Source: Lectures 35–37
Tags: reproduction, asexual, sexual, gametogenesis, spermatogenesis, oogenesis, menstrual cycle, ovulation, fertilization, pregnancy, hormones, FSH, LH, estrogen, progesterone, placenta, lactation
Difficulty: Intermediate Prerequisites: Cell division (mitosis, meiosis), basic endocrinology (hormone signalling, feedback loops), and the hypothalamic-pituitary axis.
This block covers animal reproduction from the broadest possible view (asexual vs sexual) down to the molecular details of hormonal regulation of the menstrual cycle and pregnancy. You will compare reproductive strategies across animals, trace the pathways of sperm and egg production, and learn how the hypothalamic-pituitary-gonadal axis coordinates the entire process through feedback loops. The material culminates with fertilisation, implantation, pregnancy, birth, and lactation. If you are behind on meiosis or hormone signalling, revisit those first.
Animals reproduce either asexually (clones, no genetic variation) or sexually (genetic recombination via meiosis and fertilisation). Sexual reproduction is regulated by the hypothalamic-pituitary-gonadal axis, where GnRH drives FSH and LH release, which in turn control gametogenesis and steroid hormone production. In females, the menstrual cycle coordinates follicle development, ovulation, and endometrial preparation through shifting feedback from estradiol and progesterone. Pregnancy is maintained by hormones from the corpus luteum and later the placenta, and birth is triggered by a positive feedback loop involving oxytocin and prostaglandins.
Parthenogenesis
Asexual reproduction in which an egg develops without fertilisation. Offspring can be haploid or diploid.
Hermaphrodite
An organism that produces both eggs and sperm. Can be simultaneous (both at once) or sequential/serial (changes sex over time: protogynous = female first, protoandrous = male first).
Spermatogenesis
The process of sperm production: spermatogonium (2n) to primary spermatocyte (2n) to meiosis I to secondary spermatocytes (n) to meiosis II to spermatids (n) to mature sperm (n). Continuous throughout life.
Oogenesis
The process of egg formation: oogonium to primary oocyte to meiosis I (produces secondary oocyte + first polar body) to meiosis II (completed only upon fertilisation, produces one mature ovum + polar bodies). Unequal division keeps most cytoplasm in the egg.
GnRH (gonadotropin-releasing hormone)
Produced by the hypothalamus; stimulates the anterior pituitary to release FSH and LH.
FSH (follicle-stimulating hormone)
Stimulates follicle development in ovaries and spermatogenesis (via Sertoli cells) in testes.
LH (luteinising hormone)
Triggers ovulation and corpus luteum formation in females. Stimulates Leydig cells to produce testosterone in males.
Estradiol
Major oestrogen produced by ovaries (granulosa cells). Drives follicle development, endometrial growth, and at high levels triggers the LH surge (positive feedback). At low-to-moderate levels, inhibits GnRH/FSH/LH (negative feedback).
Progesterone
Produced by the corpus luteum (and later the placenta). Maintains the endometrium, inhibits GnRH/FSH/LH (negative feedback), and decreases uterine contractions during pregnancy.
Corpus luteum
Structure formed from the ruptured follicle after ovulation. Secretes progesterone and oestradiol to maintain the endometrium.
Capacitation
Process in the female reproductive tract that makes sperm capable of fertilising an egg.
Placenta
Structure formed from maternal and foetal tissues (trophoblast-derived) that allows gas, nutrient, and waste exchange between mother and foetus. Also produces hormones (hCG, progesterone, oestrogen).
Oxytocin
Peptide hormone from the posterior pituitary. Stimulates uterine contractions during birth and milk ejection during lactation.
Prolactin
Peptide hormone from the anterior pituitary. Stimulates milk production in mammary glands.
Asexual reproduction: one parent produces genetically identical (or nearly identical) offspring without fertilisation. Examples include budding, fragmentation, and parthenogenesis. Whiptailed lizards use parthenogenesis, where two females simulate copulation to trigger ovulation and eggs develop without fertilisation.
