produces an impulse with a similar amplitude.

Stronger stimuli are coded mainly by impulse frequency, not by a larger action-potential amplitude.

Impulse conduction speed increases with axon diameter and myelination because both allow local currents to influence the next excitable membrane region more rapidly.

Describe a positive correlation when conduction speed rises as axon diameter rises, and a negative correlation when one variable falls as the other rises. The correlation coefficient r gives direction and strength; R² estimates the proportion of variation in conduction speed explained by the fitted relationship.

If r = 0.90 for diameter and speed, the association is strong and positive; R² = 0.81 means about 81% of the observed variation in speed is explained by the fitted relationship, not that diameter is proven to be the sole cause.

Correlation does not by itself prove causation. Faster impulses do not have larger action-potential amplitudes; speed and signal strength are different properties.

A synapse is a junction where a presynaptic cell communicates with a postsynaptic cell, usually through neurotransmitter release.

The synaptic cleft separates membranes, creating a one-way delay in chemical synapses. Receptors on the postsynaptic membrane convert transmitter binding into ion-flow or intracellular effects. The synapse is a junction, so the signal must be converted before it can cross to the next cell.

Describe a chemical synapse:

• presynaptic terminal
• vesicles and cleft
• postsynaptic receptors
• signal termination

An action potential at a motor neuron terminal releases transmitter that binds receptors on a muscle fibre.

A synapse is not simply a physical gap; receptor type and transmitter removal determine the response.

Arrival of an action potential at a presynaptic terminal opens voltage-gated calcium channels and triggers vesicle fusion.

Ca²⁺ entry binds release machinery, causing exocytosis of neurotransmitter into the synaptic cleft. Enzymatic breakdown, reuptake or diffusion then terminates the signal. This one-way sequence explains why changing calcium entry can alter how strongly a synapse communicates.

Trace release:

• action potential arrives
• Ca²⁺ channels open
• vesicles fuse
• transmitter binds and is cleared

Blocking presynaptic calcium entry reduces transmitter release even if the action potential still reaches the terminal.

The electrical impulse triggers release; it does not cross the cleft as the same electrical current.

An excitatory postsynaptic potential (EPSP) is a graded depolarization that makes the postsynaptic neuron more likely to reach action-potential threshold.

Neurotransmitter released from the presynaptic terminal diffuses across the synaptic cleft and binds a transmembrane receptor. Acetylcholine can open ligand-gated channels, allowing net positive charge to enter and depolarize the postsynaptic membrane.

Sequence: transmitter release → diffusion across cleft → receptor binding → channel opening → local depolarization. Acetylcholine acts at many synapses, including neuromuscular junctions.

One acetylcholine input may produce a small EPSP below threshold; overlapping excitatory inputs can sum at the axon hillock until an action potential is triggered.

An EPSP is local and graded, not an all-or-none action potential. The neurotransmitter does not carry the electrical impulse across the cleft; receptor-controlled ion movement changes voltage.

Integration joins specialised parts into a working whole.

In a multicellular organism, tissues, organs and organ systems exchange information and materials so the organism can coordinate one response. Nervous impulses are fast; hormones travel in blood and can act on distant targets.

Name the parts; identify the signal or material crossing between them; then state the coordinated outcome.

During exercise, receptors and the brain increase heart and ventilation activity while blood delivers oxygen to working muscle.

Integration is more than a list of organs: the explanation must include communication and a shared function.

Organisation builds new properties at each level.

Cells of one type form tissues, different tissues form organs, and organs form systems. Interactions between parts can produce an emergent capability that no isolated cell performs alone.

cell → tissue → organ → system → organism; at each step ask what cooperation adds.

Cardiac muscle, connective tissue and blood vessels combine in a heart that pumps blood; no one tissue performs the whole job.

Hierarchy is not just size ranking; it is a functional relationship between levels.

Animal organs are integrated by nervous and hormonal messages and by blood transport of materials and energy between organs.

During exercise, motor nerves stimulate skeletal muscles, epinephrine coordinates responses in several organs, and blood carries oxygen and glucose to muscle while transporting carbon dioxide away.

Blood is both a transport route for hormones and a carrier of non-message materials. Integration requires source, route, target and coordinated outcome—not just a list of organs.

