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PHPY 303 > Lecture 1+2 > Flashcards

Lecture 1+2 Flashcards

1
Q

Pairs of similarly sized chromosomes:

A

Females have 8, including the 2X.

Males have 7.5, because Y is smaller.

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2
Q

Reasons that genetic identity is maintained in mitosis:

A

Homologous chromosomes don’t exchange genetic material - sister chromatids are identical.

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3
Q

Meiosis events:

A

Meiosis I: recombination and reduction to haploid. homologues split.
Meiosis II: chromatids separate.

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4
Q

Spermatogenesis:

A 
Spermatogonium (2N)
-- duplication --
Primary spermatocyte (4N)
-- telophase I --
2 secondary spermatocytes (2N)
-- after meiosis II --
4 spermatids (1N) 
-- after maturation --
4 spermatozoa (1N)
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5
Q

Oogenesis:

A 
Oogonium (2N)
-- duplication -- 
Primary oocyte (4N) 
-- prophase I --
Arrested primary oocyte (4N) 
-- meiosis I --
Secondary oocyte (2N) and polar body #1
-- separation of chromatids --
Mature oocyte (1N) and polar body #2
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6
Q

Sex determination: genetic sex

A

Determined at fertilization: whether sperm bears X or Y.

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7
Q

Sex determination: genotypic sex

A

Determined by parental sex chromosomes.

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8
Q

Sex determination: gonadal sex

A

Determined by genotypic sex at 9 weeks of gestation.

External genitalia is expressed after gestation, 38-40 weeks.

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9
Q

Sex determination: phenotypic sex

A

Determined by gonadal sex at puberty.

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10
Q

Epigenetics:

A

A change in phenotype without a change in genotype.
Probably happen due to DNA methylation and histone modification.
In fetuses, epigenomes direct stem cell differentiation.

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11
Q

Development of testes:

A

Cortex regresses into tunica albuginea. Medulla develops. Primary sex cords hollow out to become seminiferous tubules.

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12
Q

Development of ovaries:

A

Cortex becomes more pronounced and more vascularized at the expense of the medulla.

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13
Q

Default sex:

A

Female. Need lots of conditions to make male.

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14
Q

Testis-determining effect of Y chromosome:

A

Male sex is established when Y tells primary sex cords to differentiate into seminiferous tubules.

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15
Q

TDF/SRY:

A

A single gene located on the short arm of the Y chromosome. Needed for testicular development.

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16
Q

Translocation of TDF:

A

XX male. During father’s meiosis, X and Y chromosomes recombine at distal end of short arms.
Sterile with small testes and feminine traits.

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17
Q

Gonadal dysgenesis: XO

A

Loss of one X chromosome. Gonads appear as a streak or line in the adult pelvic sidewall.

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18
Q

Gonadal dysgenesis: Turner syndrome

A

Most common example of gonadal dysgenesis.

45 XO. Females with short stature, primary amenorrhea, sexual infantalism.

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19
Q

SRY-related abnormalities: 46 XX

A

True hermaphrodites. No Y chromosome but still have testes - possess both male and female sex organs.

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20
Q

SRY-related abnormalities: 45 XO

A

Pseudohermaphrodites - only one type of gonadal tissue, but morphological characteristics of both sexes. Testes and ovary streak.

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21
Q

Male development of genital ducts:

A

Paramesonephric/Mullerian duct degenerates. Mesonephric/Wolffian duct develops into vas deferens, seminiferous tubules, ejaculatory duct.

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22
Q

Female development of genital ducts:

A

Mesonephric/Wolffian duct degenerates. Paramesonephric/Mullerian duct develops into oviduct, uterus, and upper third of vagina.

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23
Q

Removing both testes:

A

Stops production of testosterone and anti-Mullerian hormone. Mullerian ducts will develop and Wolffian ducts will degenerate. Chromosomal male but phenotypic female.

24
Q

Removing ovaries:

A

Mullerian development continues as normal. Ovaries aren’t necessary for female duct development.

25
Q

Removing one testis before puberty:

A

Ipsilateral development of mullerian duct. Other side develops normally - virilization of external genitalia occurs as normal.

26
Q

Removing both testes and administering testosterone:

A

Wolffian ducts develop normally. Mullerian ducts do not regress in the absence of AMH.

27
Q

Treating a female with testosterone:

A

Promote development of Wolffian ducts. Mullerian ducts develop normally in absence of AMH.

