IB Biology SL Continuity and Change Concepts

DNA replication produces exact copies of DNA with identical base sequences, apart from rare copying errors.

Accurate copies preserve genetic information when cells or organisms reproduce. In multicellular organisms, replication supplies genomes for cell division during growth and replacement of damaged or worn tissues.

Original DNA sequence → replication → two matching DNA molecules → genetic continuity in reproduction, growth and tissue replacement.

Before a skin cell divides to replace lost tissue, its DNA is copied so both daughter cells can inherit the same base sequence.

Replication copies DNA; transcription makes RNA and translation makes polypeptide. ‘Identical’ describes base-sequence information, not two newly synthesized strands without templates.

Semi-conservative replication produces DNA molecules in which each double helix contains one parental strand and one newly synthesized strand.

When the original strands separate, each acts as a template. Complementary base pairing preserves information while retaining one physical strand from the original molecule in each product.

Identify a product by checking: one old strand; one new strand; complementary pairing between them.

After one round, heavy parental DNA in a density experiment is replaced by two intermediate molecules, each containing one old and one new strand.

Semi-conservative does not mean half the bases are copied randomly; the strand pattern is the key prediction.

Helicase separates the two DNA strands, while DNA polymerase builds complementary DNA strands from the exposed templates.

Helicase unwinds the double helix and breaks hydrogen bonds between complementary bases. DNA polymerase selects complementary DNA nucleotides and joins them into a growing strand.

Helicase: unwind and break inter-strand hydrogen bonds. DNA polymerase: use each original strand as a template and join complementary nucleotides.

At a replication fork, helicase exposes template bases; polymerase then places A opposite T and C opposite G while extending the new DNA.

Helicase does not synthesize DNA, and polymerase does not separate the original strands. Detailed 5′/3′ directionality belongs to the later HL objective.

PCR amplifies a selected DNA region; gel electrophoresis then separates DNA fragments mainly by length.

Primers define the target ends. Each thermal cycle uses high temperature to separate strands, lower temperature for primer binding, and a suitable extension temperature for heat-stable Taq DNA polymerase to synthesize new DNA.

Load amplified fragments into wells. Negatively charged DNA moves toward the positive electrode through the gel; shorter fragments move farther than longer fragments in the same time.

Primers amplify a variable DNA locus; electrophoresis separates the resulting fragments, and a size marker allows their approximate lengths to be compared.

PCR increases the amount of target DNA; electrophoresis separates fragments. Primer specificity, contamination controls and the size marker affect interpretation.

PCR and gel electrophoresis support DNA profiling by amplifying and comparing variable DNA markers.

In a paternity investigation, a child's marker alleles must be explainable by the biological parents. In a forensic investigation, a crime-scene DNA pattern can be compared with reference samples.

Use several independent markers: each additional matching marker reduces the probability that an unrelated person shares the full pattern by chance. Include positive/negative controls and guard against contamination.

A child's allele not supplied by the known parent must match the candidate parent's allele at each tested marker; one matching marker is weak, whereas a consistent multi-marker pattern is stronger evidence.

A profile supports or excludes a biological relationship/source; it does not alone prove when or how DNA reached a location. More markers reduce false-match probability but do not make laboratory error impossible.

Transcription is the synthesis of an RNA strand using one DNA strand as the template.

RNA polymerase binds the selected DNA region, separates a short section, matches RNA nucleotides to exposed template bases and joins the nucleotides into RNA.

DNA template exposed → complementary RNA nucleotides pair → RNA polymerase forms the RNA backbone → RNA separates and DNA re-forms its double helix.

For a protein-coding gene, RNA polymerase produces an mRNA transcript whose base sequence can later be translated.

Transcription synthesizes RNA, not DNA or polypeptide. Promoter/transcription-factor detail belongs to the later HL initiation objective.

Temporary hydrogen bonds between complementary bases allow an RNA sequence to be specified from a DNA template during transcription.

DNA hydrogen bonds separate locally while the covalent sugar–phosphate backbones remain intact. RNA nucleotides form complementary hydrogen bonds to exposed template bases before RNA polymerase joins them.

DNA template A pairs with RNA U; DNA template T pairs with RNA A; DNA C pairs with RNA G; DNA G pairs with RNA C.

A DNA template segment 3′-TACG-5′ specifies RNA 5′-AUGC-3′: template adenine is represented by uracil in RNA, not thymine.

Complementary does not mean identical. Hydrogen bonds guide base choice; phosphodiester bonds form the stable RNA backbone.

A single DNA strand can act repeatedly as a transcription template without its base sequence changing.

RNA polymerase reads the template and joins separate RNA nucleotides; it does not consume or replace the DNA bases. After the transcription bubble passes, the DNA strands pair again.

DNA opens locally → RNA copy is synthesized → RNA leaves → original DNA sequence remains conserved and available for later transcription.

A non-dividing neuron may transcribe the same essential gene many times while conserving that gene's DNA sequence throughout the life of the cell.

Stable does not mean inaccessible: local opening permits transcription. The RNA transcript can change or degrade while the DNA template sequence remains unchanged.

Transcription is the first stage of gene expression and a key point at which expression can be switched on or off.

