Compiled Notes

SPERMATOGENESIS
STAGES, MECHANISM AND CONTROL

Spermatogenesis is the biological process of gradual transformation of germ cells into

spermatozoa over an extensive period of time within the boundaries of
the seminiferous tubules of the testis. This process involves cellular
proliferation by repeated mitotic divisions, duplication of chromosomes,
and genetic recombinations through crossover reduction division by
meiotic division to produce haploid spermatids and terminal
differentiation of the spermatids into spermatozoa. Thus
spermatogenesis can be divided into three phases of proliferation,
reduction-division (meiosis) and differentiation. These phases are also
associated with specific germ cell types, i e spermatogonia,
spermatocytes and spermatids respectively.

Spermatogenesis occurs within extensive seminiferous tubular structures, the testes.

Seminiferous tubules are lined by the seminiferous epithelium and contain a fluid filled
lumen; into which fully formed spermatozoa are released. The seminiferous epithelium
consists of two basic cells types, somatic and germinal cells. The germ cells are found
at different levels from the base of the epithelium tubules to the lumen and are
surrounded by cytoplasm of somatic cell, the sertoli cells. Sertoli cell cytoplasm
extends the entire height of the epithelium because the cell serves to nurture the
germ cells through their cycles of development. As the germ cells divide and develop
into different types of cells, they move from the basement membrane region through
tight functional complexes of adjacent sertoli cells until they reside in the adluminal
compartment. The Sertoli-Sertoli cell junctions form the blood-testis barrier, which
helps to protect the developing germ cells from potentially harmful blood borne
chemicals. The germ cells develop as syncytium or clonal unit connected to one
another by intercellular bridges after cell division. This unique process of incomplete
division ensures synchronous development and permits rapid communication between
the cells. Synchrony of germ cell development results in large number of cells at the
same level of development, the specific identification of which scientists refer to as
stages.

PHASES OF SPERMATOGENESIS
Proliferation
Proliferation spermatogonia, which constitute the first phase, are the most immature
cells and are located along the base of the seminiferous epithelium. They proliferate
by mitotic division and multiply repeatedly
continually replenish the germinal
epithelium. Spermatogonia are capable of
self-renewal and thus also produce stem cells
that remain along the base as well as
committed cells that are on one-way tract
leading to spermatozoa. In most species, the
B spermatogonium is the last one to divide
by mitosis. Its division produces the first cell
of the second phase, the preleptotene
spermatocyte, which migrates upwards away
from the base of the seminiferous tubule and
crosses through the sertoli-sertoli junction.

Meiosis
Reduction division by meiosis involves
numerous types of spermatocytes that range
in size from cells smaller than a red blood
cell to very large that occupy portions of
every cross section of seminiferous tubules.
Reduction division is a biological mechanism
Compiled Notes

by which a single germ cell can increase its DNA content, then divide twice to produce
four individual germ cells containing a single strand of each chromosome or half the
number of chromosomes normally found in cells of the body. The process of meiosis is
extended over a long period of time; therefore' spermatocytes are found in every
stage of spermatogenesis, and in some stages two different types; of spermatocytes
are observed. During meiosis, the changes that take place in the chromosomes are
easily recognized .
DNA synthesis occurs in pre-leptotene spermatocytes. Prophase of the first meiotic
division may, last nearly 3 weeks; during which time other chromosomes first unravel
as thin unpaired filaments. Homologous chromosomes become paired in the zygote
cell, forming the synaptonemal complex Pachytene spermatocytes begin as small cells
but their nuclei enlarge greatly as the chromosomes become shorter and thicken.
Genetic recombination occurs through crossover between paired chromosomes.
Pachytene cells also exhibit an increase in RNAs and protein synthesis in preparation
for the next phase. Diplotene spermatocytes separate the synaptonemal complexes
and the chromosomes are spread apart in the nucleus. In diakinesis the nuclear
envelope disappears and chromosomes condense. Both meiotic divisions occur
rapidly, thus limiting these cell to one stage. Small secondary spermatocytes (2N) are
produced by meiosis I which then rapidly divide again by meiosis II, with unique
metaphase formations by the chromatin. Meiosis II produces very small haploid (1N)
cells called round spermatids that enter the next phase called differentiation.
Differentiation
The haploid germ cells undergo a prolonged phase of terminal differentiation known as
spermiogenesis. The cells undergo dramatic changes including the following three
major modifications: (1) the nucleus elongates and chromatin condenses into a very
dark staining structure having unique shapes that are species specific. (II) The Golgi
apparatus produces a lysosome-like granule that elaborates over the nucleus to form
the future acrosome. The acrosomic system contains the hydrolytic enzymes required
for sperm-egg interaction and fertilization. and (III) the cells forms a long tail lined
with mitochondria in the proximal region and it loses excess cytoplasm, which is
added first as the cytoplasmic lobe that eventually is phagocytized by the sertoli cell
as the residual body. Recognizable changes in the differentiation of a spermatid are
called "steps" of spermiogenesis. In the rat, the first step is the small round step
spermatid produced by meiosis II. Step I occurs in the first stage of the cycle. In all
species, the tail elongate spermatids, steps 15-19 in the rat, overlap with the younger
round spermatids thus, in some stages tow generation of spermatids are present in
the same tubule cross section

