BIO Revision - Reproduction review qs PDF

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Review: Reproduction 1● What two main processes are key to sexual reproduction? ○ Meiosis → involving the halving of the number of chromosomes ○ Fertilization → involving the fusion of two gametes and the restoration of the original number of chromosomes ● What is asexual reproduction? Give 3 exampl...

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Review: Reproduction 1 ●

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What two main processes are key to sexual reproduction? ○ Meiosis → involving the halving of the number of chromosomes ○ Fertilization → involving the fusion of two gametes and the restoration of the original number of chromosomes What is asexual reproduction? Give 3 examples of types of asexual reproduction. ○ Asexual reproduction does not involve the fusion of gametes or change in the number of chromosomes ○ The offspring that arise by asexual reproduction from a single cell or from a multicellular organism inherit the genes of that parent - a clone, genetically identical to parent ○ Haploid gametes not involved in this reproduction ○ ALL prokaryotic and some eukaryotic organisms reproduce this way ○ Fission: separation of a parent cell into 2 binary daughter cells (which should be identical to the parent cell) ■ E.g. sea anemone (multicellular organism), hydra ○ Parthenogenesis: egg develops into a new individual without fertilization ■ Komodo dragon ■ Bees and wasps ● Fertilized eggs = female (2 sets of chromosomes, ‘diploid’) ● Unfertilized eggs = male (1 set of chromosomes, ‘haploid’) ○ Fragmentation: when parent organism breaks into fragments, or pieces, and each fragment develops into a new organism ■ Starfish, worms

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Haploid cell vs diploid cell

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A diploid cell contains two complete sets of chromosomes Haploid contains one set of chromosomes

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Explain mitosis and the characteristics of the product in terms of number of product cells and their chromosomes ○ Mitosis: major purpose = to replace worn out cells, for growth ■ Product - a single cell divides into 2 daughter cells genetically identical to parent cells (cell division) ● Dividing cells = growing ■ The “goal” of mitosis is to make sure that each daughter cell gets a perfect, full set of chromosomes ■ From zygote to a baby ■ From baby to adult

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■ Does NOT make sperm or egg cells ■ Not dividing all the time - cancer is uncontrolled cell growth Stages of Mitosis: ■ Interphase: ● Growth ● DNA replication ● Cell function ■ PMAT - prophase, metaphase, anaphase, telophase ● Pro - chromosomes are condensing (thickening) ● Meta- chromosomes line up in middle of cell ● Ana- “away”, move to opp sides of cell ● Telo - chromosomes are at complete opposite ends, new nuclei forming on both sides to make new cells ■ Cytokinesis: final separation into 2 cells, splits cytoplasm

● and the cells versus mitosis in terms of the number of cells and their chromosomes

Compare contrast product of meiosis

Key diff: Mitosis= two genetically identical cells produced, Meiosis: produces four cells that are genetically different ●

Meiosis: 4 daughter cells - sex cells ○ Genetic material can cross over / shift ○ Pieces of DNA are exchanged ○ Gametes (sex cells) are generated in organisms that reproduce sexually ■ These cells are produced in male and female gonads (testes, ovary) ■ Contain one-half the number of chromosomes as the original cell ■ New gene combinations are introduced in a population through the genetic recombination that occurs during meiosis ■ Produces 4 haploid cells ○ Chromosomes: ■ Anaphase I → Homologous chromosomes migrate toward opp poles of cell, sister chromatids do not separate

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Mitosis: 2 daughter cells - body cells ○ Daughter nuclei expected to be genetically identical to parent cell ○ Genetic material (DNA) is duplicated and divided equally between two cells

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Dividing cell goes through an ordered series of events called the cell cycle Somatic cells of the body replicate by mitosis ■ E.g. fat cells, blood cells, skin cells, or any body cell that is not a sex cell Produces 2 diploid cells Chromosomes: ■ Anaphase → sister chromatids separate, migrate toward opposite poles of cell ■ Separated sister chromatid = full daughter chromosome

List the advantages of sexual reproduction over asexual reproduction ○

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Genetic variation in offspring ■ → Facilitates response to environmental change more readily, survival advantage Recombination can purge deleterious (damaging) mutations ■ Disease less likely to affect population Allows natural selection to more easily work on combinations of traits Allows genome of species to carry significantly more information than genome of an individual Encourages fruitful collaborations (investment) Asexually producing species often thrive for a time, but are slower to adapt to change Evidence: some organisms that usually reproduce asexually: can reproduce sexually, but often only do so in times of stress or uncertainty

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Possible disadvantages of costs attributed to sexual reproduction?

