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BIOL 432 Final > Gonadal Differentiation > Flashcards

Gonadal Differentiation Flashcards

1
Q

What is sexual differentiation in mammals driven by?

A
  • presence of androgens in males and their decreased amounts in females
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2
Q

What does the presence of androgens induce in males?

A
  • irreversible changes

- genital differentiation, secondary sex characteristics

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3
Q

What does the lower amount of androgens induce in females?

A
  • female genital differentiation, secondary sex characteristics
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4
Q

What is sex?

A
  • biological and physiological characteristics that define men and women
  • male and female
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5
Q

What is gender?

A
  • socially constructed roles, behaviours, activities, and attributes that a given society considers appropriate for men and women
  • masculine and feminine
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6
Q

What is this section “gonadal differentiation” about?

A
  • conditions that leave people with a reproductive inability not a health abnormality
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7
Q

In what chromosomal gene/region is FISH helpful?

A
  • ID
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8
Q

What initiates testes development?

A
  • sex-determining region Y (SRY) protein, is a DNA-binding protein
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9
Q

What is SF-1 important for?

A
  • gonadal and adrenal development, reproduction and anti-mullerian hormone
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10
Q

What do mutations in SF-1 lead to?

A
  • range of problems

- adrenal insufficiency i 46, XY females (low androgens), gonadal dysgenesis

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11
Q

What does translocation of SRY cause?

A
  • 46, XX males (SRY functional), but mutation of SRY leads to 46XY females (loss of SRY function)
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12
Q

What are testicular and ovarian differentiation influenced by?

A
  • combination of hormonal and environmental factors
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13
Q

What does the undifferentiated gonad have the unique characteristic of?

A
  • has potential o form either of two organs: testes or ovaries
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14
Q

Currently, how many genes have been identified that regulate sex differentiation processes? What do these genes do?

A
  • more than fifty genes

- encode transcription factors, gonadal steroids, peptide hormones and tissue-specific receptors

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15
Q

Currently, how many genes have been identified that regulate sex differentiation processes? What do these genes do?

A
  • more than fifty genes

- encode transcription factors, gonadal steroids, peptide hormones and tissue-specific receptors

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16
Q

What are mullerian ducts?

A
  • paired ducts of the embryo that run down the lateral sides of the urogenital ridge
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17
Q

What do the mullerian ducts develop into?

A
  • in female: form the fallopian tubes, uterus, and the upper portion of the vagina
  • in male: lost
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18
Q

When is the default form female?

A
  • when there is no exposure or sensitivity to androgens
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19
Q

What is the wolffian duct?

A
  • paired organ also found in humans during embryogenesis
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20
Q

What does the wolffian duct develop into?

A
  • males: epididymis, vas deferens and seminal vesicle
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21
Q

What must wolffian ducts be exposed to? When?

A
  • testosterone during embryogenesis for development
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22
Q

What controls stabilization of wolffian ducts?

A
  • anti-mullerian hormone (or mullerian inhibiting factor) produced by sertoli cells and leydig cells
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23
Q

Testicular differentiation precedes ___ ____.

A

ovarian differentiation

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24
Q

What are some of the conditions associated with females?

A
  • amenorrhea: GnRH deficiency, functional hypothalamic amenorrhea, hyperprolactinemia
  • menopause
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25
Q

What is amenorrhea? What could this be a possible sign of?

A
  • lack of menstrual cycle after age 16 or 3 missed periods

- genetic, endocrine or anatomic abnormalities

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26
Q

What is GnRH deficiency (Kallmann’s syndrome)?

A
  • example of amenorrhea
  • adhesion molecule gene mutation
  • no migration of GnRH producing cells or olfactory neurons to the hypothalamus
  • no sexual maturity or smell
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27
Q

What is Functional hypothalamic amenorrhea?

A
  • reduced GnRH pulse frequency and amplitude
  • low FSH and LH, leptin implicated, minor activation of HPA axis and incidences of psychological stress, strenuous exercise or poor nutrition precede
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28
Q

What is hyperprolactinemia?

A
  • example of amenorrhea

- usually dopamine not inhibiting prolactin release

29
Q

What is menopause?

A
  • ovary ceases to function at average age 51
30
Q

Which country made a third gender option legal?

A

Germany

31
Q

What is Klinefelter’s syndrome? What are the conditions associated with it?

A
  • male 47, XXY

- gonadal dysgenesis, low testosterone, sometimes no clear secondary sex characteristics, may be mental retardation

32
Q

How common is Klinefelter’s syndrome?

A
  • 1/500 males
  • most common form of male hypogonadism
  • most common found human sex chromosomal abnormality
  • low androgens
33
Q

What is Turner’s syndrome? What are the conditions associated with it?

A
  • female 45, X
  • gonadal dysgenesis, almost no estrogen or progesterone, no secondary sex characteristics
  • numerous developmental problems: short, web neck, hearing and kidney loss of function
34
Q

How common is Turner’s syndrome?

A
  • mostly fatal to fetus so 1/5000
35
Q

What is the cause of Turner’s syndrome?