Cells contain many genes but do not express all of them at the same time. If a gene is not transcribed, its mRNA is unavailable for translation; starting transcription makes expression possible.

Regulatory state → transcription on/off → mRNA absent/present → translation possible/not possible. Different cell types express different subsets of the same genome.

A cell can switch on transcription of an enzyme gene when the enzyme is needed while other genes remain untranscribed.

Transcriptional control is a key switch, not the only possible control. More mRNA does not guarantee proportionally more protein if later steps are limiting.

Translation uses a ribosome to read mRNA codons and join amino acids in the encoded order.

tRNA molecules pair anticodons with codons and deliver specific amino acids. The ribosome forms peptide bonds as it moves from start toward stop.

Trace: start codon; tRNA matching; peptide bond; codon movement; stop codon.

A ribosome reading three codons adds three specified amino acids before a stop signal ends the chain.

Translation reads RNA; it does not copy mRNA back into DNA. The ribosome assembles the chain; later folding and modification determine whether the polypeptide becomes functional.

During translation, mRNA supplies codon order, tRNAs deliver specific amino acids and the ribosome positions the molecules and catalyses peptide-bond formation.

mRNA first binds to the small ribosomal subunit. The large subunit forms the catalytic complex and can hold two tRNAs simultaneously so the amino acid on one can be linked to the growing chain on the other.

mRNA: ordered codons. tRNA: anticodon plus specific amino acid. Small subunit: binds/positions mRNA. Large subunit: binds two tRNAs and supports peptide-bond formation.

One tRNA holds the growing chain while a second matching tRNA places the next amino acid beside it; a peptide bond extends the polypeptide.

No component determines the protein alone: mRNA sets sequence, tRNAs match codons, and the ribosome coordinates assembly.

A three-base tRNA anticodon forms complementary base pairs with a three-base mRNA codon during translation.

Correct codon–anticodon pairing positions the tRNA carrying the amino acid specified by that codon, transferring mRNA sequence information into polypeptide sequence.

Read the mRNA codon 5′→3′; write the antiparallel complementary anticodon; pair A–U and C–G; identify the amino acid from the mRNA codon, not the anticodon.

mRNA codon 5′-AUG-3′ pairs with tRNA anticodon 3′-UAC-5′, positioning the tRNA carrying methionine.

Codon and anticodon are complementary and antiparallel, not identical. DNA–RNA pairing during transcription is a different Objective.

The genetic code is a triplet, degenerate and nearly universal mapping from mRNA codons to amino acids or stop signals.

Four bases taken two at a time give only 16 combinations, fewer than the 20 amino acids; triplets give 4³ = 64 codons, enough for all amino acids plus stop signals.

Degenerate means more than one codon can specify the same amino acid. Universal means the same codon usually specifies the same amino acid across organisms, with limited exceptions.

UUU and UUC both code for phenylalanine, showing degeneracy; UUU has one defined meaning, so degeneracy is not ambiguity.

Read codons in a fixed triplet frame. Universality is a broad biological pattern, not a claim that no exceptions exist.

A genetic-code table is used by reading mRNA codons 5' to 3' and matching each to its amino acid.

The first, second and third bases select positions in the table. Reading-frame errors shift every later codon, so strand labels and grouping matter.

Use: locate start; split triplets; read each codon; stop at a stop codon; report amino-acid order.

For 5'-AUG-GCU-UAA-3', AUG starts, GCU adds alanine and UAA terminates. If one base is omitted before AUG, every later triplet may be regrouped, so the table must be used from the correct start frame.

Do not use the DNA template directly as if it were mRNA; transcribe first.

During elongation, a matching tRNA enters, a peptide bond forms and the ribosome moves to the next codon.

Repeating this cycle extends the chain in a fixed direction while mRNA advances through the ribosome. Energy from charged tRNAs and factors supports the process.

Track each cycle: codon recognition; chain transfer; translocation; empty tRNA exit.

After one cycle the chain has one additional amino acid and the next codon is exposed.

Elongation is not random amino-acid addition; codon recognition controls the order. The cycle stops at a termination signal rather than continuing until the physical end of the mRNA.

A point mutation can change one mRNA codon, replace one amino acid and alter how a polypeptide folds or functions.

The effect depends on code degeneracy, mutation position and the chemical properties of the original and replacement amino acids. Some substitutions are synonymous; others alter interactions stabilizing protein structure.

In sickle-cell disease, a point substitution changes a β-globin codon from GAG to GUG in mRNA, replacing glutamic acid with valine. The hydrophobic replacement promotes abnormal haemoglobin association and changes red-cell shape under low oxygen.

DNA base substitution → changed mRNA codon → possible amino-acid replacement → altered side-chain interactions → altered protein structure/function.

A mutation is not automatically harmful or structure-changing: degeneracy can make it synonymous, and some amino-acid replacements have little effect.

A gene mutation is a structural change in the base sequence of DNA within a gene.

Changing 5′-ACT-3′ to 5′-AGT-3′ is a substitution; changing it to 5′-ACCT-3′ is an insertion.

A mutation is the DNA sequence change itself. Its effect on a codon, protein or phenotype is a possible consequence, not part of the definition.