PROCESS
Once the vertebrate primordial germ cells (PGC) arrive at the genital ridge of male in
embryonic stage of development, they become incorporated in to the sex cords. They
remain there until maturity, at which time the sex cords hollow out to form the
seminiferous tubules, and the
epithelium of the tubules
differentiates into the sertoli
cells. These sertoli cells nourish
and protect the developing
sperm cells, and
SPERMATOGENESIS- meiotic
divisions giving rise to the
sperm-occurs in the recesses of
the sertoli cells. The process by
which the PGCs generate sperm
has been studied in detail in
several organisms, but it shall be
focused here on
spermatogenesis in mammals.
After reaching the gonad, the
PGCs divide to form TYPE A1
Compiled Notes

SPERMATOGONIA. These cells are smaller than the PGCs and are characterized by an
ovoid nucleus that contains chromatin associated with the nuclear membrane. The A1
spermatogonia are found adjacent to the outer basement membrane of the sex cords.
At maturity, these spermatogonia are thought to divide so as to make another type A1
spermatogonium as well as a second, paler type of cell, the TYPE A2
SPERMATOGONIUM. Thus, each type A1 spermatogonium is a stem cell capable of
regenerating itself as well as of producing a new cell type. The A2 spermatogonia
divide to produce the A3 spermatogonia, which then beget the type A4 spermatogonia
divide to form the TYPE B SPERMATOGONIA, and these cells divide mitotically to
generate the PRIMARY SPERMATOCYTES-the cells that enter meiosis.

It is found that during the spermatogonial divisions, cytokinesis is not complete.

Rather, the cells form a syncytium whereby each cell communicates to the other via.
cytoplasmic bridges about 1 micron in diameter (Dym and Fawcett, 1971). The
successive divisions produce clones of interconnected cells, and because ions and
molecules readily pass through these intercellular bridges, each cohort, row of
soldiers, matures synchronously.

Each primary spermatocyte undergoes the first meiotic division to yield a pair of
SECONDARY SPERMATOCYTES, which complete the second division of meiosis. The
haploid cells formed are called spermatids, and they are still connected to each other
through their cytoplasmic bridges.

The spermatids that are connected in this manner have haploid nuclei, but are
functionally diploid, since the gene product made in one cell can readily diffuse into
the cytoplasm of its neighbors (Braun et al., 1989a). During the divisions from typeA1
spermatogonium to spermatids, the cells move farther and farther away from the
basement membrane of the seminiferous tubule and closer to its lumen. Thus, each
type of cell can be found in a particular layer of the tubule. The spermatids are located
at the border of the lumen, and here they lose their cytoplasmic connections and
differentiate into sperm cells.

SPERMIOGENESIS
The haploid spermatid is a round, unflagellated cell that looks nothing like the mature
vertebrate sperm. The next step in sperm maturation, then, is SPERMIOGENESIS (or
SPERMATELIOSIS), the differentiation of the sperm cell. IN order for fertilization to
occur, the sperm has to meet and bind
with the egg, and spermiogenesis
differentiates the sperm for these
functions of motility and interaction. The
first steps involve the construction of
the acrosomal vesicle from the Golgi
apparatus. The acrosome forms a cap
that covers the sperm nucleus. As the
cap is formed, the nucleus rotates so
that the acrosomal cap will then be
facing the basal membrane of the
seminiferous tubule. This rotation is
necessary because the flagellum is
beginning to form from the centrioles on
the other side of the nucleus, and this
flagellum will extend into the lumen.
During the last stage of spermiogenesis,
the nucleus flattens and condenses, the
remaining cytoplasm (the “cytoplasmic
droplet”) is jettisoned, and the
Compiled Notes

mitochondria from a ring around the base of the flagellum. The resulting sperm then
enter the lumen of the tubule.

