D3.1 Reproduction

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.

Puberty begins when increased hypothalamic GnRH release stimulates the pituitary to release more LH and FSH.

LH and FSH act on the gonads, increasing gamete production and secretion of steroid sex hormones such as testosterone and oestradiol. These hormones drive primary reproductive maturation and secondary sexual characteristics.

Hypothalamus: GnRH ↑ → pituitary: LH/FSH ↑ → ovaries/testes: gametogenesis and sex-steroid secretion ↑ → developmental changes of puberty.

In a typical male pathway, rising LH supports testicular testosterone secretion while FSH contributes to sperm production; testosterone promotes reproductive maturation and secondary traits.

Puberty timing and visible changes vary among individuals; the defining control is the endocrine signal chain, not one external trait.

Human gametogenesis combines mitosis, cell growth, two meiotic divisions and differentiation to produce haploid sperm or eggs.

One primary spermatocyte can yield four sperm, whereas unequal cytokinesis directs most cytoplasm from one primary oocyte into one ovum.

Both pathways halve chromosome number; the different product numbers arise mainly from equal versus unequal cytokinesis, not a different number of meiotic divisions.

Two linked reactions allow one sperm to enter an egg and then prevent additional sperm from causing polyspermy.

Blocking additional sperm preserves the normal paternal chromosome contribution and prevents an abnormal polyploid zygote.

The acrosome reaction enables penetration; the cortical reaction creates the later block. Reversing these roles gives the wrong mechanism.

After early cleavage, the embryo forms a blastocyst whose outer cells attach to and invade the uterine lining during implantation.

The inner cell mass forms the embryo; the outer trophoblast helps attachment and later placenta formation. Implantation connects embryonic development to maternal support.

Distinguish cleavage; blastocyst formation; implantation; and later organ development in sequence.

A blastocyst reaches the uterus and its trophoblast attaches to the endometrium, allowing implantation to begin.

Fertilization in the oviduct is not implantation; implantation requires later attachment to the uterine lining.

Pregnancy tests detect human chorionic gonadotropin (hCG) using monoclonal antibodies that bind specifically to the hormone.

The early embryo or developing placenta secretes hCG after implantation. hCG maintains the corpus luteum, allowing progesterone secretion to continue, and enters maternal blood and urine.

Urine moves along the test strip → labelled anti-hCG antibody binds hCG if present → the complex is captured by another anti-hCG antibody at the test line → a control line confirms flow and reagent function.

A test taken before urine hCG reaches the detection threshold can be negative even if implantation later produces a detectable concentration.

The test detects hCG, not the embryo directly. A control line does not indicate pregnancy; it indicates that the strip operated correctly.

The placenta supports foetal development by exchanging materials across placental villi while maternal and foetal blood normally remain separate.

Numerous villi provide a large surface area and a short exchange path. Oxygen, nutrients and maternal antibodies move toward foetal blood; carbon dioxide, urea and other wastes move toward maternal blood; placental hormones help maintain pregnancy.

The placenta allows the foetus to remain and develop inside the uterus to a later stage than in mammals without a placenta, while maternal physiology supplies continuous exchange.

Oxygen diffuses down its concentration gradient from maternal blood across a villus into foetal capillaries, while carbon dioxide moves in the opposite direction.

Large surface area does not mean the two blood supplies mix. The placental barrier is selective but not complete; some drugs and pathogens can cross.

Progesterone maintains pregnancy, whereas its decrease near childbirth permits an oxytocin-driven positive-feedback loop of uterine contractions.

After implantation, hCG maintains the corpus luteum so it continues secreting progesterone. Later the placenta becomes the main progesterone source, maintaining the endometrium and reducing uterine contractions.

Near childbirth, progesterone levels fall. Cervical stretch promotes oxytocin release; oxytocin strengthens uterine contractions, which increase cervical stretch and cause still more oxytocin release.

Corpus luteum progesterone → placental progesterone → progesterone falls → contractions/stretch → oxytocin ↑ → stronger contractions → more stretch.

Positive feedback applies to the escalating childbirth loop; pregnancy maintenance is continuity through progesterone, not an LH-surge mechanism from the ovarian cycle.

Evidence about hormone replacement therapy (HRT) and coronary heart disease (CHD) changed when randomized controlled trials tested a correlation reported by observational studies.

HRT users in the observational studies tended to have higher socioeconomic status. Socioeconomic status itself is causally associated with lower CHD risk, so it confounded the apparent protective association.

If lower CHD is caused by healthcare access, diet or other factors linked to socioeconomic status, comparing self-selected HRT users with non-users can wrongly attribute that difference to HRT.

A strong correlation can still be non-causal. The syllabus conclusion is not that HRT prevents CHD: randomized trials found a small increase in risk.