The brain is a central integration organ that combines information from several inputs before coordinating responses.

Current sensory inputs can be compared with stored information. Changes in neural connections support learning, while stored and retrievable information supports memory; both influence how later inputs are interpreted and acted on.

Trace input from several receptors → combined processing in the brain → comparison with learned or remembered information → coordinated output. Detailed slow-acting neurotransmitter mechanisms are not required.

A learner sees a traffic signal, hears an approaching vehicle and recalls the crossing rule; the brain combines these inputs and memory before coordinating whether to step forward or wait.

Integration is not simple forwarding of one sensory message. The objective concerns combining inputs plus learning and memory, not memorizing detailed functions of many brain regions.

The spinal cord can integrate a rapid response.

The spinal cord links body and brain, but grey matter can connect sensory input to motor output without waiting for conscious brain processing. White matter carries impulses along longer pathways.

receptor → sensory neurone → spinal integration → motor neurone → effector.

Touching a hot surface triggers a withdrawal through a spinal reflex; the brain receives information as the movement is already beginning.

A reflex is not brain-free information: the spinal cord handles the immediate response, while the brain can receive the signal afterwards.

Sensory neurones carry transduced information to the CNS.

A receptor detects a stimulus and converts its energy into a change in membrane potential. If threshold is reached, an action potential travels along a sensory neurone to the CNS.

identify stimulus; receptor type; transduction; threshold; direction to CNS.

Salt ions entering taste-receptor channels depolarise the receptor cell, which then excites a sensory neurone carrying the signal to the brain.

A stronger stimulus is not encoded by a larger action potential; it can increase firing frequency or recruit receptors.

Motor neurones turn CNS decisions into muscle action.

Motor neurones carry action potentials from the CNS to an effector. At a neuromuscular junction, acetylcholine depolarises the muscle membrane and starts the calcium-controlled contraction sequence.

CNS signal → motor axon → acetylcholine release → muscle action potential → calcium release.

An impulse at a motor end plate opens ion channels; the resulting muscle action potential travels along the fibre and triggers calcium release from the sarcoplasmic reticulum.

The motor neurone does not contract the muscle directly; transmitter and membrane events link the two cells.

A peripheral nerve is a bundle of many nerve fibres—axons—from sensory and motor neurons, protected and organized by connective tissue sheaths.

In transverse section, each fibre appears cut across. Some have a visible myelin sheath around the axon and others are unmyelinated; groups of fibres are surrounded by protective connective tissue and supplied by blood vessels.

Identify outer protective sheath, bundles of fibres, myelinated fibres and unmyelinated fibres. Sensory axons carry input toward the CNS; motor axons carry output toward effectors.

A mixed nerve to a limb can contain sensory fibres carrying touch information toward the spinal cord and motor fibres carrying impulses back to skeletal muscle.

A nerve is not one giant neuron. Myelinated and unmyelinated fibres remain separate signal pathways inside the same protective bundle.

A pain withdrawal reflex is an involuntary response integrated in the spinal cord, with skeletal muscle as the effector.

A free sensory nerve ending in the hand detects a damaging stimulus. The sensory neuron enters the spinal cord and synapses with one interneuron in grey matter, which synapses with a motor neuron; the motor neuron stimulates a skeletal muscle to withdraw the hand.

Free nerve ending → sensory neuron → single interneuron in spinal grey matter → motor neuron → skeletal-muscle contraction. The short spinal route starts withdrawal before conscious pain processing is complete.

Touching a hot object activates the pain receptor; flexor muscle contraction withdraws the hand while impulses also travel to the brain and pain becomes conscious.

The reflex does not bypass the CNS—the spinal cord is part of the CNS. The brain can be informed in parallel but is not required to initiate this immediate response.

The cerebellum coordinates movement and balance.

The cerebellum compares intended movement with sensory feedback and adjusts motor output. It helps timing, posture, balance and smooth coordination rather than choosing the goal of a movement.

separate movement planning from coordination; link sensory feedback to corrective output.

If balance shifts while walking, cerebellar processing helps alter muscle activity before the person falls.

The cerebellum does not initiate every voluntary action; it refines the accuracy and timing of movement.

Melatonin links darkness to the body clock.

Melatonin released by the pineal gland rises in darkness and helps synchronise circadian timing, including sleep propensity. Light reaching the retina can suppress its release.

light input → clock pathway → pineal melatonin → timing effect.