A single-nucleotide polymorphism (SNP) results from a base substitution, but the substitution may or may not change one amino acid in a polypeptide.

An mRNA codon change from GAA to GAG is silent because both specify glutamate; a change to a stop codon can shorten the polypeptide.

A substitution does not automatically change protein function. First identify the new codon and its amino-acid or stop outcome.

Insertions and deletions are likely to stop a polypeptide functioning when they shift its reading frame or change a large section of its sequence.

Ribosomes read mRNA in triplets. Adding or removing a number of bases that is not a multiple of three regroups every downstream codon, often changing many amino acids and creating an early stop codon.

Not a multiple of three → frameshift and changed downstream codons. Multiple of three → no frameshift, but amino acids are added or removed. A major insertion or deletion can still disrupt structure and function even without a frameshift.

Deleting one base near the start of a coding sequence shifts the triplet grouping for most of the remaining mRNA and is therefore likely to produce a non-functional polypeptide.

A three-base insertion or deletion avoids a frameshift, but it is not automatically harmless because the added or missing amino acid may be important.

Gene mutations can result from errors in DNA replication or repair and from DNA damage caused by mutagens.

Damage is not yet a permanent mutation if accurate repair restores the original sequence. It becomes a mutation when the altered sequence remains and is copied.

A mutagen increases mutation probability; it does not produce the same mutation in every exposed cell.

Mutations occur randomly with respect to an organism's need: no known natural mechanism deliberately changes a particular base in order to create a useful trait.

A mutation can occur anywhere in the genome before its consequence is tested by the environment. Natural selection later changes variant frequencies because some carriers reproduce more successfully.

Random relative to need does not mean uniform probability. Base identity and sequence context, DNA repair, gene activity and mutagen exposure can make some sites or cells more likely to mutate than others.

Antibiotic exposure does not instruct bacteria to make a resistance mutation. A resistant variant may already exist, then increase in frequency when susceptible cells die.

Mutation bias can make some changes more frequent without making them purposeful or directed toward advantage.

The consequence of a mutation depends on whether it occurs in the germ line or in a somatic cell lineage.

A mutation in a sperm cell may be inherited by a child, whereas a mutation acquired in one skin cell can spread through a local clone but is not normally passed to offspring.

Somatic does not mean harmless: a non-inherited mutation can still cause cancer or other serious effects in the individual.

Gene mutation is the original source of new alleles and therefore of all genetic variation.

Most mutations are neutral or harmful to an individual, but a population needs heritable variants for natural selection to act on. Selection changes allele frequencies; it does not create the initial DNA differences.

Mutation creates a new allele → inheritance can place it in a population → environmental conditions affect reproductive success → natural selection can change its frequency over generations.

A new allele that improves drought survival may spread when carriers leave more offspring in dry conditions, while the same allele may provide no advantage in another environment.

Mutation alone is not adaptation. The variant must be heritable and influence reproductive success in the relevant environment.

In every living organism, cell division generates new cells when one parent cell divides to produce two daughter cells.

Producing daughter cells allows an organism to grow, replace worn cells, repair damaged tissue or reproduce asexually. The genetic material must be distributed before the cytoplasm separates so both daughters can function.

A skin cell can divide into two daughter cells that replace cells lost from the surface, while a single-celled organism can divide to produce two organisms.

The parent cell is sometimes called a mother cell, but this does not imply sex or fertilization. Cell division means generation of daughter cells, not growth of one cell alone.

Cytokinesis splits the cytoplasm of a parent cell between its daughter cells, but animal and plant cells achieve the split differently.

An animal cell pinches from its outer edge toward the centre, whereas a plant cell builds the separating plate from the centre outward.

Cytokinesis divides cytoplasm; mitosis or meiosis divides the nucleus. The events can overlap in time but are not the same process.

Cytokinesis is usually equal, but unequal cytokinesis can give daughter cells very different amounts of cytoplasm.

Whatever their final sizes, both daughters must receive at least one mitochondrion and any other organelle that can arise only by growth and division of a pre-existing organelle.

Unequal cytoplasm does not mean unequal nuclear DNA: chromosomes can still be segregated correctly before asymmetric cytokinesis.

Eukaryotic cells use mitosis to maintain chromosome number and genome, whereas meiosis halves chromosome number and generates genetic diversity.

Nuclear division must occur before cell division so each daughter receives a nucleus rather than becoming an anucleate cell.

Meiosis is not simply mitosis twice: homologous chromosomes pair and separate in its first division, creating the reduction in chromosome number.

DNA replication occurs before nuclear division so each daughter nucleus can receive a complete chromosome set.

During S phase, each chromosome becomes two sister chromatids joined at a centromere. Division then separates chromatids or homologues according to the process.

Trace: replication; duplicated chromosome; spindle attachment; chromosome separation; daughter nuclei.

If a cell entered mitosis without replicating DNA, one daughter could receive too little genetic material.

Replication doubles DNA amount, not chromosome number in the usual chromosome-counting convention.

Mitosis and meiosis both condense chromosomes and move them accurately between new nuclei.

