1. Gametogenesis and Fertilization

2. Oogenesis
Primary Oogenesis: formation of the primary oocyte in the ovary
Occurs during embryological development
Oogonia (sex cells) divide and undergo meiosis until prophase I  primary oocyte
stop and are quiescent (silent) and housed in protective cells called the follicle

3. At puberty, FSH stimulates the follicle to reinitiate meiosis (FSH = Follicle Stimulating Hormone)
Cell divides unequally giving one cell a greater amount of cytoplasm than the other
Larger cell  secondary oocyte
Smaller cell  polar body  dies
Secondary Oocyte proceeds until it reaches Metaphase II
Remains in this stage until it is fertilized
When fertilized it rapidly undergoes the second division removing a second polar body and forming a haploid nucleus for fusion with the sperm nucleus

4. Primary germ cell in embryo
Ovary
Primary germ cell in embryo
Differentiation
Oogonium
in ovary
Mitotic
division
Primary oocyte,
arrested in prophase
of meiosis I
(present at birth)
Completion of meiosis I
and onset of meiosis II
Primary
oocyte
within
follicle
Secondary oocyte,
arrested at meta-
phase of meiosis II
First
polar
body
Ovulation
Entry of
sperm triggers
completion of
meiosis II
Ovum
Growing
Mature follicle
Ruptured
Ovulated
secondary oocyte
Corpus luteum
Degenerating
corpus luteum 2n n
Figure 46.11

5. Menstrual and Ovarian Cycles – balance of hormonal regulation
1. Release of GnRH (gonadotropin releasing hormone) from the hypothalamus
2. stimulate the release of FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone) from the anterior pituitary
3. FSH – causes the development of an egg cell in a follicle

6. Figure 45.7 Hypothalamus Neurosecretory cells of the hypothalamus Axon
Anterior
pituitary
Posterior
HORMONE
ADH
Oxytocin
TARGET
Kidney tubules
Mammary glands,
uterine muscles

7. Figure 45.8 Tropic Effects Only FSH, follicle-stimulating hormone
LH, luteinizing hormone
TSH, thyroid-stimulating hormone
ACTH, adrenocorticotropic hormone
Nontropic Effects Only
Prolactin
MSH, melanocyte-stimulating hormone
Endorphin
Nontropic and Tropic Effects
Growth hormone
Neurosecretory cells
of the hypothalamus
Portal vessels
Endocrine cells of the
anterior pituitary
Hypothalamic
releasing
hormones
(red dots)
HORMONE
FSH and LH
TSH
ACTH
MSH
TARGET
Testes or
ovaries
Thyroid
Adrenal
cortex
Mammary
glands
Melanocytes
Pain receptors
in the brain
Liver
Bones
Pituitary hormones (blue dots)
Figure 45.8

8. 4. Developing follicle releases estrogen
Estrogen causes the lining of the uterus (endometrium) to thicken and become highly vascularized – prepping for implantation of embryo

9. Increased levels of estrogens cause the amount of FSH and LH to eventually spike (initially inhibited until levels of estrogens are high) – positive feedback
– LH causes for more estrogen to be released

10. Control by hypothalamus Uterine (menstrual) cycle
Figure 46.13a–e
Control by hypothalamus
Inhibited by combination of
estrogen and progesterone
Stimulated by high levels
of estrogen
Inhibited by low levels of
estrogen
Hypothalamus
Anterior pituitary
GnRH
FSH LH
Pituitary gonadotropins
in blood
FSH and LH stimulate
follicle to grow
LH surge triggers
ovulation
Ovarian cycle
Growing follicle
Mature
follicle
Corpus
luteum
Degenerating
corpus luteum
Estrogen secreted
by growing follicle in
increasing amounts
Progesterone and
estrogen secreted
by corpus luteum
Follicular phase
Luteal phase
Ovulation
Ovarian hormones
Peak causes
LH surge
Estrogen
Progesterone
Estrogen level
very low
Progesterone and estro-
gen promote thickening
of endometrium
Uterine (menstrual) cycle
Endometrium
Menstrual flow phase
Proliferative phase
Secretory phase 5 10 14 15 20 25 28
Days 1
(a)
(b)
(c)
(d)
(e) 3 6 7 8 4 2 9

11. 5. High levels of LH cause the follicle to mature and burst and the secondary oocyte ruptures from the ovary (ovulation) for possible fertilization in the fallopian tube