A bright screen late at night can delay the melatonin rise, shifting the timing signal even if the person feels tired.

Melatonin is a timing hormone, not an instant anaesthetic; sleep also depends on behaviour and other signals.

Epinephrine prepares several organs for immediate demand.

Epinephrine from the adrenal medulla binds receptors in target tissues during acute stress. It raises cardiac output, widens airways and mobilises glucose so muscles can respond quickly.

hormone source; receptor-bearing target; response in heart, airways and liver; adaptive purpose.

A sudden threat increases epinephrine, accelerating heart rate and glycogen breakdown while reducing investment in digestion.

The hormone does not affect every cell equally: receptor type and tissue context determine the response.

The hypothalamus coordinates endocrine control through the pituitary.

The hypothalamus links neural information to hormone release and regulates the pituitary with releasing or inhibiting signals. Pituitary hormones then act on distant glands or tissues.

stimulus or brain signal → hypothalamus → pituitary → target gland/tissue → feedback.

A hypothalamic signal can control pituitary FSH release, which then influences reproductive tissues.

The hypothalamus and pituitary are control centres, not the final target for every hormone they regulate.

Heart rate is adjusted by negative feedback after baroreceptors and chemoreceptors send sensory information to the medulla.

Baroreceptors in the carotid sinus and aortic arch monitor arterial pressure. Chemoreceptors in carotid and aortic bodies and the brainstem monitor blood pH and oxygen/carbon-dioxide concentrations.

The medulla integrates this input and changes autonomic nerve impulses to the heart. This alters heart rate and the strength of contraction, changing stroke volume so circulation opposes the detected disturbance.

If arterial pressure falls, reduced baroreceptor firing causes medullary output that increases heart rate and contraction strength, helping restore cardiac output and pressure.

Heart rate is only one component of cardiac output: cardiac output = heart rate × stroke volume. Receptors detect changes; the medulla coordinates the response.

Ventilation rate is controlled by negative feedback from chemoreceptors that detect blood-pH changes linked mainly to carbon dioxide.

CO₂ dissolves and forms carbonic acid, increasing H⁺ and lowering pH. Chemoreceptors in the brainstem detect the change; the respiratory control centre sends nerve impulses to the diaphragm and intercostal muscles to alter breathing rate and depth.

Raised CO₂ → lower pH → brainstem chemoreceptor input → stronger or more frequent signals to diaphragm/intercostals → increased ventilation → more CO₂ removed → pH moves back toward normal.

During exercise, increased respiration produces extra CO₂. Ventilation rises, increasing gas exchange and limiting the fall in blood pH.

The lungs do not directly decide how to correct pH. Chemoreceptor detection and nervous output to breathing muscles coordinate the response.

Control of movement through the digestive tract shifts between voluntary CNS actions at the endpoints and involuntary enteric control between them.

The central nervous system voluntarily initiates swallowing and participates in voluntary control of faecal egestion. Between these points, the enteric nervous system coordinates circular and longitudinal smooth-muscle contractions that move contents by peristalsis.

Voluntary initiation of swallowing → involuntary ENS-coordinated peristalsis through gut → voluntary component of egestion. Local stretch and chemical signals help the ENS coordinate contraction behind and relaxation ahead.

After a person chooses to swallow, an oesophageal peristaltic wave moves the bolus to the stomach without conscious control.

Peristalsis is not one simultaneous squeeze and is not consciously directed along the whole gut; the ENS coordinates the travelling pattern between voluntary endpoints.

Pathogens cause disease by entering and damaging a host.

A pathogen is a disease-causing organism or particle. Bacteria, viruses, fungi and protists reproduce or use host cells in ways that disrupt tissues, release toxins or trigger damaging inflammation.

classify the pathogen; route of entry/transmission; host process disrupted; resulting signs.

A respiratory virus enters droplets, infects airway cells and spreads before the immune response clears it.

Pathogen presence is not identical to symptoms: dose, host susceptibility and immune response also affect disease.

Skin and mucous membranes block entry.

Keratinised skin forms a physical barrier, while mucus traps particles and cilia move them away. Secretions such as lysozyme, tears and stomach acid add chemical protection.

barrier; trapped or killed agent; route out; limitation if the barrier is breached.