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Costs of sex: ○ Cost of presenting yourself / making yourself look attractive to partner (peacocks - huge energetic cost) ○ Courtship & mating involves risks ○ Spread of disease ○ Childbirth risks ○ Some organisms die after reproduction ○ Competition - fight off other possible mates

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Describe the advantages of internal fertilization over external fertilization

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External vs Internal: ○ Internal = when the male deposits his sperm directly into the female's body ○ External= when the male and female gametes unite outside the female's body External fertilization ○ Depends on availability of moisture ○ Synchrony required - what types?

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○ Probability of fertilization low ○ Without parental care, the odds of subsequent survival can be also be low ○ Can include parental care ○ Doesn’t necessarily mean lack of physical contact Internal fertilization ○ Environment - drier ■ Successful even in harsh environmental conditions ○ Synchrony required - in the mood, right age, right nutrition ○ Probability of fertilization (and subsequent survival) higher than for external ○ Requires physical contact

46 chromosomes in most human body cell nuclei

Review: sex determination ●

Describe some intersex conditions that are not based on chromosomal disorders

5-Alpha Reductase Deficiency ● Affects male sexual development before birth and during puberty ● Genetically male → one X and one Y chromosome in each cell, male gonads (testes) ● Lack enzyme that converts testosterone to dihydrotestosterone (DHT) - a more potent form of testosterone ○ (kicks in during puberty) ○ development of penis and scrotum needs potent DHT ● 12 years = just prior to puberty, phenotype is still female (internal testes) ● Testosterone surge at puberty → male phenotype ● Are fertile (thus condition can be passed on) and appear phenotypically as men for rest of life - Dominican Republic Congenital adrenal hyperplasia (CAH) ● deficiency of one of the enzymes needed to make specific hormones ● Progesterone diverted into different pathways (cortisol) ● Mutation in CYP21A2 gene = developmental problems ○ Can't convert OH-progesterone to cortisol ○ Adrenaline, stress, water retention, glucose production, immune response are all affected ○ Can't convert progesterone to corticosterone ○ When adrenal glands can’t make cortisol, the progesterone heads to androgen pathway ■ Hormone overflow is directed to production of androgens ■ Females display masculinized genitals ●

Describe the genetic complement and symptoms of

5-alpha reductase deficiency ● Genetically male, with one X and one Y chromosome in each cell, and they have male gonads (testes) ● Symptoms: ○ Early years = appearance female but internal testes present ○ Age 8 years = DHT in utero essential for normal development of male genitalia ○ 12 years = just prior to puberty, phenotype is still female ○ Testosterone surge at puberty → male phenotype (sparse beard growth, no acne) ○ Are fertile, appear phenotypically as men for rest of life Androgen insensitivity syndrome ● Complete or partial testicular feminisation syndrome ● Affected individuals are genetic males (XY) ● Testosterone receptor defect on X chromosome (X-linked inheritance) ● Neither testosterone nor dihydrotestosterone (DHT - most active potent form) can bind to receptors ○ Cells are only responsive to hormones if they have receptors for those hormones ○ Human androgen receptor proteins are encoded by a gene located on the X chromosome ● The body is ‘blind’ to testosterone (complete AIS) ● Symptoms: ○ External genitalia is female - testes in abdomen, little pubic hair, well developed breasts ○ Gonads develop based on genetics (XY) - this is fixed development ○ BUT hormones act as modifying agents (default female phenotype) ■ Because the body cannot respond to the androgens secreted ○ CAIS = complete Androgen Insensitivity Syndrome ○ Genetically (chromosomally) male (XY) ○ Phenotypically female but lacks uterus CAH ● ●

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Progesterone diverted into different pathways (cortisol) Mutation in CYP21A2 gene = developmental problems ○ Can't convert OH-progesterone to cortisol ■ Symptoms: adrenaline, stress, water retention, glucose production, immune response are all affected ○ Can't convert progesterone to corticosterone ○ When adrenal can’t make cortisol, the progesterone heads to androgen pathway - Symptoms: ■ Hormone overflow is directed to production of androgens ■ Females display masculinized genitals What does the phrase “two-fold cost of sex” refer to?