Histones organize DNA into nucleosomes, and further supercoiling condenses the long chromatin fibres into compact chromosomes that can be moved without tangling.

Spindle microtubules attach to chromosomes, and microtubule motors plus microtubule shortening or growth generate directed movement. Alignment and separation differ between divisions, but the same general machinery organizes chromosome distribution.

In both mitosis and meiosis II, sister chromatids move toward opposite poles; in meiosis I, homologous chromosomes move apart while sister chromatids remain together.

Shared condensation and movement mechanisms do not make the outcomes identical: the chromosome partners separated and the number of divisions differ.

Mitosis proceeds through prophase, metaphase, anaphase and telophase, each solving a different chromosome-distribution problem.

Chromosomes condense and attach to spindle fibers, align at the equator, separate sister chromatids and re-form nuclei at opposite poles. Cytokinesis follows.

Use the sequence: condense; align; separate chromatids; rebuild nuclei.

A metaphase cell has chromosomes aligned at the equator; anaphase begins when sister chromatids move apart.

Interphase is not a mitosis stage, although it prepares the cell by growing and replicating DNA.

Identify a mitosis phase from the position and appearance of chromosomes, using several features rather than cell shape alone.

Two groups of V-shaped chromatids moving away from the equator indicate anaphase, whether seen in a diagram, a prepared root-tip cell or a micrograph.

A dark stain or rounded cell outline is not enough to identify a phase. Confirm chromosome condensation, alignment or separation and nuclear-envelope state.

Meiosis is a reduction division: one diploid nucleus undergoes two nuclear divisions after one DNA replication to produce four haploid nuclei.

Diploid nuclei contain two homologous chromosome sets; haploid nuclei contain one. Homologous chromosomes separate in meiosis I, halving the number of sets, and sister chromatids separate in meiosis II without another round of replication.

Diploid nucleus → DNA replication → homologous pairs segregate in meiosis I → two haploid nuclei with duplicated chromosomes → chromatids segregate in meiosis II → four haploid nuclei.

In a sexual life cycle, haploid gametes produced by meiosis fuse at fertilization, restoring the diploid chromosome number instead of doubling it in every generation.

Chromosome number is reduced in meiosis I, even though each chromosome still has two chromatids until meiosis II.

Nondisjunction is failure of homologous chromosomes or sister chromatids to separate, producing gametes with abnormal chromosome numbers.

If an extra chromosome enters a gamete, fertilization can create a zygote with three copies of one chromosome. The phenotype depends on chromosome and gene dosage.

Trace: division error; abnormal gamete; fertilization; chromosome count; developmental consequence.

A gamete containing two copies of chromosome 21 can combine with a normal gamete to produce trisomy 21.

Nondisjunction is a chromosome-segregation error, not a point mutation in one gene.

Meiosis generates genetic diversity through random orientation of bivalents and crossing over between non-sister chromatids.

At metaphase I, each bivalent can face either pole independently. The maternal and paternal homologues therefore segregate into many possible whole-chromosome combinations.

During prophase I, non-sister chromatids of homologous chromosomes exchange corresponding DNA at chiasmata, producing recombinant chromatids with new combinations of linked alleles.

One gamete can receive a maternal chromosome carrying a short paternal segment after crossing over, plus a different random mixture of the remaining maternal and paternal homologues.

Random fertilization adds further variation but is not a meiotic process. Meiosis does not direct combinations toward future advantage.

Solvation occurs when polar water molecules surround and interact with dissolved ions or polar solute molecules.

Water's partially negative oxygen is attracted to positive ions, while its partially positive hydrogens are attracted to negative ions. Polar solutes can also form hydrogen bonds with water.

These attractions form hydration shells, separate solute particles and keep them dispersed. Water molecules engaged around solutes have less freedom of movement than in pure water.

When sodium chloride dissolves, oxygen ends of water face Na⁺ and hydrogen ends face Cl⁻, producing oriented hydration shells.

Water does not form hydrogen bonds with every solute: ion–dipole attraction hydrates ions, while hydrogen bonding requires suitable polar groups.

Across a partially permeable membrane, net water movement is from the less concentrated solution toward the more concentrated solution.

If solution A is 0.10 mol dm⁻³ sucrose and solution B is 0.40 mol dm⁻³, A is hypotonic to B and net water movement is from A to B if water can cross but sucrose cannot.

At SL, express the comparison using solute concentration—not 'high water concentration'. Tonicity is relative and depends on solutes that do not freely cross the membrane.

Osmosis is the net movement of water across a partially permeable membrane, and the cell's environment determines its direction.

In an isotonic environment, water molecules continue crossing in both directions at equal rates. This is dynamic equilibrium, not an absence of molecular movement.

A cell placed in hypertonic solution loses water and decreases in volume because more water leaves than enters.

Always state the solution relative to the cell. 'Hypotonic' or 'hypertonic' without a comparison has incomplete meaning.

Changes in plant-tissue mass or length across a series of sucrose concentrations can be used to estimate the isotonic concentration.

Prepare equal tissue pieces, record initial mass or length, incubate them for the same time in known sucrose solutions, blot consistently, record final values and calculate change.

