18 Flashcards

(24 cards)

1
Q

what determines sex?

A

the chromosomal complement of sperm

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2
Q

6 weeks

A

the foetus has a biopotential primordium and rudimentary reproductive tracts

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3
Q

define a bipotential primordium

A

an embryonic structure with the capacity to develop into either a male (testis) or female (ovary) gonad

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4
Q

how does the bipotential primordium develop if the Y chromosome is present?

A

testis
Wolffian duct -> epididymis, vas deferens, seminal vesicle

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5
Q

how does the bipotential primordium develop if the Y chromosome is absent?

A

ovary
Mullerian duct -> fallopian tube, uterus, upper vagina

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6
Q

development of structures in XX embryos

A

10 weeks:
1. gonadal cortex becomes ovary in the absence of SRY protein and under the influence of female-specific genes
2. absence of testosterone causes Wolffian duct to degenerate
at birth:
3. absence of anti-Mullerian hormone (AMH) allows the Mullein duct to become the fallopian tube, uterus, and upper part of the vagina

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7
Q

development of structures in XY embryos

A

10 weeks:
1. SRY protein in male embryo directs the medulla of the bipotential gonad to develop into testis
2. Anti-Mullerian hormone from testis causes the Müllerian ducts to disappear
at birth:
3. testosterone from testis converts Wolffian duct into seminal vesicle, vas deferent, and epididymis. DHT controls prostate development

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8
Q

what is so special about the Y chromosome?

A

has SRY gene that promotes testes development

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9
Q

how does SRY promotes testes development

A

encodes TDF (testes-determining factor) a transcription factor

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9
Q

describe the genetic mechanism through which the testes form

A
  1. SF1 is expressed in the bipotential primordium and acts together with SRY to activate the transcription of the SOX9 gene
  2. SOX9 activates transcription of FGF9, AMH, DHH, SF1
  3. this leads to development of Sertoli cells (AMH) and testes, development of Leydig cells (testosterone), and repression of female structures (via AMH)
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10
Q

SF1 stands for

A

steroidogenic factor 1 (transcription factor)

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11
Q

high levels of SOX9 in males suppress

A

β-catenin

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12
Q

β-catenin in females suppresses

A

SOX9

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13
Q

how does SOX9 initiate Sertoli cell differentiation?

A
  • growth factors cause the proliferation of Sertoli precursors
  • Sertoli precursors organise around clusters of germ cells
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14
Q

what cellular events downstream of SOX9 help to organise testis structure?

A

proliferation, migration, organisation, vascularisation, Leydig cell differentiation

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15
Q

label a flow chart of how hormones help to regulate structural differentiation in males

16
Q

label the localisation of testosterone and DHT in common XY structures

17
Q

hormones in common XX structures

A
  • β-catenin suppresses SOX9 expression
  • no AMH or testosterone
  • estrogens and estradiol
18
Q

What causes variations in sex development due to atypical hormone levels or action in XY and XX individuals?

A

XY – atypical androgen synthesis (e.g., 5-a-reductase) or action
XX - excessive exposure to androgens during early gestation

19
Q

XY individual with androgen insensitivity

A
  • testes (undescended)
  • vagina (lower portion, closed end)
  • androgens high, LH high
20
Q

what is activated at the onset of puberty?

A

the GnRH system

21
Q

describe puberty in girls

A
  • growth spurt
  • menarche
  • pubic hair, breasts
  • between ages of 8-14
22
Q

describe puberty in boys

A
  • growth spurt
  • testes
  • penis
  • pubic hair
  • between ages of 8-16
23
Q

how is puberty activated?

A

neurons stimulate GnRH pulsatility → anterior pituitary releases LH & FSH → gonads produce sex steroids (testosterone/estrogen) → secondary sexual characteristics, growth, gametogenesis.