Mucus in an airway traps microbes and cilia move the mucus toward the throat, reducing access to lung tissue.

These are first-line defences, not antigen-specific memory responses.

Blood clotting rapidly seals a cut in the skin, limiting blood loss and pathogen entry.

Platelets at damaged tissue release clotting factors that start a cascade. The cascade produces thrombin, which rapidly converts soluble fibrinogen into insoluble fibrin strands.

Cut → platelet activation and clotting-factor release → cascade → thrombin → fibrinogen converted to fibrin → fibrin mesh traps erythrocytes → clot seals wound.

At a skin cut, the fibrin mesh stabilizes the platelet plug and traps red blood cells, forming a clot that can dry into a protective scab.

Thrombin converts fibrinogen to fibrin; it is not the mesh itself. Further clotting-factor details are outside this objective.

Innate immunity responds to broad pathogen categories and remains essentially unchanged during life; adaptive immunity targets particular antigens and forms memory.

Phagocytes can engulf unfamiliar bacteria immediately, while a later exposure to the same antigen triggers a faster antibody response from retained adaptive memory cells.

Innate does not mean weak, and adaptive does not mean immediate. For this objective, no innate component other than phagocytes needs to be named.

Phagocytes control infection by leaving the blood, moving amoeboidly to infected tissue, recognizing pathogens, engulfing them and digesting them.

Chemical signals guide phagocytes to an infection site. The flexible cell membrane changes shape during amoeboid movement and encloses a recognized pathogen by endocytosis in a vesicle.

Blood → amoeboid movement into infected tissue → pathogen recognition → endocytosis/phagosome → lysosome fusion → lysosomal enzymes digest pathogen.

A neutrophil leaves a capillary, crawls through tissue, encloses a bacterium and digests it after lysosomes fuse with the phagosome.

Phagocytosis is an innate cellular response, not antibody production. Engulfment contains the pathogen; lysosomal enzymes perform digestion.

Lymphocytes are adaptive immune cells that circulate in blood and are also concentrated in lymph nodes, where antigen-specific cells cooperate to produce antibodies.

An individual has a very large number of B lymphocytes with different receptors. Each B-cell clone is capable of making one specific type of antibody, so the population collectively recognizes many antigens.

Location: blood and lymph nodes. Diversity: many B-cell specificities. Cooperation: antigen-specific helper T cells help activate matching B cells, which can form antibody-secreting cells.

Only the small B-cell population with receptors complementary to a viral surface antigen is selected to produce antibodies against that antigen.

One B cell does not make every antibody. Large population diversity plus cooperation between lymphocytes creates the adaptive repertoire.

An antigen is a recognition molecule that can bind a specific antibody or lymphocyte receptor and trigger antibody production.

Most antigens are glycoproteins or other proteins and are located on the outer surface of a pathogen, where immune receptors can encounter them.

Antigen = molecular target, not the whole pathogen. Complementary receptor binding selects an antigen-specific response; different surface antigens select different lymphocyte clones.

Erythrocyte surface antigens from an incompatible blood group can stimulate antibody binding and production after transfusion, causing dangerous cell agglutination or destruction.

An antigen is not automatically an entire foreign organism. It is a recognizable molecule or molecular region, commonly a surface protein or glycoprotein.

An antigen-specific B lymphocyte is activated only after it interacts directly with its matching antigen and receives contact-dependent help from an activated helper T lymphocyte specific to the same antigen.

The two matching signals confirm antigen identity before the B cell divides. After activation, the B cell can produce antibody-secreting plasma cells and retained memory cells.

Specific antigen binds B-cell receptor → helper T cell activated by the same antigen contacts B cell → B cell activates → clonal expansion → plasma and memory cells.

A B cell recognizing one viral protein receives help only from a helper T cell activated by that same antigen type, preventing an unrelated B-cell clone from expanding.

Direct antigen binding alone is not sufficient in this model, and helper T-cell contact must be antigen-matched. Unactivated B cells do not yet secrete large antibody quantities.

Because only a small number of B cells recognize a given antigen, an activated B cell divides repeatedly by mitosis to form a large clone.

Clonal expansion supplies enough plasma cells to secrete an effective quantity of one antibody type. Every plasma cell in the clone inherits the selected antibody specificity.