Plot mean percentage change against sucrose concentration. The x-intercept, where change is 0%, estimates the isotonic concentration. Replicates allow standard deviation to compare spread and standard error/error bars to compare uncertainty in means.

Positive mass change at 0.20 mol dm⁻³ and negative change at 0.30 mol dm⁻³ place the isotonic estimate between those concentrations; interpolate from the fitted graph rather than choosing the nearest raw point.

Zero mean change estimates isotonic conditions; it does not mean water molecules stopped moving. Consistent blotting, initial size and incubation time are needed for a fair comparison.

Cells without a wall can burst in hypotonic solution or shrink in hypertonic solution because their plasma membrane cannot resist large volume changes.

Freshwater unicellular organisms continually gain water from their hypotonic environment, so contractile vacuoles collect and expel excess water. Multicellular animals instead maintain near-isotonic tissue fluid around cells.

A plasma membrane can deform but does not provide the rigid mechanical restraint of a cell wall; active water removal is an adaptation, not a reversal of osmosis.

A cell wall resists expansion when water enters, converting osmotic water uptake into turgor pressure.

The wall’s rigidity balances the inward tendency of water. If water leaves, pressure falls and the membrane can pull away from the wall, producing plasmolysis.

Distinguish wall restraint from membrane transport: water direction first, then pressure and shape.

A plant cell in dilute solution becomes turgid rather than bursting because the wall pushes back as the vacuole expands.

A wall prevents unlimited swelling but does not stop osmosis or guarantee that a severely dehydrated cell survives.

Medical fluids are made isotonic with body tissues to avoid harmful net water gain or loss by cells.

An isotonic saline infusion replaces extracellular fluid without causing appreciable net movement of water into or out of red blood cells.

Isotonic means matched effective osmotic concentration relative to the tissue; it does not mean the solution has the same chemical composition as cytoplasm.

Asexual reproduction uses one parent without gamete fusion and normally produces genetically identical offspring; sexual reproduction uses meiosis and fertilization to produce new allele combinations.

A strawberry runner produces a clone suited to the parent's current habitat, whereas a seed formed after fertilization carries a new allele combination.

Asexual offspring can still differ after mutation or environmental effects; 'clone' refers to their inherited genome, not guaranteed identical phenotype.

Meiosis halves chromosome number in gametes, and fusion of two gametes restores the diploid number in the zygote.

The alternation prevents chromosome number doubling every generation. Independent assortment and crossing over also create combinations before fusion adds another random combination.

Track chromosome number through meiosis; then track the fusion event and the first embryo cell.

A diploid human cell with 46 chromosomes produces gametes with 23; fusion returns the zygote to 46.

Meiosis does not simply make ‘smaller’ cells; its defining outcome is reduced chromosome number plus variation.

In anisogamous species, the male produces smaller motile gametes and the female produces larger nutrient-rich gametes.

The distinction is based on gamete type, not on every secondary trait or an individual’s identity. Different species organise reproductive roles around these gametes in different ways.

Identify the gametes first, then infer the biological sex category used in the syllabus model.

In humans, sperm are small and motile while ova are large and non-motile, so the model labels their producers male and female.

Gamete definitions do not justify assumptions about behaviour, gender, or all reproductive biology.

Human reproductive systems link gamete production, transport, fertilization, implantation and birth through specialized structures.

A labelled diagram must show position and connections as well as names. Fertilization normally occurs in an oviduct; implantation occurs later in the endometrium.

The menstrual cycle combines ovarian and uterine cycles controlled by FSH, LH, oestradiol and progesterone through negative and positive feedback.

A sharp LH peak follows the high-oestradiol positive-feedback switch and occurs just before ovulation.

Feedback direction changes with hormone concentration and cycle stage; oestradiol is not always a positive-feedback signal.

Human fertilization begins in the oviduct when sperm and egg cell membranes fuse and ends with paternal and maternal chromosomes sharing the first zygotic mitosis.

Sperm membrane fuses with egg membrane → sperm nucleus enters while its tail and mitochondria are destroyed → sperm and egg nuclear membranes dissolve → both condensed chromosome sets attach to one mitotic spindle → chromosomes segregate to form two diploid nuclei.

This sequence brings one haploid paternal and one haploid maternal chromosome set into a diploid zygote genome while preventing paternal sperm mitochondria becoming part of the embryo.

The 23 paternal and 23 maternal chromosomes participate together in the first mitosis, so each of the first two embryonic nuclei receives a diploid set.

Fertilization is not implantation: nuclear union begins in the oviduct, while attachment to the endometrium happens later.

IVF treatment temporarily takes control of normal reproductive hormone signalling so artificial hormone doses can induce superovulation.

Normal pituitary hormone secretion is first suppressed to prevent an uncontrolled ovulation. Carefully timed FSH-like stimulation matures several follicles, and an LH-like trigger completes egg maturation before collection.

Suppress normal cycle → stimulate multiple follicles → trigger maturation → collect oocytes → fertilize outside the body → culture embryo(s) → transfer selected embryo(s) to uterus.

Producing several mature oocytes in one controlled cycle gives more opportunities for fertilization and embryo selection than the usual release of one oocyte.