12. Figure 46.13a–e Control by hypothalamus Inhibited by combination of
estrogen and progesterone
Stimulated by high levels
of estrogen
Inhibited by low levels of
estrogen
Hypothalamus
Anterior pituitary
GnRH
FSH LH
Pituitary gonadotropins
in blood
FSH and LH stimulate
follicle to grow
LH surge triggers
ovulation
Ovarian cycle
Growing follicle
Mature
follicle
Corpus
luteum
Degenerating
corpus luteum
Estrogen secreted
by growing follicle in
increasing amounts
Progesterone and
estrogen secreted
by corpus luteum
Follicular phase
Luteal phase
Ovulation
Ovarian hormones
Peak causes
LH surge
Estrogen
Progesterone
Estrogen level
very low
Progesterone and estro-
gen promote thickening
of endometrium
Uterine (menstrual) cycle
Endometrium
Menstrual flow phase
Proliferative phase
Secretory phase 5 10 14 15 20 25 28
Days 1
(a)
(b)
(c)
(d)
(e) 3 6 7 8 4 2 9

13. 6. LH then causes the follicle tissue to thicken and form the corpus luteum
Corpus luteum releases progesterone and estrogen
Shut down secretion of FSH and LH – negative feedback

14. Figure 46.13a–e Control by hypothalamus Inhibited by combination of
estrogen and progesterone
Stimulated by high levels
of estrogen
Inhibited by low levels of
estrogen
Hypothalamus
Anterior pituitary
GnRH
FSH LH
Pituitary gonadotropins
in blood
FSH and LH stimulate
follicle to grow
LH surge triggers
ovulation
Ovarian cycle
Growing follicle
Mature
follicle
Corpus
luteum
Degenerating
corpus luteum
Estrogen secreted
by growing follicle in
increasing amounts
Progesterone and
estrogen secreted
by corpus luteum
Follicular phase
Luteal phase
Ovulation
Ovarian hormones
Peak causes
LH surge
Estrogen
Progesterone
Estrogen level
very low
Progesterone and estro-
gen promote thickening
of endometrium
Uterine (menstrual) cycle
Endometrium
Menstrual flow phase
Proliferative phase
Secretory phase 5 10 14 15 20 25 28
Days 1
(a)
(b)
(c)
(d)
(e) 3 6 7 8 4 2 9

15. 7. degeneration of corpus luteum causes the levels of estrogen and progesterone to fall and results in the shedding of the thickened endometrium (menstruation)
allows for renewed secretion of FSH and LH to allow a new follicle to form

16. Control by hypothalamus Uterine (menstrual) cycle
Figure 46.13a–e
Control by hypothalamus
Inhibited by combination of
estrogen and progesterone
Stimulated by high levels
of estrogen
Inhibited by low levels of
estrogen
Hypothalamus
Anterior pituitary
GnRH
FSH LH
Pituitary gonadotropins
in blood
FSH and LH stimulate
follicle to grow
LH surge triggers
ovulation
Ovarian cycle
Growing follicle
Mature
follicle
Corpus
luteum
Degenerating
corpus luteum
Estrogen secreted
by growing follicle in
increasing amounts
Progesterone and
estrogen secreted
by corpus luteum
Follicular phase
Luteal phase
Ovulation
Ovarian hormones
Peak causes
LH surge
Estrogen
Progesterone
Estrogen level
very low
Progesterone and estro-
gen promote thickening
of endometrium
Uterine (menstrual) cycle
Endometrium
Menstrual flow phase
Proliferative phase
Secretory phase 5 10 14 15 20 25 28
Days 1
(a)
(b)
(c)
(d)
(e) 3 6 7 8 4 2 9

17. Effects of Pregnancy
Embryo implants in endometrium and secretes human chorionic gonadotropin – simulates release of progesterone and estrogen from the corpus luteum to maintain the endometrium and prevents menstruation
Embryo is at first nourished by the endometrium, but then tissue grows out of the embryo and intermingles with the endometrium to form the placenta

18. Menopause Cessation of ovulation and menstruation
Ovaries lose responsiveness to FSH and LH

19. Gametogenesis in Males – Page 975
GnRH causes release of FSH and LH
LH causes the release of testosterone from the Leydig cells which causes spermatogenesis (meiosis)
FSH stimulates Sertoli cells which produce nutrients for developing sperm in the seminiferous tubules of the testicles

20. Secondary spermatocyte
Epididymis
Seminiferous tubule
Testis
Cross section
of seminiferous
tubule 2n
Spermatogonium
Mitotic division,
producing large numbers
of spermatogonia
Sertoli cell
nucleus
Differentiation and onset of meiosis I 2n
Primary spermatocyte
(in prophase of meiosis I)
Meiosis I completed n n
Secondary spermatocyte
Meiosis II
Lumen of
Seminiferous tubule n n n n
Early
spermatids
Spermatids
(at two stages of
differentiation)
Differentiation
(Sertoli cells provide
nutrients) n n n
Sperm cells n
Neck
Head
Midpiece
Tail
Plasma membrane
Mitochondria
Nucleus
Figure 46.12
Acrosome