Rare matching B cell → activation → repeated mitosis → clone of genetically matching cells → many plasma cells secrete the same specific antibody; some cells can become memory cells.

A selected B cell responding to a bacterial surface antigen produces thousands of plasma-cell descendants, all releasing antibodies complementary to that antigen.

Antibodies are secreted in quantity by differentiated plasma cells, not by every inactive B cell. Mitosis increases cell number without changing specificity.

Memory cells accelerate a second response.

Some activated B and T cells persist as memory cells. On re-exposure they respond more rapidly and strongly, often preventing noticeable disease.

primary exposure; memory formation; secondary exposure; faster/larger response.

A booster vaccine re-stimulates memory cells, producing protective antibody levels sooner than the first dose.

Memory is antigen-specific and can weaken; it does not make a person immune to every pathogen.

HIV spreads through particular body-fluid routes.

HIV transmission requires infected blood, semen, vaginal fluids or breast milk to reach susceptible tissue. It is not spread by casual contact, food sharing or intact skin.

source fluid; route of exposure; susceptible tissue; prevention barrier.

Sharing a contaminated needle can transfer infected blood directly into circulation, whereas a handshake cannot.

Transmission risk depends on exposure and viral load; a positive test does not identify the route by itself.

HIV can cause AIDS by reducing CD4 T cells.

HIV infects and progressively destroys CD4 helper T cells. As immune coordination falls, opportunistic infections and cancers become more likely; this clinical state is AIDS.

HIV entry/replication; CD4 decline; loss of coordination; opportunistic disease.

A person with low CD4 counts may develop an infection that a healthy immune system would normally control.

HIV infection and AIDS are not synonyms: treatment can delay or prevent progression to AIDS.

Antibiotics are chemicals that block processes in bacteria while having little or no effect on corresponding processes in eukaryotic host cells.

Selective targets include bacterial cell-wall synthesis or bacterial ribosomes. Human cells lack bacterial walls and their cytoplasmic ribosomes differ, allowing a susceptible bacterial infection to be treated without the same target effect on human cells.

Identify bacterial target → explain disrupted bacterial process → explain why eukaryotic cells lack or differ in that target → predict treatment only for susceptible bacteria.

An antibiotic that blocks bacterial peptidoglycan-wall synthesis can stop dividing bacteria, while human cells have no peptidoglycan wall to block.

Viruses have no bacterial cell wall, ribosome or independent bacterial metabolism; they replicate using host-cell machinery. Antibiotics therefore do not control viral infections.

Antibiotic exposure selects resistant bacterial variants, allowing strains resistant to several antibiotics to evolve and spread.

Resistance genes arise through mutation or are acquired from other bacteria. An antibiotic kills susceptible cells, while resistant survivors reproduce and pass resistance vertically or transfer genes horizontally.

Existing genetic variation → antibiotic selection → resistant survival → reproduction/gene transfer → resistance frequency rises → different resistance genes can accumulate in one multiresistant strain.

Repeated exposure to different antibiotics can successively select a pathogenic strain carrying resistance to several drug classes, leaving fewer effective treatments.

Antibiotics do not direct bacteria to mutate. Careful use—only when appropriate, with the prescribed agent and regimen—reduces unnecessary selection pressure but cannot make evolution impossible.

A zoonosis is an infectious disease that can transfer from another animal species to humans, through several different transmission routes.

Zoonoses are prevalent among human infectious diseases because humans interact with livestock, wildlife, food systems and vectors. Ecology and behaviour change the opportunities for cross-species exposure.

Animal origin does not guarantee efficient human-to-human spread. Identify the reservoir or animal link, the transfer route and whether onward human transmission occurs.

Vaccination stimulates immunity to a specific pathogen without causing the disease itself.

A vaccine supplies pathogen antigens directly, or supplies DNA or RNA sequences that host cells use to make the antigen. Adaptive immune activation produces specific effector cells and retained memory cells.

Antigen vaccine: antigen is delivered. Nucleic-acid vaccine: DNA/RNA code for antigen is delivered. Both expose the immune system to the target antigen and develop memory without the full infection.

After immunization, later exposure to the pathogen reactivates antigen-specific memory cells, producing a faster response that can prevent disease.