Sexual reproduction: two parents contribute haploid gametes (sperm + egg) that fuse to form a diploid zygote. Generates genetic variation through meiosis (independent assortment, crossing over) and fertilisation (unique combinations).
Why sexual reproduction? Genetic variation at multiple levels: production of haploid gametes from diploid parents, recombination creating hybrid chromosomes, and fertilisation producing unique genotype combinations. This diversity is advantageous for adapting to changing environments.
XY system (mammals): males XY, females XX
ZW system (birds, butterflies): females ZW, males ZZ
Haplodiploidy (honeybees): fertilised eggs become diploid females, unfertilised eggs become haploid males
Temperature-dependent (reptiles): incubation temperature determines sex; may also be influenced by hormone levels in the egg
Ovipary: eggs expelled from the body; development occurs externally using yolk nutrients. Fertilisation can be external (fish) or internal (birds, reptiles).
Vivipary: embryos develop inside the mother; nourishment comes from the mother (common in mammals).
Ovo-vivipary: eggs retained within the female; embryos develop using yolk (no direct maternal nourishment) and hatch internally or just before release.
Fertilisation (zygote) then cleavage (cell division, forming blastula) then gastrulation (ectoderm, mesoderm, endoderm established) then morphogenesis (body shape and organ formation) then metamorphosis (in species that have it) then reproductive development then senescence and death.
Anatomy: testes (in scrotum for temperature regulation) contain seminiferous tubules (spermatogenesis) and Leydig cells (testosterone). Sperm travel from seminiferous tubules through efferent ductules to the epididymis (maturation and storage), then via the vas deferens to the ejaculatory duct and urethra. Accessory glands add fluid: seminal vesicles (fructose-rich alkaline fluid), prostate (citrate-containing fluid), bulbourethral glands (lubricating mucus).
Seminiferous tubule organisation: from outer wall inward: basal lamina with spermatogonia, developing spermatocytes, spermatids, lumen with mature sperm. Sertoli cells support and nourish developing sperm. Leydig cells sit outside the tubules and produce testosterone.
Spermatogenesis: spermatogonium (2n) to primary spermatocyte (2n) to meiosis I to secondary spermatocytes (n) to meiosis II to spermatids (n) to differentiation (lose cytoplasm, develop flagellum, condense DNA) to mature sperm (n). Continuous from puberty onward.
Sperm release and maturation: nearly mature but non-motile sperm are released into the seminiferous tubule lumen, transported to the epididymis where they mature and gain motility. During ejaculation, smooth muscle contractions propel sperm through the vas deferens to the urethra, where they mix with seminal fluid. Sperm become capable of fertilisation only after capacitation in the female reproductive tract.
Hormonal control in males:
FSH pathway: hypothalamus releases GnRH, anterior pituitary releases FSH, FSH acts on Sertoli cells to stimulate spermatogenesis and inhibin production. Inhibin provides negative feedback on FSH.
LH pathway: hypothalamus releases GnRH, anterior pituitary releases LH, LH acts on Leydig cells to stimulate testosterone production. Testosterone supports spermatogenesis and provides negative feedback on hypothalamus and pituitary.
Androgens: testosterone promotes male secondary sex characteristics (axillary hair, voice deepening, libido) and supports spermatogenesis. Synthesised from cholesterol via progesterone and androstenedione. Can be converted to dihydrotestosterone (DHT).
Anatomy: ovaries (produce oocytes and secrete oestrogen/progesterone), oviducts (fallopian tubes, site of fertilisation), uterus (embryo implantation and development, muscular wall = myometrium, inner lining = endometrium), cervix (passage between uterus and vagina), vagina (receives sperm, birth canal).
Follicle structure (vertebrate): oocyte surrounded by zona pellucida (glycoprotein layer for sperm binding), granulosa cells (inner follicle cells, convert androgens to oestrogens via aromatase), and theca cells (outer cells, produce androgen precursors).