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Two-fold cost of sex: ○ Map of heredity of genetic material ○ 2 costs: ■ half of offspring are males ● Males cannot asexually reproduce on their own, they need a female ● Females CAN reproduce without a male asexually ■ Only half of each parent’s genes are passed on ○ Recombination scrambles genotypes, can disrupt favorably adapted gene combinations ○ Asexual reproduction can preserve advantageous genotypes ○ Sexual reproduction = slower process ■ Meiosis & fertilisation take longer than mitosis (and finding a mate slows process)

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Describe each of the 4 stages of reproductive development in humans

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Four stages: ○ Formation of urogenital ridge (tissues that will develop into testes or ovaries) ○ Gonad formation - (testes or ovaries) - determined by presence and activity of SRY gene (Sex determining Region of Y chromosome) ○ Sex determination - typically occurs as a consequence of gonad formation ○ Sex differentiation - recognizing how the sexes are phenotypically differentiated

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What factors interact to determine gender in humans?

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SRY gene ○ Crucial event in whether an embryo will develop into male or female: ■ If Y chromosome is present in the embryo’s cells, the gene SRY will turn on → initiating a chemical chain reaction that will simulate the production of male hormones ■ If X chromosome is present (or if SRY gene is missing from Y chromosome), embryo will develop into female ○ SRY gene sends instructions to the gonads to make developmental hormones, signal to develop testes, then will develop testosterone

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Describe types of chromosomal irregularities and the effect of each on the human phenotype.

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Turner Syndrome ○ 45X (or XO) - only affects females ○ Not inherited ○ Phenotype = Short stature, usually infertile

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Shox gene (on X chromosomes) important for bone development and growth - short stature Klinefelter syndrome ○ 47 XXY (only affects males) ○ Men with extra X chromosome ○ Phenotype: Low production of testosterone - feminizing influences ○ High chance of infertility Androgen Insensitivity Syndrome

Review: Puberty What does the term secondary sexual characteristics describe? ● Secondary sex characteristics are features that appear during puberty in humans. ● Include: ○ Pubic hair ○ Enlarged breasts and widened hips of females ○ Facial hair and Adam's apples on males What is the definitive trait for a male and female that signals they have reached puberty? ● ●

Girls - Menarche (first menstrual bleeding) Boys - Ejaculation (wet dreams)

Of the 3 recognised hormonal axes, which one describes the reproductive one? Write it out. ● 3 hormonal axes = ● Activation of Hypothalamic-(anterior)-Pituitary-Gonadal Axis aka HPG axis= a major physiological event ○ Feedback loop (most cases is a negative feedback loop - switches off) ● Hypothalamic-Pituitary Axes ○ 3 main axes involving hypothalamus and pituitary control muc of endocrine system ○ Mostly operate by negative feedback ■ HypothalamicPituitary-Thyroid axis ■ HypothalamicPituitary-Adrenal axis Hypothalamic■ Pituitary-Gonadal axis (HPG) = reproductive hormonal axes

● Hypothalamus sends a signal for gonadotropin releasing

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hormone (GnRH) to the anterior pituitary Anterior pituitary releases luteinizing hormone (LH) and follicle stimulating hormone (FSH) These hormones act upon testes or ovaries Testes produces testosterone, ovaries produces estrogen & progesterone

What organs differ between male and female phenotype? ● Female: ovaries, uterus, vagina ● Male: penis, scrotum Factors known to affect age of puberty: ● The age at menarche has declined → clear trend for earlier onset ● Distinguish between first signs of puberty (breast development = thelarche) and menarche (first menstruation) ● USA data ○ Caucasian menarche constant, african americans = advancing in age more than others ● Hypotheses for early onset of puberty ○ Increased body fat / nutrition? ■ Hypthesised that females should maintain adequate body fat to both commence menstruation and fertility ○ Social factors? ■ E.g. overt sexuality of popular media (no evidence for this), family stress, presence / absence of fathers ○

Environmental contaminants - endocrine disrupting chemicals? ■ E.g. industrial products ○ Body shape ■ Body fat in breasts, hips and thighs

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Relationship between fertility and BMI ■ If BMI is too low or too high, less successful conception