In the mouse, the entire development from stem cell to spermatozoan takes 34.5
days. The spermatogonial stages last 8 days, meiosis lasts 13 days, and
spermiogenesis takes up another 13.5 days. In humans, spermatic development takes
74 days to complete. Because the type A1 spermatogonia are ///stem cells,
spermatogenesis can occur continuously. Each hour, some 100 million sperm are
made in each human testicle, and each ejaculation releases 200 million sperm.
Unused sperm is either reabsorbed or passed out of the body in urine.

GENE EXPRESSION DURING SPERM DEVELOPMENT

Gene transcription during spermatogenesis takes place predominantly during the
diplotene stage of meiotic prophase. This transcription has been observed in many
organisms, but the documented case is probably that of Y chromosome transcription
in Drosophila hydei. Here, RNA transcripts originating from the Y-chromosome are
seen to be essential for controlling spermiogenesis. When we recall the function of the
Y chromosome in Drosophila, this is not surprising, for the Y chromosome is not
involved in sex determination here. Rather, it is needed for the formation of viable
sperm. The difference between XY Drosophila and XO Drosophila is that the latter are
sterile. Both are male. In Drosophila hydei, the Y chromosome extends five prominent
loops of DNA .If any of these loops is deleted; the organization of the sperm tail will be
abnormal. All the component parts of the sperm will be present, but not properly
organized (Hess, 1973). It appears, then, that Y-specific RNA made during meiotic
prophase is utilized later during spermiogenesis.

The genes that are transcribed specifically during spermatogenesis are often those
whose products are necessary to sperm motility or binding to the egg. In Drosophila
melanogaster, one of the sperm –specific genes transcribed is for b2-tubulin. This
isoform of b-tubulin is only seen during spermatogenesis, and it is responsible for
forming the meiotic spindles, the axoneme, and the microtubules associated with the
lengthening mitochondria. Hoyle and Raff (1990) have shown that another b-tubulin
isoform; b3-tubulin (which is normally expressed in mesodermal cells and epidermis)
cannot substitute for the b2-tubulin. When this gene was expressed in the absence of
the b2-tubulin gene, the resulting germ cells failed to undergo meiosis, axoneme
assembly, or nuclear shaping. Only the mitochondrial elongation occurred. This
indicates that the formation of the meiotic spindles and axoneme of sperm cells
cannot be accomplished by just any b-tubulin and that the transcription of sperm-
specific isoform is important.

Those genes whose products are necessary for the binding of the sperm and the extra
cellular matrices of the egg are also transcribed during spermatogenesis. The gene for
sea urchin bindin is transcribed relatively late in spermatogenesis and its m’RNA is
translated into bindin shortly after being made (Nishioka et al., 1990). The bindin
accumulates in vesicles that fuse together to form the single acrosomal vesicle of the
mature sea urchin sperm.

Like the oocyte, the spermatid can store m’RNA for later use. In mammals and birds, a
specific form of lactate dehydrogenate – SDH-X – is made during spermatogenesis.
(This protein enables the developing sperm to utilize can be identified in spermatocyte
cytoplasm during meiotic prophase (Blanco, 1980). Similarly, in many species, small
proteins called PROTAMINES appear in the nucleus during the final stages of
spermiogenesis. These proteins contain about 32 amino acids, all but four or five of
which are arginine residues. They replace the nuclear histones and cause the DNA to
form a compact, almost crystalline, array (Marushige and Dixon, 1969). DNA
complementary to trout protamine m’RNA can detect protamine m’RNA can detect
protamine message sequences in the primary spermatocyte. However, these
messages are stored in ribonucleoprotein particles. Only during the spermatid stage,
approximately a month after its synthesis is the protamine message translated into
Compiled Notes

protein (Itarou et al., 1978). The regulation of this m’RNA appears to be controlled by
its 3 untranslated region. If placed onto another message, this 3 untranslated region
will give the new message, the same translational regulation as the protamines
m’RNA. We find, then, that just like the oocyte, which can synthesize RNA in the
diplotene stage and store it for late use, the sperm can also package messages for
later translation.

In addition to gene transcription during meiotic prophase, there is also evidence that
certain genes are transcribed in the spermatids (reviewed in Palmiter et al., 1984).
This evidence for HAPLOID GENE EXPRESSION comes from studies involving
heterozygous mice in which two different populations of sperm are seen to exist – one
population expressing the mutant phenotype and one population expressing the wild-
type trait. If the synthesis of the RNA or protein were to occur while the cells were still
diploid, all the sperm would show the same phenotype.