21. Figure 46.14 Stimuli from other areas in the brain Hypothalamus
GnRH from the
hypothalamus reg-
ulates FSH and LH
release from the
anterior pituitary.
FSH acts on the
Sertoli cells of the
seminiferous
tubules, promoting
spermatogenesis.
LH stimulates the
Leydig cells to make
testosterone, which
in turn stimulates
sperm production.
Anterior
pituitary
Negative
feedback
Leydig cells
make
testosterone
Primary and
secondary sex
characteristics
Sertoli cells
Spermatogenesis
Testis
Figure 46.14

22. Sperm anatomy Head – - acrosome - Contains digestive enzymes
- actin – forms acrosomal process
- nucleus – haploid DNA
Collar – filled with mitochondria
Tail - flagellum

24. Fertilization Process
Sperm hit outer layer (jelly coat) of the egg cell and releases digestive enzymes that start to digest the outer layer away
Actin filaments grow forming the acrosomal process
Actin filaments fuse with the surface proteins of the egg – this ensures the correct type of sperm (species) is fertilizing the egg
Sperm membrane unites with the membrane of the egg cell

25. Figure 47.3 Sperm nucleus Sperm plasma membrane Hydrolytic enzymes
Cortical
granule
Cortical granule
EGG CYTOPLASM
Basal body
(centriole)
head
Acrosomal
process
Actin
Acrosome
Jelly coat
Egg plasma
Vitelline layer
Fused plasma
membranes
Perivitelline
space
Fertilization
envelope
Cortical reaction. Fusion of the
gamete membranes triggers an
increase of Ca2+ in the egg’s
cytosol, causing cortical granules
in the egg to fuse with the plasma
membrane and discharge their
contents. This leads to swelling of the
perivitelline space, hardening of the
vitelline layer, and clipping of
sperm-binding receptors. The resulting
fertilization envelope is the slow block
to polyspermy. 5
Contact and fusion of sperm
and egg membranes. A hole
is made in the vitelline layer,
allowing contact and fusion of
the gamete plasma membranes.
The membrane becomes
depolarized, resulting in the
fast block to polyspermy. 3
Acrosomal reaction. Hydrolytic
enzymes released from the
acrosome make a hole in the
jelly coat, while growing actin
filaments form the acrosomal
process. This structure protrudes
from the sperm head and
penetrates the jelly coat, binding
to receptors in the egg cell
membrane that extend through
the vitelline layer. 2
Contact. The
sperm cell
contacts the
egg’s jelly coat,
triggering
exocytosis from the
sperm’s acrosome. 1
Sperm-binding
receptors
Entry of
sperm nucleus. 4
Figure 47.3

26. Fusion of the gamete membranes causes the egg cell to depolarize by the release of Ca2+
Depolarization initiates the release of cortical granules = Cortical Reaction – this causes the membrane of the egg to change preventing other sperm from fertilizing the egg.
This also activates the egg cell and the second phase of meiosis is completed

27. Figure 47.3 Sperm nucleus Sperm plasma membrane Hydrolytic enzymes
Cortical
granule
Cortical granule
EGG CYTOPLASM
Basal body
(centriole)
head
Acrosomal
process
Actin
Acrosome
Jelly coat
Egg plasma
Vitelline layer
Fused plasma
membranes
Perivitelline
space
Fertilization
envelope
Cortical reaction. Fusion of the
gamete membranes triggers an
increase of Ca2+ in the egg’s
cytosol, causing cortical granules
in the egg to fuse with the plasma
membrane and discharge their
contents. This leads to swelling of the
perivitelline space, hardening of the
vitelline layer, and clipping of
sperm-binding receptors. The resulting
fertilization envelope is the slow block
to polyspermy. 5
Contact and fusion of sperm
and egg membranes. A hole
is made in the vitelline layer,
allowing contact and fusion of
the gamete plasma membranes.
The membrane becomes
depolarized, resulting in the
fast block to polyspermy. 3
Acrosomal reaction. Hydrolytic
enzymes released from the
acrosome make a hole in the
jelly coat, while growing actin
filaments form the acrosomal
process. This structure protrudes
from the sperm head and
penetrates the jelly coat, binding
to receptors in the egg cell
membrane that extend through
the vitelline layer. 2
Contact. The
sperm cell
contacts the
egg’s jelly coat,
triggering
exocytosis from the
sperm’s acrosome. 1
Sperm-binding
receptors
Entry of
sperm nucleus. 4
Figure 47.3

28. Basic Development - Zygote - Cleavage: cell division
- Blastula: Hollow ball of cells

30. Gastrulation: infolding of ball (deflated ball) - forms gastrula - point of infolding = blastopore
infolding results in tissue layers Video
Ectoderm: outer layer
Endoderm: inner layer
Archenteron: space formed by the infolding of gastrula – becomes the digestive tract

31. Blastula, Gastrulation, Gastrula