Oogenesis: oogonium to primary oocyte (arrested before birth) to meiosis I (produces secondary oocyte + first polar body, completed at ovulation) to meiosis II (completed only upon fertilisation, produces one mature ovum + polar bodies). Division is unequal: most cytoplasm stays in the egg.
Folliculogenesis: maturation of ovarian follicles before ovulation. Oocytes grow by receiving materials from surrounding follicle cells. The follicle eventually ruptures, releasing the ovum into the coelom, where it typically enters the oviduct.
Vitellogenesis: yolk production in the liver, stimulated by hormones along the axis: external cue, hypothalamus releases GnRH, pituitary releases FSH, follicle cells are stimulated, oestrogen is released, liver produces vitellogenin (yolk precursor), which is transported to and processed by the oocyte. Absent in placental mammals.
Estrous vs menstrual cycle:
Estrous cycle: sexual receptivity occurs only during a specific phase (oestrus); minimal to moderate uterine lining shed
Menstrual cycle: sexual receptivity can occur throughout the cycle; substantial shedding of uterine lining (menstruation)
Three phases of the menstrual cycle:
Follicular phase: GnRH, FSH, and oestrogen rise, driving follicle development. Low oestradiol provides negative feedback, keeping LH low.
Ovulation: high oestradiol (late follicular phase) switches to positive feedback, triggering a sharp LH surge that causes the follicle to rupture and release the oocyte.
Luteal phase: the ruptured follicle becomes the corpus luteum, which secretes progesterone and oestradiol. These provide strong negative feedback, suppressing GnRH/FSH/LH. If no fertilisation occurs, the corpus luteum degenerates, hormones drop, and the endometrium sheds (menstruation). FSH begins to rise again, starting the next cycle.
Uterine cycle (parallel to ovarian cycle):
Menstrual phase: endometrium sheds
Proliferative phase: endometrium rebuilds under oestrogen
Secretory phase: endometrium thickens and becomes glandular under progesterone, preparing for implantation
Hormonal feedback summary:
Low oestradiol = negative feedback (suppresses GnRH/FSH/LH)
High oestradiol (late follicular) = positive feedback (triggers LH surge and ovulation)
Progesterone + oestradiol (luteal phase) = strong negative feedback (suppresses GnRH/FSH/LH)
External fertilisation (aquatic animals): gametes released into water; requires large numbers, synchronised release, and specific behaviours.
Internal fertilisation (terrestrial animals): sperm transferred to the female reproductive tract via copulation. Prevents desiccation and protects developing embryos.
Control of erection: nerve signals from the brain trigger nitric oxide (NO) release, which activates guanylate cyclase, increases cGMP, activates protein kinase G (PKG), relaxes vascular smooth muscle, and increases blood flow to the penis.
Sperm guidance: chemokinetic molecules increase sperm motility (swim faster); chemotaxic molecules direct sperm toward higher concentrations of a signal (guide them toward the egg). Some females store sperm in specialised compartments for extended periods.
Egg structure varies by habitat:
Aquatic: permeable to water, gelatinous, protective coating added in the reproductive tract
Terrestrial: hard or leathery shell (calcium carbonate in reptiles/birds), extraembryonic membranes (chorion for gas exchange, amnion for cushioning, allantois for waste storage and gas exchange, yolk sac for nutrient transfer). Fertilisation must be internal.
Placental mammals: no eggshell; embryo develops internally
Successful cycle hormones: after fertilisation, the embryo produces hCG (human chorionic gonadotropin), which maintains the corpus luteum. Progesterone and oestradiol remain high, maintaining the endometrium and suppressing FSH/LH. No menstruation occurs.
Ovulation to implantation: ovulation releases oocyte, fertilisation occurs in the oviduct, cleavage produces a morula, then a blastocyst. The blastocyst travels to the uterus and implants: trophoblast cells invade the uterine lining, the inner cell mass forms the embryo.