A vaccine does not need to contain a live pathogen. Protection is antigen-specific and may require multiple doses or boosters.

Herd immunity protects some people indirectly.

When enough people are immune, an infectious case has fewer susceptible contacts and transmission chains are interrupted. The required coverage depends on pathogen transmissibility and mixing.

immune fraction; contact network; effective reproduction; vulnerable people left unprotected.

High measles vaccination coverage can prevent an imported case from reaching many susceptible people.

A simple percentage threshold is not universal; immunity may wane and coverage can be clustered unevenly.

COVID-19 data must be compared using consistent definitions, time windows and denominators, with percentage change and percentage difference chosen for different questions.

Use percentage change for movement from an earlier baseline to a later value. Use percentage difference to compare two values when neither is designated as the original baseline. Check whether counts, rates or proportions are being compared.

Cases rising from 100 to 130 gives percentage change = (30 ÷ 100) × 100 = 30%. Comparing rates 40 and 50 gives percentage difference = (10 ÷ 45) × 100 = 22.2% (3 s.f.).

A percentage is only interpretable with its denominator and context. Testing effort, case definitions, reporting delays, population size and time window can change apparent trends; association alone does not establish cause.

A population is an interacting group of organisms of the same species living in a defined area at the same time.

Members normally have opportunities to breed with one another. Reproductive isolation—little or no gene flow through breeding—can distinguish one population of a species from another.

State the species, spatial boundary and time; show interaction or breeding opportunity; use reproductive isolation to separate neighbouring populations when relevant.

Frogs of one species breeding in a connected pond system can form one population, while a geographically isolated group with no interbreeding is treated as a separate population.

A population is not every organism in a habitat—that is closer to a community. Sharing a species name alone is insufficient if groups are reproductively isolated.

Population size is estimated by random sampling when counting every individual is impractical, disruptive or impossible.

Random selection gives locations or individuals an unbiased chance of inclusion, making a sample more representative before its mean or marked fraction is extrapolated to the whole area.

Define target population and area → select positions or individuals randomly → standardize sampling effort → repeat → calculate estimate and uncertainty.

Random quadrat coordinates across a large meadow give an average plant density that can be multiplied by meadow area, avoiding convenient locations near a path.

Sampling error is the difference between the sample-based estimate and the true population size. Randomness reduces placement bias but cannot remove sampling error.

Random quadrat sampling estimates abundance of sessile plants or animals whose individuals can be counted within a known area.

Map the study area, generate random coordinates, place equal-area quadrats at those positions, count individuals using a consistent boundary rule, repeat many times, and scale the mean count per quadrat to the total habitat area.

Use a calculator to obtain the standard deviation of quadrat counts. A small standard deviation suggests counts are similar and distribution is relatively even; a large standard deviation suggests strong spatial variation or clumping.

If 1 m² quadrats average 4 plants and the habitat is 250 m², the estimated population is 4 × 250 = 1,000 plants; the standard deviation shows how variable the counts were around that mean.

Quadrats suit sessile organisms, not freely moving animals. Random placement does not guarantee representation if too few or poorly sized quadrats are used; the standard-deviation formula need not be memorized.

Capture–mark–recapture estimates mobile populations.

A first sample is captured, marked harmlessly and released. After mixing, a second sample is taken; the marked fraction helps estimate the total population.

N≈(first caught × second caught)/marked recaptured; check mixing, mark retention and equal catchability.

If 40 fish are marked, 50 are caught later and 10 are marked, the estimate is about 200 fish.

The calculation fails if marks are lost, animals learn the trap or the population changes between samples.

Carrying capacity is a resource-limited population size.

Carrying capacity is the population size an environment can support over time under specified conditions. Resource limits and feedback make growth slow as the population approaches it.

identify limiting resource; link density to birth/death rate; state that capacity can change.

A drought lowers available food, so the carrying capacity for grazing animals falls even if the species is unchanged.

Carrying capacity is not a fixed species constant; it depends on environment and timescale.

Negative feedback restrains population growth.

As density rises, competition, disease or predation can reduce births or increase deaths. The response opposes the change and tends to return population size toward a range.

disturbance → density-dependent response → birth/death change → correction.

Crowding increases disease transmission, lowering survival and slowing further population growth.

Not every population change is negative feedback; density-independent storms can reduce numbers without crowding.