Superovulation increases the number of available oocytes but does not guarantee fertilization, implantation or live birth.

Flowering-plant reproduction is sexual because male and female gametes fuse, even when one hermaphroditic flower produces both pollen and ovules.

Male gametes develop inside pollen grains in anthers; female gametes develop inside ovules in the ovary. Pollination transfers pollen to a stigma, the pollen grain develops a tube, and male nuclei travel to the ovule for fertilization.

Fusion produces a diploid zygote that develops into an embryo; the ovule develops into a seed that contains the embryo.

Pollen carried by an insect reaches a compatible stigma, grows a tube down the style and delivers a male nucleus to the egg cell in an ovule.

Pollination is transfer, not fertilization. A hermaphroditic flower still reproduces sexually when gamete nuclei fuse.

An insect-pollinated flower attracts a pollinator and positions its reproductive structures so pollen is picked up and later deposited on a stigma.

As a bee reaches nectar, the flower's anthers brush pollen onto its body; a later visit places some pollen on another flower's stigma.

For a diagram, annotate each named structure with its function; colour alone does not establish insect pollination.

Plants promote cross-pollination by separating pollen and receptive female structures in time, space or among different plants, then using animals or wind as transfer vectors.

If pollen matures before the stigma of the same flower, pollen arriving later from another plant is more likely to fertilize its ovules.

Cross-pollination increases new gene combinations but is not guaranteed on every visit; self-incompatibility is a separate genetic recognition mechanism.

Self-incompatibility is a genetic recognition system that prevents self-pollen from fertilizing ovules and thereby promotes cross-fertilization.

Matching incompatibility alleles in pollen and stigma can block pollen germination or pollen-tube growth. Compatible pollen from another plant can continue to the ovule.

Self-pollination increases inbreeding, which reduces genetic diversity and can reduce vigour by increasing expression of harmful recessive alleles. Rejecting self-pollen helps maintain variation within the species.

Pollen sharing the stigma's incompatibility class is rejected, while pollen carrying a different compatible class grows a tube and can fertilize the ovule.

Self-incompatibility is not pollen sterility or physical separation; the same pollen may function normally on a genetically compatible plant.

Seed dispersal separates offspring from the parent, and germination begins when water, oxygen and a suitable temperature allow metabolism and growth.

Dispersal reduces crowding and competition. During germination, water activates enzymes, oxygen supports respiration, and the embryo uses stored food until photosynthesis begins.

Check each condition before deciding whether a seed can germinate.

A bean seed kept dry does not germinate; after water and warmth are supplied, respiration rises and the radicle emerges.

A seed can be viable but remain dormant; failure to germinate does not prove it is dead.

In the sexual life cycle common to eukaryotes, meiosis makes haploid gametes and fertilization fuses two gametes to form a diploid zygote.

Meiosis halves chromosome number from 2n to n. Fusion combines one maternal and one paternal set, restoring 2n without chromosome number doubling in every generation.

A diploid individual normally carries two copies of each autosomal gene, one on each homologous chromosome. Each gamete carries one copy, and the zygote receives two again.

A human sperm and ovum each contain 23 chromosomes; after nuclear fusion the zygote contains 46.

Fertilization combines two haploid sets; it does not copy one gamete or make the zygote genetically identical to either parent.

A flowering-plant cross transfers pollen carrying male gametes to a stigma so fertilization can combine known parental alleles.

Pollen is the practical source of male gametes; female gametes are inside ovules in the ovary. Pea flowers can self-pollinate, which helps maintain pure-breeding lines and produce controlled F2 generations.

Cross two pure-breeding parents with contrasting traits, record a uniform F1, then self-pollinate the F1 and compare the F2 counts with the predicted genotype and phenotype ratios.

A Punnett grid predicts probabilities, not exact counts. Controlled crosses are used in crop and ornamental breeding, but pollination is transfer of pollen, not fertilization itself.

A gene is a DNA sequence affecting a characteristic; an allele is one version of that gene; a genotype is the allele combination carried at one or more loci.

Writing Aa identifies the genotype at one locus; it does not by itself name the visible phenotype until the allele relationship is known.

Do not use gene, allele, genotype and phenotype as synonyms. An individual has two alleles at an autosomal locus, while a population may contain more than two.

Phenotype is an observable or measurable characteristic produced by genotype, environment, or an interaction between them.

Genotype sets biological possibilities, while environmental conditions can alter gene expression, development or physiology; the size of each contribution depends on the trait.

A phenotype is not always visible, and an environmental effect does not necessarily change DNA sequence or become inherited.

For a complete-dominance locus, the dominant allele determines the heterozygous phenotype; the recessive phenotype appears only when no dominant allele is present.

One dominant allele may produce enough functional product for the dominant phenotype, so AA and Aa look alike in this model, whereas aa lacks that contribution.

In Aa × Aa, the expected genotypes are 1 AA : 2 Aa : 1 aa but the expected phenotypes are 3 dominant : 1 recessive.

Dominant does not mean common, beneficial or stronger. Dominance describes the phenotype of a heterozygote.

Phenotypic plasticity is the capacity of one genotype to produce different phenotypes under different environmental conditions.

