1. Gametogenesis is the process by which primordial germ cells mature into functional gametes through meiosis and cellular differentiation. In females, primordial germ cells become oogonia then enter meiosis to become primary oocytes, while in males they become gonocytes then spermatogonia. 2. Primordial germ cells form early in development and migrate to the developing gonads, inducing their formation. In the gonads, germ cells proliferate then enter gender-specific meiotic and developmental pathways. 3. Differences between male and female gametogenesis include the timing and location of meiosis. In females, oocytes arrest in prophase I until ovulation, while in males

1. Dr. Komal Parmar
GAMETOGENESIS

2. TYPES OF CELL DIVISION

8. • Gametes are derived from the
primordial germ cells
(PGCs) that are formed in the
epiblast during the second
week and that move to the wall
of the yolk sac.
• Gametogenesis: It refers
to the maturation of germ cells
into functional gametes. It
involves Meiosis and
Cytodififfrentiation of
the primordial germ cell.
GAMETOGENESIS

9. Stage Approximate
Age in Days
Event Cell Population
1. 1 Fertilization and First
Clevage
Oocyte to Ootid formation and Zygote
formed.
2. 2-3 Perimplantaion and
Compaction.
4-8-16 cell blastula
3. 4-5 Free Blastula hatches
from Zona
• Trophoblast
• Inner cell mass differentiationg into
Epiblast and Hypoblast
4. 6 Implantation • Syncytio and Cytotrophoblast
• Hypoblast and Epiblast further
differentiating
5a, 5b,
5c.
7-12 Implanted Previllus • Lacunae, Chorion, Amnion, Primary Yolk
Sac, extraembryonic mesoblast, Amnion
6a, 6b 16-18 Secondary Yolk Sac,
Primitive Streak
• Villi
• Secondary Yolk Sac
• Amnion
• Primordial Germ cells
• Primitive Streak formed in later half

11. • The primordial germ cells are formed
very early from the epiblast (2nd
week). They are larger than most
somatic cells, and are characterized by
vesicular nuclei with well-defined
nuclear membranes.
• Primordial germ cells spend the early
stages of development within the
extraembryonic tissues (Yolk Sac)
near the end of the primitive streak. In
this situation they are away from the
inductive influences to which the
majority of the somatic cells are
subjected during early development.
• During the fourth week these cells
begin to migrate from the yolk sac
toward the developing gonads, where
they arrive by the end of the fifth
week.
PRIMORDIAL GERM CELLS

12. • When the tail fold has
formed they appear within
the endoderm and the
splanchnopleuric
mesenchyme and
epithelium of the hindgut
as well as in the adjoining
region of the wall of the
yolk sac.
• They migrate
dorsocranially in the
mesentery, by amoeboid
movements and by growth
displacement, and reach
the genital ridges.
• Primordial germ cells
proliferate both during and
after migration to the
mesonephric ridges. Cells
which do not complete this
migration degenerate.
After segregation, when
they are often termed
primary gonocytes, they
divide to form secondary
gonocytes

13. • The Urogenital System develops
from a common mesodermal
ridge (intermediate mesoderm)
along the posterior wall of the
abdominal cavity.
• Gonadal Ridges are formed by
proliferation of the epithelium
and a condensation of underlying
mesenchyme. Germ cells do not
appear in the genital ridges until
the sixth week of development.
• If the PGC fail to reach the
ridges, the gonads do not
develop. Hence the primordial
germ cells have an inductive
influence on development of the
gonad into ovary or testis.
THE GONADAL RIDGE

14. • Human PGCs proliferate by mitosis
during migration and after reaching
the Gonadal ridges (GR).
• During this journey, while undergoing
proliferation, PGCs begin extensive
nuclear reprogramming to regain
differentiation totipotency and reset
the genomic imprinting.
• Once relocated in the GRs, PGCs are
rapidly surrounded by cords of
somatic cells.
• They undergo mitosis and meiosis as
per their gender specific pattern.
GROWTH OF PRIMORDIAL
GERM CELLS (PGC)

15. • During the 6th to 8th week of female
(XX) embryonic development, the
primordial germ cells grow and begin
to differentiate into oogonia.
• Oogonia proliferate via mitosis during
the 9th to 22nd week of embryonic
development. There can be up to
600,000 oogonia by the 8th week of
development and up to 7,000,000 by
the 5th month.
• The mitotic proliferation of oogonia
lasts several weeks and overlaps the
period of their entry into meiosis (10–
11 weeks). In fact, until the fifth
month of fetal life, mitotic oogonia
and primary oocytes in different stages
of meiosis coexist
DIFFERENTIATION OF PRIMORDIAL
GERM CELLS IN FEMALES

16. • In the male, after reaching the
developing testis, PGCs are usually
termed gonocytes.
• During the first trimester, gonocytes
are mitotically active. Of relevance,
gonocytes continue to express markers
typical of pluripotent cells and despite
some morphological differences,
gonocytes are basically equivalent to
PGCs.
• During the second trimester, most but
not all gonocytes progressively lose
mitotic activity together with the
pluripotency and PGC markers. At this
time, two new types of germ cells have
been described, intermediate germ
cells still able to proliferate and mitotic
quiescent prespermatogonia.
DIFFERENTIATION OF PRIMORDIAL
GERM CELLS IN MALES