Placenta development: trophoblast contributes to the chorion, chorionic villi invade the endometrium, and maternal and foetal tissues form the placenta. The placenta handles gas, nutrient, and waste exchange between mother and foetus. Early in pregnancy, the chorion secretes hCG to maintain the corpus luteum; later, the placenta itself produces oestrogen and progesterone.
Altricial vs precocial species:
Altricial: short gestation, many offspring, underdeveloped at birth, require extensive care
Precocial: long gestation, fewer offspring, well-developed and relatively independent at birth
Parturition (birth): driven by a positive feedback loop. Progesterone decreases while oestradiol increases oxytocin receptors on the uterus. Oxytocin (from foetus and maternal posterior pituitary) stimulates uterine contractions. The placenta releases prostaglandins, which amplify contractions. The loop escalates until the foetus and placenta are expelled.
Prolactin (anterior pituitary) stimulates milk production but is inhibited during pregnancy by high oestrogen and progesterone. After birth, the drop in these hormones allows milk production. Continued suckling maintains prolactin release.
Oxytocin (posterior pituitary) stimulates milk ejection: suckling triggers sensory afferent nerves, which signal the hypothalamus, which triggers oxytocin release. Oxytocin binds receptors on myoepithelial cells surrounding mammary gland alveoli, causing contraction and milk ejection.
Glandular cells synthesise and secrete milk. Myoepithelial cells contract around the alveoli in response to oxytocin to squeeze milk out.
Oral contraceptives work by delivering synthetic oestrogen and progesterone, which maintain negative feedback on GnRH/FSH/LH throughout the cycle, preventing the LH surge and therefore preventing ovulation.
Fertility treatments often involve administering FSH to stimulate multiple follicles to develop simultaneously, followed by an hCG injection to trigger ovulation (mimicking the LH surge).
Students often think oestradiol always provides negative feedback on LH. It does not. At low-to-moderate levels, oestradiol inhibits LH (negative feedback). At high, sustained levels during the late follicular phase, it switches to positive feedback and triggers the LH surge. This switch is critical for ovulation.
Students confuse spermatogenesis and oogenesis timing. Spermatogenesis is continuous from puberty onward. Oogenesis begins before birth (primary oocytes are arrested), with meiosis I completing at ovulation and meiosis II completing only if fertilisation occurs.
Students assume the corpus luteum persists throughout pregnancy. Early in pregnancy, hCG from the embryo maintains the corpus luteum. Later, the placenta takes over hormone production and the corpus luteum degenerates.
Students think oxytocin during birth operates by negative feedback. Birth is a positive feedback loop: contractions trigger more oxytocin release, which triggers stronger contractions, until delivery.
Be able to trace the hypothalamic-pituitary-gonadal axis for both males and females, including which hormones provide negative and positive feedback.
Know the three phases of the menstrual cycle and the corresponding hormonal changes (FSH, LH, oestradiol, progesterone) and how they drive ovarian and uterine events.
Understand the switch from negative to positive feedback by oestradiol and why it matters for ovulation.
Compare spermatogenesis and oogenesis: timing, number of gametes produced, division symmetry.
Be able to explain what happens hormonally in a successful cycle (fertilisation and hCG) versus an unsuccessful cycle (corpus luteum degeneration and menstruation).
Know the birth positive feedback loop (oxytocin and prostaglandins) and how it differs from the negative feedback loops elsewhere in the system.
Understand the roles of prolactin and oxytocin in lactation and how suckling maintains milk production.
True or false: Parthenogenesis requires fertilisation by a male.
False. Parthenogenesis is development of an egg without fertilisation.
Fill in the blank: The LH surge that triggers ovulation is caused by ___ feedback from high levels of ___.
Positive; oestradiol.
True or false: Spermatogenesis produces four functional sperm from each primary spermatocyte, while oogenesis produces one functional ovum.