In some species, sperm provides important developmental information that cannot be

compensated by the egg. We have discussed the imprinting of mammalian
chromosomes wherein the sperm and egg DNA differ in their methylation pattern.
There are also cases of paternal effect genes. Here, homozygous recessive alleles in
the male cause abnormal development in the embryo even if the female is
homozygous for the wild-type allele, while the reciprocal cross, where the father is
wild-type and the mother is homozygous for the mutant allele, leads to normal
embryos. One such paternal effect gene is spe-11 in C. elegans. The sperm containing
mutant alleles at the locus are unable to direct chromosomal movements that orient
the mitotic spindle of the embryo, suggesting that the mutation affects the
microtubule organizing regions such as centrioles.

Eventually, the haploid genome is condensed as the histones are replaced by

protamines or by specifically modified histones. Many of the sperm histones become
modified in the late spermatid stage during spermiogenesis. These modifications (such
as dephosphorylating the N-terminal regions of certain histones) cause the chromatin
to condense. Condensation results in severely reduced transcription. Thus,
transcription from the male genome is not detected again until it is reactivated
sometime during development (Poccia, 1986; Green and Poccia, 1988).

HORMONAL CONTROL OF SPERMATOGENESIS

The production of spermatozoa and testosterone, is the primary functions of the adult
mammalian testis, depends on stimulation of the testes by the gonadotropic
hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
Both hormones are produced by the pituitary gland in response to
gonadotropin releasing hormone (GnRH) from the hypothalamus. In response
to LH, testosterone is produced by the Leydig cells. It has been clear for
decades that testosterone is a necessary prerequisite for the initiation of
spermatogenesis in the peripubertal mammal, the maintenance of
established spermatogenesis (and fertility) in adults induced experimentally
to become oligospermic or azoospermic. It also is well established that FSH is
involved in the peripubertal initiation of spermatogenesis. Whether or not
FSH is also involved in regulating spermatogenesis in the adult mammal
continues to be debated.

Although the effects of testosterone and FSH administration or with drawl on

spermatogenesis have been studied for years, the mechanisms by which they regulate
spermatogenesis remain uncertain. Androgen and FSH receptors are localized to
sertoli cells, making it likely that the effects of both testosterone and FSH are
mediated via. these cells. Over the past 10 years, it has become well established that
the testosterone concentration normally present within the testis is very high relative
to the concentration that should be required to saturate androgen receptors, and that
although intratesticular testosterone concentration is also very high. There is no good
explanation for this observation. Recent studies have shown that increased germ cell
Compiled Notes

apoptosis occurs when testosterone is withdrawn from the mammalian testis, pointing
to testosterone as a cell survival factor. The molecular mechanisms by which
testosterone acts in this way only recently have begun to be considered. FSH also may
act to prevent cell death, though this is less certain.

This article focuses on the roles of testosterone and FSH in mammalian

spermatogenesis. Discussion will center on the relationship between intratesticular
testosterone concentration and spermatogenesis, controversy regarding the
requirement for FSH, and the possible mechanisms by which testosterone and FSH act
to regulate spermatogenesis.

TESTOSTERONE AND FSH REQUIRED FOR SPERMATOGENESIS ?

Testosterone
In the rat, the concentration of testosterone in blood serum is approximately 2 ng/ml.
Because Leydig cells are located in the interstitial compartment of the testis, it is not
surprising that the concentrations of testosterone in the interstitial fluid (IF; 70ng/ml)
and seminiferous tubule fluid (STF; 50ng/ml) of untreated rats are far greater than
those in serum. Similar relationships between serum and intratesticular testosterone
concentrations occur in the human. Interestingly, when testosterone is administered
to rats in circumstances in which its local production by Leydig cells is suppressed,
testosterone concentration does not equilibrate throughout the body, as might be
expected; rather, a concentration gradient is established that is similar to the gradient
that occurs normally, with testosterone concentration in IF>STF>serum. Thus, even
when there is no local testosterone production, testosterone becomes concentrated
within the testis. Whether or not administered testosterone also becomes
concentrated in the human testis is not known