NUTRITION ● Ballet dancers, models, athletes who do not increase food intake to compensate for energetic demands ○ Menstrual irregularities - athletes= delayed onset of menstruation ○ Amenorrhea (cessation of menstruation) ■ Correlation with intensity (distance run) ■ More pronounced in young females with immature HPG i.e. hypothalamic/pituitary/ovarian axis ○ Diminished libido ○ Diminished sexual activity ● When energy is plentiful, animals can afford to engage in optimal levels of all activities ● Priorities → not enough food, reproduction deferred until energy is available and chances of reproductive success are greater ● Infertility can result from the expenditure of extraordinary amounts of energy in processes, e.g. keeping warm or exercise ○ Increase in emphasis on thermoregulation (growth, exercise) ○ As with food deprivation, reproduction is deferred ○ Fat stores are mobilized ● Excess energy expenditure does not lead to infertility, but where there is an imbalance between intake & output Leptin ● Protein that signals to the body how well endowed your fat cells are ● Humans more fertile when injected with leptin ● Conclusion: ○ Leptin (a hormone that signals fat levels) is one factor contributing signals thought to be just one permissive cue: not a trigger ○ Leptin’s presence is necessary but not sufficient on its own to support sexual maturation for the onset of puberty ● For males, nutrition might affect puberty ○ Tanner stages (for males) ■ Tanner stages = a scale of physical development based on external primary and secondary sex characteristics ○ Prader orchidometer - measurement of testicular volume aka dick size Chemicals ● Endocrine disruptors interfere with normal hormone action ○ E.g. industrial pesticides, PCBs in electrical equipment, dioxins (long term exposure) ● Affect one of the many stages in the hormonal system ○ Prevent synthesis of hormones

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Directly bind to hormone receptors Interfere with hormone degradation

What does an early pubescent event mean? ●

Precocious puberty → appearance of physical and hormonal signs of pubertal development at an earlier age than considered normal ○ Males = ■ Prader orchidometer - measurement of testicular volume (penis size) ■ Precocious puberty = >3 ■ Onset of puberty before 9 y/o ■ Measurement of serum testosterone ○ Females = ■ Used to be younger than 8 y/o, recent study = black girls aged 6-8 showing signs ○ Levels of adrenal androgens usually elevated

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Large incidence in Puerto Rico in 1978-1981 (3x) Probable oestrogenic contamination of food but no single cause identified Extensive Thelarche and gynecomastia (male breasts) in 1-2 year old children

Review: Male reproduction Where do sertoli cells occur? What is their function? ● = is a cell of the testicles that is part of a seminiferous tubule and helps in the process of spermatogenesis, the production of sperm ● support and nourish the immature sperm cells by giving them nutrients and blood products ○ As the young germ cells grow, Sertoli cells help to transport them from the outer surface of the seminiferous tubule to the central channel of the tubule. ● Activated by follicle-stimulating hormone (FSH) secreted by the adenohypophysis, and has FSH receptor on its membranes ● Sperm develop within Seminiferous tubules (highly coiled 120m) supported by Sertoli cells ● Sertoli cells form tight junctions that further separate the tubular compartment creating a blood-testis barrier ○ Reason for this: stop things from blood from impacting sperm (e.g. alcohol, drugs, medication) ○ Allows sperm to develop in a chemical environment different from blood & lymph ○ Prevents sperm leaking out into blood / immune response / inflammatory disease / antibodies that destroy sperm

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The primary hormonal control of spermatogenesis is via testosterone produced by the Leydig cells ○ Appropriate levels are maintained by an interaction between the hypothalamic gonadotropin releasing hormone (GnRH), pituitary hormones, luteinizing hormone (LH), follicle stimulating (FSH), and inhibin from Sertoli cells ■ inhibin inhibits further production, signals no more sperm needs to be produced ■ Sperm washed away from sertoli cells by fluid

What do Leydig cells produce? ● ● ● ●

They produce testosterone in the presence of luteinizing hormone (LH) (from pituitary) Androgens are synthesised between tubules in Leydig Cells The primary hormonal control of spermatogenesis is via testosterone produced by the Leydig cells They are adjacent to the seminiferous tubules in the testicle

At what stage of development and for what reason does a testis-blood barrier develop? ●

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Sertoli cells form tight junctions that further separate the tubular compartment creating a blood-testis barrier ○ Reason for this: ■ Stop things from blood from impacting sperm (e.g. alcohol, drugs, medication) ■ Allows sperm to develop in a chemical environment different from blood & lymph ■ Prevents sperm leaking out into blood / immune response / inflammatory disease / antibodies that destroy sperm Stage: during the initiation of spermatogenesis in response to gonadotropin stimulation

Describe process of spermatogenesis and where it occurs Spermatogenesis→ the production of sperm ● Process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis ○ 1. Mitotic proliferation - (mitosis) ■ Pro-spermatogonial cells: quiescent (quiet) until puberty ■ Mitosis: morphologically distinct spermatogonia ■ Mitosis: several times into primary spermatocytes ■ Occurs in basal part of tubules ● Duplicate DNA ● Push into adluminal compartment - chemically distinct

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2. Meiotic Division ■ In adluminal compartment (non-fluid area) ● Meiosis I: haploid secondary spermatocytes ● Meiosis II: spermatids ● 4 spermatids should be produced 3. Cytodifferentiation ■ Conversion of...