Environmental signals can change which genes are expressed and how much product is made, altering physiology or form without changing the DNA sequence.

Many plastic responses can reverse during an individual's lifetime if the environment changes again; the inherited genotype remains the same.

The same plant genotype may form broader leaves in shade and smaller leaves in bright, dry conditions because development responds to the local environment.

Plasticity is not mutation and does not guarantee that the acquired phenotype is inherited by offspring.

Phenylketonuria (PKU) is an autosomal recessive disorder in which mutation reduces the enzyme that converts phenylalanine to tyrosine.

With insufficient enzyme activity, phenylalanine accumulates and tyrosine production is reduced. Two recessive disease alleles are normally required for the affected phenotype.

Genotype → reduced phenylalanine-hydroxylase activity → disrupted phenylalanine-to-tyrosine conversion → altered metabolite concentrations and phenotype.

Restricting dietary phenylalanine lowers the substrate entering the blocked pathway and can reduce the severity of the phenotype.

Diet can change the phenotype but does not remove or rewrite the inherited PKU alleles.

A SNP is a common one-base DNA difference; multiple alleles are variants of one locus present in a population.

A base change may affect coding, regulation or nothing observable; a diploid person carries at most two alleles even when a population has many. Trace the allele combination through the stated biological mechanism before predicting the result.

Separate population allele variety from the two alleles in one individual.; compare the stated alleles and outcome

The ABO locus has three common alleles, while one person may carry only IA and IB. This gives a concrete prediction from the stated parental information.

A SNP is not automatically harmful or visible. Interpret the result within the stated inheritance model and its sample or environmental limits.

ABO phenotype is determined by IA, IB and i: IA and IB are codominant, while i is recessive to either.

IA makes A antigen; IB makes B; i makes neither; IAIB therefore displays both antigens. Trace the allele combination through the stated biological mechanism before predicting the result.

List the two alleles; apply dominance; identify antigens and phenotype.; compare the stated alleles and outcome

IAi × IBi can produce AB, A, B or O offspring. This gives a concrete prediction from the stated parental information.

Blood type requires alleles from both parents. Interpret the result within the stated inheritance model and its sample or environmental limits.

In incomplete dominance the heterozygote has an intermediate phenotype; in codominance both allele products are detectably expressed.

Self-crossing two pink Mirabilis F1 plants predicts a 1 red : 2 pink : 1 white phenotype ratio when the two alleles show incomplete dominance.

Codominance is not blending: both products remain present. Incomplete dominance does not make either allele 'partly dominant' in every genotype.

In the simplified human model, eggs carry X, whereas sperm carry X or Y; therefore the sperm's sex chromosome determines whether the zygote is typically XX or XY.

The X chromosome carries far more genes than the Y chromosome. Sex-chromosome inheritance therefore also affects many genes unrelated to sex determination.

An X-bearing and a Y-bearing sperm are expected in roughly equal proportions, so each fertilization has approximately equal model probabilities of XX and XY.

XX/XY is a simplified model of typical development; chromosome variation and differences in gene function can produce other biological outcomes.

Haemophilia alleles on the X chromosome reduce a clotting factor; the recessive pattern makes affected XY individuals more common.

An XY individual has one X allele; an XX individual may have a second functional allele; a carrier mother can pass the allele to sons or daughters. Trace the allele combination through the stated biological mechanism before predicting the result.

Write X-linked genotypes and track which parent supplies each X.; compare the stated alleles and outcome

Carrier mother XH Xh and unaffected father XH Y can have an affected son Xh Y. This gives a concrete prediction from the stated parental information.

Probabilities describe a model, not one guaranteed child. Interpret the result within the stated inheritance model and its sample or environmental limits.

A pedigree records phenotype and family relationships across generations so inheritance patterns and possible genotypes can be deduced.

Inductive reasoning proposes a pattern from the observed family data; deductive reasoning predicts who could be affected or carry an allele if that pattern is correct.

Two unaffected parents with an affected child support a recessive hypothesis; if the trait is autosomal recessive, both parents must carry the allele.

Consanguineous partners are more likely to share a rare ancestral recessive allele, but relatedness does not guarantee an affected child. Small pedigrees may fit more than one model.

Continuous variation has many intermediate values and often results from several genes, environmental factors, or both.

In polygenic inheritance, many loci each contribute to the phenotype; environmental conditions can add further variation, often producing a broad distribution.

For student heights, the mean uses every value, the median identifies the middle position and the mode identifies the most frequent value or interval.

Continuous does not mean entirely environmental, and discrete does not mean that only one gene is always involved.

A box-and-whisker plot summarizes a continuous dataset using the minimum, lower quartile (Q1), median, upper quartile (Q3), maximum and any plotted outliers.

The box spans the middle 50% of observations, its internal line is the median, and whiskers show the non-outlying range when outliers are plotted separately.

To compare two student-height samples, compare their medians for centre, their IQRs for spread, their total non-outlying ranges and any outliers.

A longer box means a larger IQR, not necessarily a larger sample. A box plot does not display every observation or prove that two groups differ significantly.

Homeostasis maintains variables in an organism's internal environment within preset narrow limits despite external fluctuations.