Population growth is exponential while resources are abundant and limiting factors are weak, but becomes sigmoid as density-dependent limits slow growth near carrying capacity.

During exponential growth, a roughly constant per-capita growth rate produces an increasingly steep rise. In a sigmoid model, competition and other density-dependent factors reduce net growth until births plus immigration balance deaths plus emigration near carrying capacity.

Test exponential growth by plotting population size on a logarithmic vertical axis against time on a linear horizontal axis: exponential data form an approximately straight line. For the IB sigmoid model, a separate lag phase is not expected.

An introduced population with abundant food may initially show a straight line on the semi-log graph; later points fall below that line as resource limitation increases and the population approaches a plateau.

A population curve is an idealized model, not a guaranteed trajectory. A steep slope means rapid change, not the greatest population size; migration, seasons and disturbances can alter the pattern.

A sigmoid growth model can be tested by repeatedly measuring a population grown under controlled conditions, such as yeast or duckweed.

Start replicate cultures with comparable initial populations, keep temperature, nutrients, volume and light conditions controlled, measure population size at regular intervals, calculate means, and plot population size against time.

Look for an initially increasing growth rate, a transition as limiting factors intensify, and a plateau near carrying capacity. Compare replicate data with the ideal S-shaped curve and identify deviations.

Duckweed frond number can be counted daily in replicate containers; nutrient depletion, shading and crowding eventually reduce net growth and produce a plateau.

The sigmoid is a model. A plateau may shift if conditions change, and deviations must not be hidden by forcing a fitted curve through poor data.

Intraspecific relationships occur within one population: individuals compete when they require the same limited resource, but may cooperate when joint action raises survival or reproduction.

As a plant population becomes denser, individuals of the same species shade one another and compete for light; cooperative animal hunting can instead increase each participant's food access.

Competition need not involve aggression, and cooperation can have costs. An interaction between two different plant species is interspecific and does not demonstrate this objective.

A community contains interacting populations.

A community is the populations of different species living and interacting in one area. Its composition and structure depend on abiotic conditions and biotic relationships.

list populations; define boundary; identify interaction and environmental filter.

A pond community includes algae, plants, fish, bacteria and invertebrates interacting under the pond’s chemistry and light.

A community is not the same as an ecosystem: an ecosystem also includes abiotic stores and flows.

Interspecific relationships are interactions between different species that change survival, growth or reproduction within a community.

Classify from the mechanism and effects, not from proximity alone. Commensalism is a valid ecological term but is not one of the six categories required for this objective.

Mutualism is an interspecific relationship in which both species receive a net benefit.

Name the benefit to each organism. Merely living together is not enough to establish mutualism, and the balance of benefit can change with environmental conditions.

An introduced species can become invasive when it acquires limiting resources more effectively than local endemic or native species and spreads at their expense.

In southern China, the introduced vine Mikania micrantha grows rapidly over local vegetation. Its canopy captures light and space, shading slower-growing native plants and reducing their access to photosynthetic resources.

For a local case, identify introduced species → named resource → acquisition advantage → reduced resource availability or performance of local endemic/native species → spread and community impact.

Compare light interception, cover or growth of local plants in plots with and without dense Mikania; greater vine resource capture provides evidence for its competitive advantage.

Non-native does not automatically mean invasive. Spread and harm must be demonstrated, and resource competition must be separated from other mechanisms such as predation or disease.

Interspecific competition is indicated—but not proved—when one species performs better in the absence of another.

In a barnacle removal study, greater occupation of lower shore by one species after its competitor is removed supports competition as the restriction on its realized distribution.

Experiments manipulate a variable; observations do not. Better performance without a second species is evidence for competition, but alternative environmental differences must still be excluded.

A chi-squared test can test whether presence or absence of species A is associated with presence or absence of species B across several sampling sites.

Build a 2 × 2 table: both present, A only, B only, neither. Null hypothesis: the species' distributions are independent. Calculate each expected count as (row total × column total) ÷ grand total.

Compare calculated χ² with the chosen critical value or p-value. A significant result rejects independence and supports an association between distributions.

Association does not prove interspecific competition: both species may respond to the same abiotic factor, or association may reflect another interaction. Sampling sites must be independent and expected counts suitable for the test.