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Samenvatting Human Development deel 2

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Human Developement (AB_1140)

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Vrije Universiteit Amsterdam (VU)

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Lecture 15  Genetics, sex and gender
There are two kinds of sex determination (the process to become a male or a female). These are:
1. Genotypic sex determination  upon fertilization
- XX normal female (homogametic sex)
- XY normal male (heterogametic sex)
2. “Environmental” sex determination
- Gonads (6-7 weeks)
- Phenotypic (intern 8-10 weeks & extern >12 weeks)
Gender is the social meaning that is attached to being a male or a female. The sexual/gender identity is
one’s identity as a male or a female. The expectations about how a male or a female should behave is
called the gender role. Gender develops in utero throughout the childhood. Androgyny/hermaphrodism
in terms of sex means that someone possesses both male and female reproductive organs. In terms of
gender, it means possessing both male and female qualities or feelings. Often is referred to these people
as intersex. Physicians have traditionally recommended that intersex people be reared as girls. Surgery
was often conducted to make them look more feminine, assumed that children consistently raised as
female would accept that identity. Many intersex people
protest against such early surgery and many, who remain
female, feel discontent or conflict with being a female. Such
cases indicate that although hormones do not determine the
genetic sex, they are involved in determining the gender
identity by changing the brain. Intersex people are different
from transgenders, as that is expressed mostly from early
childhood onwards (3-5 years) and is dependent on the
development of the brain.
Currently, there is a dichotomy in the view of intersex people.
According to the medical model, surgery needs to be conducted as soon as possible to conform with the
‘natural’ occurrence of being male or female. However, the psychological/social model says to let the
child decide when it is able to make a decision.
The system starts bisexual, but mostly only one survives. In early fetal
development, there are two ducts: the Wolffian duct (male) and the
Müllerian duct (female). When the hormone MIF is present, the growth of
the Müllerian duct gets inhibited and the fetal becomes a male. If the MIF is
not present, the Wolffian duct spontaneously degenerates (because of the
absence of testosterone) and the fetal becomes female.
During male development, three things happen:
1. Genetic factors initiate process that directs the indifferent gonads
towards testis development.
2. Activation of Sertoli cells (sustentacular cells) to produce Müllerian inhibiting hormone, causing
the Müllerian duct to degenerate.
3. Stimulation of Leydig cells (interstitial cells) to secrete testosterone, which then directs
development of the Wolffian ducts towards epidydimes, vas deferens and seminal vesicles.
- Testosterone conversion to dihydrotestosterone (DHT)
- Directs development of the urethra, prostate gland and penis
The Y-chromosome produces the Testis Determination Factor (TDF). SRY (TDF) is a transcription factor
that via a molecular cascade activates Sertoli and Leydig cells. The Y-chromosome acts together with an

,autosomal gene SOX9. SOX9 binds to the promoter of MIH (or
AMH, anti-Müllerian hormone) and regulates its expression.
SRY/SOX9 induce FGF9: chemotactic factor for primordial germ
cells to penetrate gonadal ridge (without this no testis can be
formed).
The internal male structures (epididymis, vas deferens,
seminal vesicles and ejaculatory ducts) are formed by
testosterone. The Leydig cells converse testosterone to
dihydrotestosterone, which produces the external male
structures (urethra, prostate, penis and scrotum). This process
is called virilization, which means it makes the structures male.
When the person is XX, there is no MIH present. This results in
a continuation of the development of the Müllerian ducts
towards fallopian tubes, uterus and the upper vagina. In this
case the external genitals become feminine.
Congenital Adrenal Hyperplasia (CAH) is a genetic defect that
leads to excessive production of androgens (too little
glucocorticoids). This is caused by mutations in enzymes for glucocorticoid production, such as 21-
hydroxylase. This results in high concentrations of 17-hydroxyprogesterone (100x higher than normal).
This defect produces genotypical females (XX) that look like a male, because androgens cause virilization
of the external genitals. The state of the severity of CAH is dependent on the brain, because the brain
will dictate the gender identity of this person.
In males, testosterone is secreted into the blood and this reaches the brain. In the brain it will be
converted to estradiol and DHT. The estradiol masculinizes the brain. In the female, the alpha-
fetoprotein binds to the estradiol and prevents it from entering the brain. This protects female brains
from being masculinized.

For true hermaphrodites, adults would need to have both ovaries and testis at the same time and they
have to be functional. Pseudohermaphrodites concerns the presence of both sexes (or appearance

, thereof) in one individual, but at different stages of life. In the
Swyer syndrome, there is a lack/mutation of SRY. It results in a
complete gonadal dysgenesis. The XY ‘female’ has no testis,
because there is no testis determination factor. However, the
person has no ovaries either. The Wolffian duct fails to develop,
due to a lack of testosterone. The internal and external genitals
appear female. The person is infertile, but is able to carry a child
to term by embryo transfer. This defect arises during the spermatogenesis. Gene translocation of the
SRY to the X-chromosome is also possible (see picture). This is called the de la Chapelle syndrome (XX).
However, these ‘males’ are infertile, because spermatogenesis needs other Y-chromosome factors.
In the case of androgen insensitivity (AIS), males function as normal. The only issue is that there is no
receptor to react to testosterone and DHT. Thus, it can not respond to the androgen surge at puberty,
because testosterone and DHT use the very same receptor. In partial androgen insensitivity (PAIS) there
is partial virilization of the genitals. It is dependent on the type of mutation (severity) in dysfunction of
the androgen receptor.

Lecture 16  Anatomy of the reproductive organs
The reproductive system is the system
of organs and parts which function in
reproduction. The reproductive organs
can also be called urogenital. They are
divided in two regions: the external and
the internal reproductive organs. The
external parts for the male are the penis
and the scrotum and the internal parts
are the testicles, the epididymes, the
spermatic cord and the glands.
The penis contains the urethra. It has
two functions in males: transport of
urine and transport of ejaculate.

There can be three parts identified in the urethra:
- The prostatic part (pars prostatica)
- The membranous part (pars membranacea)
- The spongy part (pars spongiosa)
The benefit of the longer urethra in males is a
smaller risk of bladder infection (UTI), because the
bacteria’s need to travel a longer distance. The
downside of the long urethra is that there is a
larger risk of uretral blockage. This is usually caused
by enlargement of the prostate. This happens
frequently in men 40-50 years old. It has varying
symptoms:
- Mild complaints during urination (micturition)
- Obstruction of urethra  urinary catheter

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