Reproduction Lectures (8) Flashcards
Why do humans consider themselves advanced over other animals?
Humans are sexually _____.
R1
- we mate for pleasure, not just procreation
- dimorphic: males and females have distinct characteristics determines by genome
Male and female sex organs (3 sets of structures)?
R1
gonads: gamete producing organs – testes VS ovaries
internal genitalia: accessory glands and ducts – epididymis, vas deferens, seminal vesicles, prostate VS fallopian tubes, uterus, cervix, upper vagina
external genitalia: external repro structures – penis, scrotum VS labia, clitorus, opening of vagina
Sex determination depends on _____. Why is the Y chromosome so small compared to X?
R1
fusion of egg (X always) with sperm and which sex chromosome the sperm contains (X or Y)
*Y has minimal genes on it, only carries male sex characteristics
Since the X chromosome has more genes on it compared to Y, is there a genetic imbalance b/n males and females?
R1
After development of ovaries in females, once X chrom is essentially “shut off” to balance with males
- only thing left on “shut off” X is pseudoautosomal regions at ends which would essentially match a Y chromosome
- whether paternal or maternal X is shut off differs in each cells: this is shown with cats of 2 colours
Why does X-linked recessive genetic disorders more commonly affect males?
R1
only need 1 X for it to show, compared to women who need 2 X’s to show it. *Females most often carriers
Abnormal sex chromosome distribution during Meiosis?
R1
by end of 2nd meiotic division, should end with 4 monosomic gametes. if not, have nondisjunction:
- 1st meiotic division ends with all going into 1 cell, by end of 2nd division, have 2 disomic gametes and 2 nullisomic gametes
- if nondisjunction only occurs at 2nd meiotic division, end with 2 normal monosomic gametes, 1 disomic gamete and 1 nullisomic gamete
Products of abnormal sex chromosome distribution during meiosis (syndrome’s)?
XXY, X, XXX, XYY, Y
R1
- XXY (Klinefelter’s): one disomic gamete fertilizes a normal monosomic gamete, extra X causes some female characteristics to form - tall stature, small testes, female-type pubic hair, osteoporosis, breast development sometimes, bad beard growth, infertile
- X (Turner’s): nullisomic gamete fertilizes a normal monosomic gamete, missing pseudoautosomal region of 2nd X - short, neck webbing, broad chest, widely spaced nipples, streak ovaries, infertile, amenorrhoea, pigmented nevi (moles)
- Y: non viable
- XXX: no real phenotypes, 2 X’s inactivated - correlated with learning disorders
- XYY: no real phenotypes, few genes on Y anyway so extra doesn’t affect much - correlated with learning disorders
After fertilization (union of egg and sperm) \_\_\_\_\_ forms. Then, \_\_\_\_ followed by \_\_\_\_. R1
Zygote. Then, blastocyst (3 weeks after fertil, followed by embryo, and eventually fetus (9 weeks after fertilization)
Difference between gestational and developmental timeline?
R1
Gestational starts from 1st day of last period (so it’ll be 2 weeks ahead of developmental) = 40wks
Developmental starts when fetus begins developing = 38wks (fertilization length)
Internal sex organ development in males and female embryos?
R1
Begins 7th week of development, before this embryo is bipotential
DEPENDS ON PRESENCE/ ABSENCE OF SRY GENE VIA Y CHROMOSOME: females are default essentially
Bipotential gonda: outer cortex and inner medulla
Accessory ducts: mullerian and wolffian
MALE: cortex regresses and medulla forms testis. Mullerian regresses (AMH present) and wolffian forms epididymis, vas deferens, seminal vesicles (testosterone present).
FEMALE: cortex forms ovary and medulla regresses. Mullerian becomes fallopian tube, uterus, cervix, upper 1/2 of vagina and wolffian regresses.
How does the SRY gene guide male internal genitalia?
R1
Sex determining Region of Y (SRY) chromosome produces testis determining factor (TDF; transcription factor) which guides development of gondal medulla into testis
-SRY gene takes up large portion of Y chrom
Testis then produce,
- anti-mullerian hormone (AMH or MIS; sertoli cells)
- testosterone (leydig cells): cause proliferation/growth of wolffian into male accessory structures
- testosterone converted to dihydrotestosterone (DHT; leydig cells) to cause external genitalia differentiation
External sex organ development in males and female embryos?
R1
after internal has developed
DRIVEN BY PRESENCE/ABSENCE OF ANDROGENS (DHT) MADE BY SRY GENE
bipotential genital tubercle, urethral groove, urethral fold, labioscrotal swelling
if female: genital tubercle forms clitorus, urethra folds and groove forms labia minora, opening of vagina and urethra, labioscrotal swellings form labia majora
if male: genital tubercle forms glans penis (head), urethra folds and groove forms lower portion of penis shaft, labioscrotal swellings form initial portion of shaft and scrotum
**at birth, testosterone causes descent of testes from abdominal cavity into scrotum.
What is the testis determining factor?
