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UVic BIOL 432 - Spring 2019 > Gonadal Differentiation > Flashcards

Gonadal Differentiation Flashcards

1
Q

What is the main driver of sexual differentiation in mammals?

A

The presence or lack of androgens.

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2
Q

What is the default sexual morphology of human embryos at 37-45 days gestation.

A

Femaaaaaaale.

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3
Q

In males, which DNA-binding protein initiates testicular development?

A

Sex-determining region Y protein (protein SRY).

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4
Q

What were the 4 examples of amenorrhea mentioned in lecture?

A
  1. GnRH deficiency
  2. Functional Hypothalmic amenorrhea
    3, Hyperprolactinemia
  3. Menopause
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5
Q

What were the 6 examples of variations in sex characteristics mentioned in class as leading to intersex phenotypes?

A
  1. Luteinizing hormone receptor mutation
  2. 17α-hydroxylase deficiency
  3. 5α-reductase deficiency
  4. 21 α-hydroxylase deficiency
  5. Aromatase deficiency
  6. Increased androgen exposure in utero
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6
Q

Which of the variations in sex characteristics (6 mentioned) affect XY individuals?

A

XY:

  1. Luteinizing hormone receptor mutation
  2. 17α-hydroxylase deficiency
  3. 5α-reductase deficiency
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7
Q

What results from increasing prenatal androgen concentration? What effect does this have on postnatal development?

A

Prenatally: genital differentiation to male
Postnatally: development of secondary sex characteristics

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8
Q

How does the World Health Organization differentiate “sex” and “gender”?

A

Sex: biological characteristics that define men and women
Gender: socially constructed roles and “appropriate” behaviours

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9
Q

Are “masculine” and “feminine” considered sex categories or gender categories?

A

Gender categories.

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10
Q

Problems from _____ usually have a greater effect on intersex people than problems from ___ (3 letter acronym).

A

Problems from STIGMA usually have a greater effect on intersex people than problems from DSD (3 letter acronym).

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11
Q

What useful molecular tool is employed for analyzing mutations in chromosomal genes/regions?

A

Fluorescence In-Situ Hybridization.

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12
Q

Gonadal and adrenal development, reproduction, and anti-Mullerian hormone synthesis all rely on what?

A

SF-1 (a family of transcription factors).

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13
Q

What kind of sexual differentiation results from translocation of SRY?

A

46 XX males

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14
Q

What kind of sexual differentiation results from mutation of SRY? What other condition can result from this?

A

46 XY females who may also present with adrenal insufficiency.

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15
Q

How many genes have been identified which have the ability to regulate sex differentiation?

A

More than fifty! (I have no idea if that’s high or not, don’t we have like, a lot of genes?)

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16
Q

What 4 products are encoded by the genes which we’ve identified as having the capacity to regulate sex differentiation?

A
  1. Transcription factors
  2. Gonadal steroids
  3. Peptide hormones
  4. Tissue-specific receptors
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17
Q

What are the Mullerian ducts? Where are they in the body? What do they become?

A

Paired ducts of the embryo which run down the outsides of the urogenital ridge. Develop into the fallopian tubes, uterus, and vagina in females. Lost in males.

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18
Q

What occurs to an embryo exposed to too much or too little androgen during development?

A

The embryo will develop with female secondary sex characteristics regardless of chromosome set.

19
Q

What does the Wolffian duct become later in development? What must it be exposed to in order to differentiate properly?

A

In males, develops into the epididymis, the vas deferens, and the seminal vesicle. Will not develop without exposure to testosterone during embryogenesis.

20
Q

What cells produce anti-Mullerian hormone?

A

Sertolli cells and Leydig cells.

21
Q

Which comes first: testicular differentiation or ovarian differentiation?

A

Testicular differentiation.

22
Q

How does GnRH deficiency (Kallmann’s Syndrome) arise? What does it cause?

A

A gene mutation eliminating the migration of GnRH producing cells to the Hypothalamus. Results in loss of sexual maturity.

23
Q

What is the karyotype of a person with Klinefelter’s Syndrome?

A

47 XXY (male appearance).

24
Q

What is the karyotype of a person with Turner’s Syndrome?

A

45 X (female appearance).

25
Q

What are some symptoms of Klinefelter’s Syndrome?

A

Gonadal dysgenesis, low testosterone, sometimes no clear secondary sex characteristics and even mental retardation (rare).

26
Q

What syndrome is the most common cause of male hypogonadism?

A

Klinefelter’s Syndrome.

27
Q

Are persons with Klinefelter’s Syndrome fertile or infertile? What hormones do they generally lack?

A

Not always infertile, but always lacking in androgens.

28
Q

What are some symptoms of Turner’s Syndrome?

A

Gonadal dysgenesis, no estrogen or progesterone, no secondary sex characteristics, numerous developmental problems (short stature, web neck, hearing loss, kidney failure).

29
Q

What is the main cause of Turner’s syndrome?

A

Lack of sex chromosome from the father.

30
Q

How does development progress in a 46 XX female embryo which is exposed to androgens at 12 weeks?

A

The embryo develops a penis (kinda) but also ovaries. It may also develop a joined “urogenital” sinus.
= Intersex

31
Q

How does development progress in a 46 XX female embryo which is exposed to androgens very early in development (<12 weeks).

A

The embryo develops a nonfunctional penis and no ovaries. It also develops a urogenital sinus.
= Intersex

32
Q

What are 2 examples of mutations which cause Testosterone secretion defects?

A
  1. SF-1 Mutation

2. LHR Mutation

33
Q

What are the morphological symptoms of an Intersex 46 XY DSD male?

A

Have testes but genital ducts and/or external genitalia are not fully masculinized.

34
Q

How does impaired testosterone or Mullerian inhibiting factor secretion influence final mature development? What is another possible cause of this?

A

Can lead to Intersex 46 XY DSD male development.

Could also result from lack of testosterone and therefore dihydrotestosterone.

35
Q

What are the morphological symptoms of someone living with androgen insensitivity syndrome (46 XY female)?

A

External genitalia appears female, but lack wolffian ducts and have internal testis.

36
Q

What condition does someone likely suffer from if they are a female with high levels of androgens in a blood sample?

A

Likely they have a 46 XY karyotype and have androgen insensitivity syndrome. Androgen receptors are nonfunctional and so blood androgen levels remain high.

37
Q

What karyotype and symptoms result from a Luteinizing hormone receptor mutation?

A

An Intersex 46 XY DSD person from decreased androgen production and hypogonadism.

38
Q

What karyotype and symptoms result from a 17α-hydroxylase deficiency?

A

An Intersex 46 XY DSD person who lacks the ability to make androgens, resulting in feminization.

39
Q

What karyotype and symptoms result from a 5α-reductase deficiency?

A

An Intersex 46 XY DSD person who lacks the ability to make dihydrotestosterone.

40
Q

What karyotype and symptoms result from a 21α-hydroxylase deficiency?

A

An Intersex 46 XX DSD person with excess androstenedione and DHEA, leading to masculinization.

41
Q

What karyotype and symptoms result from an Aromatase deficiency?

A

An Intersex 46 XX DSD person who lacks the ability to produce estrogen.

42
Q

What karyotype and symptoms result from increased androgen exposure in utero?

A

An Intersex 46 XX DSD person with male secondary sex characteristics.

43
Q

Which of the variations in sex characteristics (6 mentioned) affect XX individuals?

A

XX:

  1. 21 α-hydroxylase deficiency
  2. Aromatase deficiency
  3. Increased androgen exposure in utero

UVic BIOL 432 - Spring 2019 (15 decks)

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