28
Q

Hormones necessary for male differentiation:

A

Testosterone (testes)
AMH (testes)
Dihydrotestosterone (peripheral tissues)

29
Q

Enzyme that converts testosterone to DHT?

A

5-alpha-reductase

30
Q

When does testicular development occur?

A

Before 9 weeks of gestation, in the presence of TDF. If TDF is not present during the critical window, ovaries will develop.

31
Q

Two major roles of androgens in male phenotypic differentiation:

A

Trigger conversion of W ducts to ejaculatory system. Direct differentiation of urogenital sinus and external genitalia.

32
Q

Wolffian phase regulated by which hormones?

A

Testosterone only. Doesn’t care about DHT.

33
Q

DHT is required for:

A

Virilization of urogenital sinus, prostate, penile urethra, and external genitalia during embryogenesis.
Sexual maturation at puberty.

34
Q

After formation of testicular cords…

A

Sertoli cells produce AMH. Leydig cells produce testosterone. If embryo doesn’t get enough androgens or doesn’t have enough androgen receptors, sexual ambiguity occurs.

35
Q

Sertoli cells produce:

A

AMH for obvious reasons.

ABP to maintain a high local concentration of testosterone, for development of W ducts/medulla/prostate.

36
Q

First site of androgen action:

A

Embryonic mesenchyme has androgen receptors.

37
Q

Do W ducts require DHT?

A

Nope. They don’t have 5-alpha-reductase, so they have to make do with reg ole (T).

38
Q

Is DHT required for development of external genitalia?

A

Yup. Absence of 5-alpha-reductase results in normal development of W duct but impaired virilization of external genitalia.

39
Q

W ducts develop into:

Medulla develops into:

A

Epididymis, vas deferens, seminal vesicles, ejaculatory duct.

Rete testis.

40
Q

Where are male steroids produced? Where are female steroids produced?

A

Male: testes, because they produce 1000x more than adrenal glands.
Female: adrenal glands.

41
Q

Cortisol:

A

Stress response.

Fights infection - hydrocortisol mimics body’s nature response to infection.

42
Q

Aldosterone:

A

Controls salt/water level in blood, regulates salt/water excretion.

43
Q

Effect of too much aldosterone:

A

Too much aldosterone -> too much salt -> more water retention -> increased blood pressure.

44
Q

Congenital adrenal hyperplasia:

A

Deficiency in 3-beta, 21-alpha, or 11-beta enzymes. Results in virilization of females. Ambiguous genitals due to hypersecretion of androgens.

45
Q

Most common congenital adrenal hyperplasia:

A

21-alpha deficiency - 95% of cases. Blocks both aldosterone and cortisol pathways, so adrenal steroid precursors are shunted to androgen pathways.

46
Q

Adrenogenital syndrome:

A

Too much androgen! Enlarged clitoris, fused/enlarged labioscrotal folds. Otherwise normal female infant.

47
Q

Androgens in feminization syndrome:

A

Testicular descent is dependent on androgens. 5-alpha-reductase deficiency and androgen resistance - testes fail to descend.

48
Q

Androgens in male pseudohermaphroditism:

A

Defect in androgen action mechanisms. Unambiguous male gonads but ambiguous genitalia or phenotypically female.

49
Q

5-alpha-reductase deficiency:

A

Autosomal recessive; only expressed in males. Lack of DHT leads to ambiguous genitalia, blind vaginal pouch, bound/hooded phallus, hypospadias (pee hole too low).

50
Q

DHT vs (T):

A

DHT binds same receptor but with 100x stronger affinity.

DHT-receptor complex binds chromatin more tightly than the (T)-receptor complex.

51
Q

Androgen receptor:

A

Present in genital tissues.

Homodimer - a member of nuclear receptor family.

52
Q

AR/AR receptor complex:

A

Transcription factor for hormone response elements on androgen-controlled genes. Increases transcription by interaction between receptor-steroid complex and chromatin.

53
Q

Absent or abnormal androgen receptors lead to:

A

Testicular feminization

54
Q

Inadequate androgen production or nonfunctioning androgen receptors lead to:

A

Sexual ambiguity

55
Q

AMH: structure

A

Homodimer of two monomeric glycoprotein subunits linked by disulfide bond.

56
Q

Mechanism of action of steroid hormones:

A

Diffuse into cell.

  1. Bind to receptor in cytosol. Diffuse into nucleus. Affect transcription.
  2. Bind to receptor in nucleus. Affect transcription.

PHPY 303 (8 decks)

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