R2
Y chromosome SRY gene product - testosterone -> DHT is what converts medulla into testes
Dihydrotestosterone (DHT) importance came to light how?
R2
during studies of male pseudohermaphrodites who had a defective gene for 5a-reductase, the enzyme converting testosterone to DHT
- had testosterone, but no male external genitalia and prostate development since no DHT
- look female at birth (external genitalia does not develop)
- at puberty the testes secrete testosterone causing masculinization of external genitalia so male can chose which gender they want to be here
Male and female gametes?
R2
ovum: largest cell in body; non-motile so smooth muscle contraction and cilia move it; born with all oocytes will ever have, cyclically released during repro years (~40 years)
sperm: small; only flagellated cells in body; move far distance in female repro tract; continually produced for entire life once reached repro maturity; sperm and testosterone production diminish with age but don’t stop
Meiosis basic overview: 4 STEPS?
R2
1 - mitosis in utero to inc number of germ cells (oogonia or spermatogonia each with 46 chrom)
2 - DNA replicates but no cell division occurs, still 1 cell with 2 pairs of sister chromatids (homologous pair of replicated diploid chromosomes)= 92 chrom: 1º gamete
3 - first meiotic division, the one 1º gamete divides into 2 seperate 2º gametes (both diploid/sister chromatids, 46 chrom in each cell)
4 - 2nd meiotic division occurs, the 2º gametes both divide to end with 4 haploid daughter 3º gametes
*end with 4 viable gametes if male, in females only 1 will be viable (polar bodies)
Female gametogenesis?
R2
germ cells = oogonia
- mitosis (step 1) and the first stage of meiosis (step 2) occur during 5th month of fetal development so by birth, have all 1º oocytes (92 chrom) will ever have
- 5th month have 5-7 million oocytes
- meiosis resumes at puberty with cyclical recruitment of 1º oocytes to enter menstrual cycle
- 1st meiotic division (step 3) produces 1 large 2º oocyte (diploid) and tiny polar body
- ovary releases this diploid 2º oocyte and will not undergo the division unless fertilized
- 2º oocyte begins 2nd meiotic division (step 4) and polar body breaks down during ovulation
- if not fertilized, is released out of body. If fertilized, undergoes the division (step 4) to yield 1 haploid gamete and a polar body
What are polar bodies and why are they non viable?
R2
uneven division in cytokinesis yield polar bodies with very little cytoplasm and few organelles, unable to thrive
- uneven distribution comes from the female gamete needing all necessary cytoplasm/proteins/organelles/energy for the zygote as sperm only supplies some DNA
Both male and female gametogenesis is under control of _____.
R2
hormones from brain (signalling cascade) and endocrine cells in gonads
Male gametogenesis?
R2
- small amnt of meiosis occurs in fetal development to inc immature germ cell numbers (spermatogonia) in testes
- at puberty: germ cell mitosis (step 1) resumes
- some spermatogonia will remain as immature germ cells and continually make more sperm (stay in mitosis step)
- some spermatogonia are recruited to enter cycle to produce 1º spermatocytes (step 2)
- 1º spermatocytes undergo 1st meiotic division to produce two 2º spermatocytes (step 3)
- both 2º spermatocytes undergo 2nd meiotic division to produce 4 immature spermatids (step 4)
All 4 viable
How does the brain direct reproduction?
R2
- peptide hormones from hypothalamus go to anterior pituitary, cause secretion of hormones which go to gonads to cause secretion of sex hormones: androgens (DHT, testosterone), estrogens (estradiol - from testosterone), progesterone (progestin)
- males make primarily androgens: 95% made in testes and 5% in adrenal cortex. Most testosterone is converted to DHT in peripheral tissues - both agonists for androgen receptors but DHT is more potent
- females make primarily estrogens and progesterone: most made in ovaries. Some testosterone made in adrenal cortex
Hypothalamic-pituitary gonadal axis (HPG axis)?
R2
control pathway for sex hormones
- gonadotropin releasing hormone (GnRH) released pulsatile-ly in hypothalamus travels to anterior pituitary
- produced either in GnRH or kisspeptin neurons
- cause secretions of 2 anterior pituitary gonadotropins from gonadotropes: follicle stimulating hormone (FSH) and luteinizing hormone (LH)
- FSH and LH act on gonads to stimulate sex hormone production and influence gamete production
Precursor for all peptide hormones?
R2
Cholesterol
Hypophyseal portal system describes _____. Explain the process.
R2
- describes how hypothalamic hormones reach anterior pituitary
- GnRH neurons release GnRH into capillaries of portal system
- portal veins carry trophic neurohormone to anterior pituitary where they act on endocrine cells
- endocrine cells release their hormones into 2nd set of capillaries for distribution to rest of body