The average testosterone concentration in rat STF (50ng/ml; 1.7x10-7 M) is

considerably higher than the Kp of testicular androgen receptors (3x10-9 M). This
suggests that the testosterone concentration in the seminiferous tubules may be
considerably in excess of that required to maintain established spermatogenesis in the
adult rat. This was found experimentally to be the case. Zirkin and colleagues
examined the quantitative relationship between intratesticular testosterone
concentration and sperm number per testis in adult rats that received testosterone of
increasing doses via testosterone filled Silastic capsules of increasing size. The
administration of testosterone in this way suppresed Leydig cell testosterone
production so that the only source of testosterone was from the capsules.
Quantitatively complete spermatogenesis was maintained at a STF testosterone
concentration of only 20 ng/ml resulted in graded reductions in sperm production,
indicative of a dose response relationship between STF testosterone concentration and
sperm produced by the testis. Similarly, in adult rats rendered azoospermic with a
contraceptive dose of LH-suppressive testosterone, the intratesticular testosterone
concentration found to be required for the restoration of quantitatively complete
spermatogenesis also was 20 ng/ml. These observations indicate that
spermatogenesis can be quantitatively maintained or restored at testosterone
concentrations far lower than those normally present within the testis but still an order
of magnitude greater than present in serum.

FSH
Though the involvement of FSH in spermatogenesis has been studied extensively,
considerable controversy remains about the circumstances in which it is required and
what it does. The uncertainty stems in part from apparent species differences in the
effects of FSH on spermatogenesis and in part from the time during the life cycle
during which FSH is either administered or withdrawn. Numerous studies have shown
that FSH is required (in addition to testosterone) for quantitatively normal
spermatogenesis in adult nonhuman primates and humans and for testicular
recrudescence in seasonally breeding rodents. There is also agreement that FSH is
integrally involved in initiating spermatogenesis in immature rats. The receptor for
FSH resides with the Sertoli cell. Given the effect of FSH on spermatogenesis initiation,
Compiled Notes

it is not surprising that FSH elicits dramatic camp production by sertoli cells from
prepubertal rat testes. Adult sertoli cells to FSH as rats approach adulthood. The
altered sensitivity to FSH has been attributed in part to age related induction of
phosphodiesterases, increased activity of G1 proteins, or induction of protein kinase
inhibitors. Whatever the mechanism, it is apparent that the response of sertoli cells to
FSH changes from the prepubertal to the adult period.

Controversy about the involvement of FSH in maintaining or restoring adult

spermatogenesis has come largely from studies of the adult rat. The administration of
testosterone to rats at the time of hypophysectomy, or after hypophysectomy-induced
testicular regression, fails to maintain or restore spermatogenesis quantitatively,
suggesting that pituitary factors in addition to LH may participate in the regulation of
spermatogenesis. A number of studies of this kind have concluded that it is the
absence of FSH, rather than the absence of other pituitary factors, that explains the
inability of testosterone to sustain or restore spermatogenesis after hypophysectomy.
Such a conclusion is consistent with studies showing synergy between FSH and
testosterone effects in the adult. For example, the administration of recombinant FSH,
by itself or together with testosterone, to hypophysectomized adult rats has been
shown in some studies to prevent germ cell loss and in others to restore
spermatogenesis (qualitatively) to germ cell depleted testes. The conclusion from such
studies, taken together is that FSH can affect adult

Does FSH affect adult spermatogenesis under non-experimental conditions? Dym and
colleagues reported that the administration of FSH antiserum to adult rats did not
affect testis weight or germ cell number, concluding that FSH has little or no effect on
spermatogenesis. Consistent with this, Awoniyi and colleagues reported that the
administration of testosterone to adult rats at the time of their active immunization
against GnRH maintained spermatogenesis quantitatively and, similarly, that
testosterone alone, when administered to rats made azoospermic by active
immunization against GnRH, restored spermatogenesis quantitatively in both cases in
the absence of detectable FSH. If FSH remained suppressed throughout these
immunization experiments, as Awoniyi and colleagues reported, these studies provide
conclusive evidence that FSH is not required for the maintenance or restoration of
spermatogenesis in adult rats. However, others have reported that at least some FSH
is restored by testosterone treatment of GnRH-immunized rats. The issue has yet to be
resolved.
The arguments for and against a role for FSH in the adult rat might be reconciled by
the thesis that under conditions in which intratesticular testosterone levels are high,
FSH may not be required for either the maintenance of spermatogenesis or its
restoration. In normal circumstances, total intratesticular testosterone concentration
in fact is very high, typically more than twice the concentration found to be required to
quantitatively maintain or restore spermatogenesis. In summary, available data
suggest (1) that FSH may not be required for spermatogenesis in the normal adult rat
because intratesticular testosterone concentrations normally are very high; but (2)
that FSH can have significant effects on spermatogenesis when intratesticular
testosterone concentrations fall. However, Griswold and colleagues reported that
immunization of adult rats against the FSH receptor resulted in reduced sperm
number, presumably despite normal high levels of testosterone. Moreover, in a setting
in which there are defects in the genes encoding FSH and its receptor,
spermatogenesis and fertility are possible. Thus, although the controversy regarding
the role of FSH continues, it is becoming apparent that complete spermatogenesis can
occur, and fertility can be realized, in the absence of FSH.