True.
Fill in the blank: The hormone produced by the embryo that maintains the corpus luteum in early pregnancy is ___.
hCG (human chorionic gonadotropin).
True or false: Parturition is driven by a negative feedback loop.
False. It is a positive feedback loop involving oxytocin and prostaglandins.
Q: Compare the hormonal control of spermatogenesis and oogenesis. Include the role of the hypothalamus, anterior pituitary, and gonads, and identify which hormones provide negative feedback in each case.
A: Both systems are controlled by the hypothalamic-pituitary-gonadal axis. The hypothalamus releases GnRH, which stimulates the anterior pituitary to release FSH and LH. In males, FSH acts on Sertoli cells to support spermatogenesis; Sertoli cells produce inhibin, which provides negative feedback on FSH. LH acts on Leydig cells to produce testosterone, which supports spermatogenesis and provides negative feedback on the hypothalamus and pituitary. In females, FSH stimulates follicle growth and oestrogen production. LH triggers ovulation and supports the corpus luteum. Low-to-moderate oestradiol provides negative feedback on GnRH/FSH/LH, but high oestradiol in the late follicular phase switches to positive feedback to trigger the LH surge. After ovulation, progesterone from the corpus luteum provides strong negative feedback.
Q: Explain why the menstrual cycle halts during pregnancy. Include the roles of hCG, the corpus luteum, and the placenta.
A: After fertilisation, the developing embryo produces hCG, which maintains the corpus luteum past its normal lifespan. The corpus luteum continues to secrete progesterone and oestradiol, keeping the endometrium intact and suppressing GnRH/FSH/LH via negative feedback, which prevents new follicle development and ovulation. Later in pregnancy, the placenta takes over production of progesterone and oestrogen, and the corpus luteum degenerates. The sustained high levels of these hormones maintain the endometrium and keep the cycle suppressed until after birth.
Q: Trace the positive feedback loop that drives parturition, starting from the initial drop in progesterone.
A: Progesterone decreases near the end of pregnancy. Oestradiol increases the number of oxytocin receptors on the uterus. Oxytocin (released from the foetus and the maternal posterior pituitary) stimulates uterine (myometrium) contractions. Contractions push the foetus against the cervix, which triggers more oxytocin release. The placenta releases prostaglandins, further strengthening contractions. This is a positive feedback loop: each contraction triggers more hormone release, which drives stronger contractions, until the foetus and placenta are expelled.
The hypothalamic-pituitary axis studied here is a specific case of the broader endocrine signalling covered earlier in the course. The same feedback logic (negative and positive) applies to other hormone systems (thyroid, adrenal).
Meiosis is the foundation of gametogenesis. Review the stages of meiosis I and II if the details of spermatogenesis or oogenesis are unclear.
The steroid hormone synthesis pathway (cholesterol to progesterone to androgens to oestrogens) connects to lipid biochemistry and will appear again in adrenal physiology.
reproduction, asexual reproduction, sexual reproduction, parthenogenesis, budding, fragmentation, hermaphrodite, protogynous, protoandrous, sex determination, XY, ZW, haplodiploidy, temperature-dependent sex determination, ovipary, vivipary, ovo-vivipary, spermatogenesis, oogenesis, seminiferous tubules, Sertoli cells, Leydig cells, epididymis, vas deferens, seminal vesicle, prostate, capacitation, GnRH, FSH, LH, testosterone, oestradiol, estradiol, progesterone, inhibin, hypothalamic-pituitary-gonadal axis, follicle, zona pellucida, granulosa cells, theca cells, folliculogenesis, ovulation, corpus luteum, menstrual cycle, follicular phase, luteal phase, LH surge, positive feedback, negative feedback, endometrium, hCG, blastocyst, implantation, trophoblast, placenta, amnion, chorion, allantois, yolk sac, parturition, oxytocin, prostaglandins, prolactin, lactation, milk ejection, altricial, precocial