A
  • father did not pass on a sex chromosome
36
Q

Are Klinefelter’s syndrome and Turner’s syndrome treatable?

A
  • both treatable with hormones for secondary sex characteristics
  • will always be infertile
37
Q

What is male hypogonadism?

A
  • developmental default is female so hypogonadism in males leads to female characteristics
38
Q

What is female 46, XX DSD - intersex (female pseudohermaphrodism)?

A
  • prenatal exposure to androgens resulting from genetic pathogenesis
  • both ovarian and testicular tissue in one or both gonads (ambiguous genitalia)
39
Q

What is the difference between early androgen exposure and at 12 weeks?

A
  • early androgen exposure: no ovaries

- androgen exposure at 12 weeks: penis and ovaries

40
Q

What is intersex 46, XY DSD (male pseudohermaphroditism)?

A
  • have testes but genital ducts or external genitalia not fully masculinized
41
Q

What causes intersex 46, XY DSD?

A
  • defect in testosterone secretion
42
Q

What are the symptoms of intersex 46, XY DSD?

A
  • testicular dysgenesis
  • impaired T or MIF secretion
  • gonadal target tissue not responsive
  • no T –> DHT conversion
43
Q

What are the symptoms of androgen insensitivity syndrome (AIS, resistance)?

A
  • testes present, absent wolffian ducts, female-appearing external genitalia
  • at puberty: female secondary sex characteristics, no menarche
44
Q

What is the cause of androgen insensitivity syndrome?

A
  • increase LH secretion results in increase in T and E2

- androgen receptor mutation is common

45
Q

What are the three causes of androgen biosynthetic dysfunction in 46, XY individuals?

A
  • luteinizing hormone (LH) receptor mutation
  • 17alpha-hydroxylase deficiency
  • 5alpha-reductase deficiency
46
Q

What results from LH receptor mutation?

A
  • decreased androgen production
  • hypogonadism
  • intersex 46, XY DSD
47
Q

What results from 17alpha-hydroxylase deficiency?

A
  • can’t make androgens
  • ambiguous gonads or feminization
  • intersex 46, XY DSD
48
Q

What results from 5alpha-reductase deficiency?

A
  • can’t make DHT

- 46, XY DSD

49
Q

What are the three causes of androgen excess in 46, XX individuals?

A
  • 21 alpha-hydroxylase deficiency
  • aromatase deficiency
  • increased androgen exposure in utero
50
Q

What results from 21 alpha-hydroxylase deficiency?

A
  • build up of androstenedione and DHEA
  • increase T, masculinization
  • intersex 46, XX DSD
51
Q

What results from aromatase deficiency?

A
  • lack of estrogen

- 46, XX DSD

52
Q

What results from increased androgen exposure in utero?

A
  • androgenic drugs

- 46, XX

53
Q

At 37-45 days of gestational age the gonads are?

A
  • biopotential - default is female
54
Q

What initiates the testes in males?

A
  • SRY protein
55
Q

What stabilizes the wolffian ducts?

A
  • anti-mullerian hormone
56
Q

What receptors do estrogens bind to and activate?

A
  • ERalpha and ERbeta
57
Q

Where is ERalpha expressed? What does it mediate?

A
  • in reproductive tissues

- the majority of the sexually dimorphic and reproductive functions

58
Q

Where is ERbeta expressed?

A
  • exhibits a distinct pattern of expression in prostate, brain and immune cells
59
Q

What are the domains and functions of the estrogen receptor structure?

A
  • A/B: transactivation, activation function (AF-1 ligand independent)
  • C: DNA binding domain, dimerization
  • D: hinge
  • E: ligand binding domain, dimerization (AF-2, ligan dependent)
  • F: function unknown
60
Q

In what domains of the estrogen receptor can phosphorylation occur?

A
  • in all domains

- affects functions

61
Q

Do ERalpha and ERbeta have similar roles?

A
  • overlapping yet unique roles in E2 signalling
62
Q

What is tamoxifen?

A
  • an antagonist of the estrogen receptor in breast tissue
63
Q

What is estrogen receptor signalling also known as?

A
  • nuclear initiated steroid signalling
64
Q

What are the specifications of estrogen receptor signalling (classical nuclear action)?

A
  • activation of txn of target gene by E2/ER
  • or no activation by antagonist tamoxifen/ER
  • with recruitment of coactivators or corepressors
65
Q

What are the specification of estrogen receptor signalling (non-classical nuclear action)?

A
  • ER regulates gene txn on genes without HRE

- interacts with TF such as SP-1, fos, jun

66
Q

What is non-genomic estrogen receptor signalling?

A
  • aka membrane initiate steroid signalling
67
Q

How is non-genomic estrogen receptor signalling mediated?

A
  • through GPCR, increase production EGF, p cascade
68
Q

How are ERalpha membrane associated?

A
  • by lipid rafts

- also direct activation of Gbetagamma leads to kinases

69
Q

What does activation of the non-genomic estrogen receptor signaling activate?

A
  • leads to pylation of nuclear ER and activation of mitogenic pathway
  • E2 signalling through GPCR30

BIOL 432 Final (14 decks)

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