Stable tissue fluid lets cells function predictably even when temperature, food intake or water availability outside the body changes.

After a meal raises blood glucose, hormonal regulation brings the concentration back toward its preset range.

Homeostasis is dynamic: values fluctuate around a set point or within limits rather than remaining perfectly constant.

Negative regulation reduces the original change so a regulated variable returns toward its normal range.

The response opposes the disturbance: a rise triggers actions that lower it, and a fall triggers actions that raise it. This stabilizes rather than amplifies the system.

Ask whether the response moves the variable in the opposite direction to the initial deviation.; identify the signal, controller and effector

If body temperature rises, sweating and vasodilation increase heat loss, reducing the rise. This gives a concrete prediction from the stated condition.

Negative means opposing the deviation, not harmful or always below the set point. Interpret the result within the stated biological model and limits.

Pancreatic endocrine cells detect blood glucose: beta cells release insulin when it rises, while alpha cells release glucagon when it falls.

The two opposing hormone responses form negative-feedback loops that reduce the original deviation.

After a carbohydrate-rich meal, rising glucose stimulates beta cells; insulin promotes uptake and storage until secretion falls as the set point is approached.

Glucagon acts mainly on the liver to raise circulating glucose; muscle glycogen is primarily a local fuel store and is not released as blood glucose in response to glucagon.

Diabetes mellitus causes persistent difficulty controlling blood glucose, but type 1 and type 2 begin with different physiological failures.

With too little effective insulin signalling, uptake and storage do not adequately reduce blood glucose after a meal, so hyperglycaemia persists.

Lifestyle is a risk modifier for type 2, not a moral diagnosis or the sole cause. A single high reading does not distinguish the two types.

Human thermoregulation detects deviation in core temperature and coordinates effectors that reverse the change.

A fall in temperature is detected, the hypothalamus coordinates reduced heat loss and increased muscle/adipose heat production, and the response decreases as core temperature recovers.

The regulated variable is core temperature; skin temperature can change more rapidly and acts partly as an early environmental signal.

Human thermoregulation combines physiological and behavioural responses; each effector changes heat transfer or metabolic heat production.

Sweating is most effective when sweat evaporates; high humidity reduces evaporation and therefore reduces cooling.

Vasodilation transfers internal heat toward skin but does not itself remove heat from the body; the environment must accept that heat.

Natural selection is differential survival and reproduction caused by heritable differences; over generations it changes populations and drives evolution.

Heritable variation exists → an environmental or biological pressure affects individuals differently → some genotypes leave more surviving offspring → their alleles become more frequent → population characteristics change.

Operating continuously over billions of years, repeated selection has contributed to life's biodiversity. It can also be observed over short timescales when pressures are strong.

Darwin supplied a convincing selection mechanism and displaced Lamarckian explanations based on inherited acquired characteristics. Replacing a dominant explanatory framework in this way is a scientific paradigm shift.

Individuals do not evolve because they need to. Selection acts on existing phenotypic differences, while evolutionary change is measured across generations.

Mutation creates new alleles by changing DNA sequence; sexual reproduction creates new combinations of existing alleles.

In a sexually reproducing plant, a mutation may introduce a drought-tolerance allele; meiosis and fertilization then place that allele into varied genetic backgrounds.

Selection does not create a needed mutation. Mutations arise without regard to usefulness, and sexual reproduction reshuffles rather than invents alleles.

Populations can produce more offspring than the environment can support, so individuals of the same species compete for limiting resources.

Food, water, light, mineral ions, territory, nesting sites or mates can limit carrying capacity. Individuals that obtain these resources more successfully are more likely to survive and reproduce.

Potential offspring exceed available resources → intraspecific competition occurs → heritable differences affect resource access → reproductive success differs.

When food limits a population, individuals whose inherited feeding traits increase food acquisition may leave more offspring than competitors.

Overproduction means reproductive potential exceeds long-term support; it does not require the population to remain permanently above carrying capacity.

Abiotic conditions can act as selection pressures when they affect survival or reproduction differently among heritable phenotypes.

High or low temperature, drought, salinity, pH and other physical conditions may affect individuals regardless of population density, so they are density-independent pressures.

Abiotic condition changes → physiological performance differs → survival or reproduction differs → alleles associated with advantageous traits become more frequent.

During repeated low-temperature events, plants with inherited frost tolerance may survive and set more seed, increasing the frequency of tolerance alleles.

A useful response is evolutionary adaptation only if it is heritable and changes reproductive contribution; temporary acclimatization alone does not alter allele frequency.

Biological fitness is a genotype's relative contribution of surviving, reproducing offspring to the next generation in a particular environment.

Intraspecific competition exposes differences in adaptation. Survival has evolutionary importance when it increases reproductive opportunity, and reproduction passes the responsible alleles onward.

Compare individuals in the same population: adaptation to current conditions → survival and mating differences → different numbers of fertile offspring → different fitness.

A genotype that survives well but produces no fertile offspring has lower fitness than a competing genotype that leaves many reproducing descendants.

Fitness does not mean strength, health or lifespan in isolation; it is relative, environment-dependent reproductive success.