17. • The period of human PGC
proliferation in the female lasts
from the beginning of the fourth
week to about the ninth week,
when oogonia become clearly
recognizable within the fetal ovary.
• In the ovaries, oogonia continue to
proliferate mititically until the fifth
month.
• Near the time of birth, all primary
oocytes have started prophase of
meiosis I.
• In the male, if we consider the
gonocytes equivalent to PGCs,
proliferation continues probably for a
little longer period until about the end
of the first trimester (10–12 weeks)
• In the testes, intermediate germ cells
proliferate while prespermatogonia
become progressively mitotically
quiescent.
• Male baby is born with these primordial
spermatogonia and the meiosis begins
only at puberty,
Females Males
DIFFERENCE BETWEEN PGC
GROWTH IN MALES AND FEMALES

18. OOGENESIS

20. After their differentiation from the PGC, oogonia increase rapidly
in number, and by the fifth month of prenatal development, the total number
of germ cells in the ovary reaches its maximum, estimated at 7 million. At this
time, cell death begins, and many oogonia as well as primary oocytes become
atretic. By the seventh month, the majority of oogonia have degenerated except
for a few near the surface. All surviving primary oocytes have entered prophase
of meiosis I, and most of them are individually surrounded by a layer of flat
epithelial cells. A primary oocyte, together with its surrounding flat
epithelial cells, is known as a primordial follicle.

21. • Primary oocytes remain in prophase and do not finish
their first meiotic division before puberty is reached. They
are arrested at the Diplotene 1.
• Oocyte maturation inhibitor (OMI), a substance
secreted by follicular cells.
• The total number of primary oocytes at birth is estimated
to vary from 7 to 2 million.
• Approximately 400,000 are present by the beginning of
puberty
• 450-500 ovulated in the lifetime.
• At puberty, a pool of growing follicles is
established and continuously maintained from the supply
of primordial follicles. Each month, 15 to 20
follicles selected from this pool begin to mature,
passing through three stages:
• 1) primary or preantral;
• 2) secondary or antral (also called
vesicular or Graafian)
• 3) preovulatory.

25. • When the secondary follicle is mature, a surge in
luteinizing hormone (LH) induces the
preovulatory growth phase. Meiosis I is completed,
resulting in formation of two daughter cells of unequal
size, each with 23 double stranded chromosomes.
• One of the cells, the secondary oocyte, receives
most of the cytoplasm.
• The other cell forms the first polar body.
• The cell then enters meiosis II but arrests in metaphase
approximately 3 hours before ovulation. Meiosis II is
completed only if the oocyte is fertilized; otherwise, the
cell degenerates approximately 24 hours after ovulation.
• The first polar body also undergoes a second division

28. SPERMATOGENESIS

29. SPERMATOGONIA TYPES

30. • Maturation of Sperm Begins at Puberty
• Supporting cells, which are derived from the surface epithelium of the gland in the same
manner as follicular cells, become sustentacular cells, or Sertoli cells
• Shortly before puberty, the sex cords acquire a lumen and become the seminiferous
tubules. At about the same time, primordial germ cells give rise to spermatogonial stem
cells (intermediate spermatogonia)
• At regular intervals, cells emerge from this stem cell population to form type A
spermatogonia, and their production marks the initiation of spermatogenesis.

33. • Spermatogonia and spermatids remain embedded in deep recesses of Sertoli cells
throughout their development.
• Sertoli cells support and protect the germ cells, participate in their nutrition, and assist in
the release of mature spermatozoa.
• Spermatogenesis is regulated by luteinizing hormone (LH) production by the pituitary.
LH binds to receptors on Leydig cells and stimulates testosterone production, which in
turn binds to Sertoli cells to promote spermatogenesis.
• Follicle stimulating hormone (FSH) is also essential because its binding to Sertoli cells
stimulates testicular fluid production and synthesis of intracellular androgen receptor
proteins.

36. CLINICAL
CORRELATES

37. TERATOMA

38. CHROMOSOMAL ANOMALIES
• About 50% of the conceptions end in spontaneous abortions and almost half of them
have some major chromosomal anomaly.
• Most common abnormalities are Turner’s Syndrome, Triploidies and Trisomy 16.
• Chromosomal abnormalities account for 10% of the major birth defects.
• Genetic Mutation accounts for additional 5%.
• Example of chromosomal number anomaly
• Down’s Syndrome
• Edward Syndrome
• Patau Syndrome
• Turner’s Syndrome
• Klinefelter’s Disease
• Triple X syndrome

39. OTHER CHROMOSOMAL
ANOMALIES
• Structural Anomalies
• Cri-du-chat
• Angelman Syndrome
• Pradser Willi Syndrome
• 22q11 Syndrome
• Fragile X Syndrome
• Single gene Mutation
• Congenital Malformations
• Congenital Errors of Metabolism

40. ABNORMAL GAMETES