SPERMATOGENESIS IN A NUT SHELL WITH RESPECT TO HUMANS

Spermatogenesis (sper’-ma-to-JEN-e-sis)
In humans, spermatogenesis takes about 74 days. The seminiferous tubules are lined
with immature cells called spermatogonia (sper’-ma-to-GO-ne-a; sperm = seed;
gonium = generation or offspring. These cells develop from primordial (primordialis
Compiled Notes

= primitive or early form) germ cells that arise from yolk sac endoderm and enter the
testes early in development. In the embryonic testes, the primordial germ cells
differentiate into spermatogonia but remain dormant until they begin to undergo
mitotic proliferation at puberty.
Spermatogonia contain the diploid (2n) chromosome number. When these stem cells
undergo mitosis, some of the daughter cells remain undifferentiated and serve as a
reservoir of stem cells. Such cells remain near the basement membrane. The rest of
the daughter cells lose contact with the basement membrane of the seminiferous
tubule, undergo certain developmental changes, and differentiate into primary
spermatocytes (SPER-ma-to-sitz’). Primary spermatocytes, like spermatogonia, are
diploid (2n); that is, they have 46 chromosomes.
Reduction Division (Meiosis I) Each primary spermatocyte enlarges before
dividing. Then two nuclear divisions take place as part of meiosis. In the first, DNA
replicates and 46 chromosomes (each
made up of two identical chromatids)
form and move toward the equatorial
plane of the cell. There they line up in
homologous pairs so that there are 23
pairs of duplicated chromosomes in the
center of the cell. This pairing of
homologous chromosomes is called
synapsis. The four chromatids of each
homologous pair then become associated
with each other to form a tetrad. In a
tetrad, portions of one chromatid may be
exchanged with portions of another. This
process, called crossing-over, permits
an exchange of genes among chromatids
those results in the recombination of
genes. Thus the spermatozoa eventually
produced are genetically unlike each
other and unlike the cell that produced
them-one reason for the great genetic
variation among humans.
Next, the meiotic spindle forms and the
kinetochore microtubules produced by
the centromeres of the paired
chromosomes extend toward the poles of
the cell. As the pairs separate, members of each pair migrate to opposite poles of the
dividing cell. The random assortment of maternally derived and paternally derived
chromosomes toward opposite poles is another reason for genetic variation among
spermatozoa and therefore among humans. The cells formed by the first nuclear
division (reduction division) are called secondary spermatocytes. Each cell has 23
chromosomes – the haploid number. Each chromosome within a secondary
spermatocyte, however, is made up of two chromatids still attached by a centromere.
Equatorial Division (Meiosis II) The second nuclear division of meiosis is
equatorial division. There is no replication of DNA. The chromosomes (each
composed of two chromatids) line up in single file along the equatorial plane, and the
chromatids of each chromosome separate from each other. The cells formed from the
equatorial division are called spermatids. Each has half the original chromosome
number, or 23 chromosomes, and is haploid. Each primary spermatocyte therefore
produces four spermatids by meiosis (reduction division and equatorial division).
Spermatids lie close to the lumen of the seminiferous tubule.
During spermatogenesis, a very interesting and unique process occurs. As the sperm
cells proliferate, they fail to complete cytoplasmic separation (cytokinesis) so that all
the daughter cells, except for the least-differentiated spermatogonia, remain in
contact via cytoplasmic bridges. These cytoplasmic bridges persist until development
of the spermatozoa is complete, at which point they float out individually into the
Compiled Notes

lumen of the seminiferous tubule. Thus the offspring of a spermatogonium remain in

cytoplasmic communication through their entire development.
This pattern of development undoubtedly accounts for the synchronized production of
spermatozoa in any given area of a seminiferous tubule. It may have survival value in
that half the spermatozoa contain an X chromosome and half a Y chromosome. The
larger X-chromosome may carry genes needed for spermatogenesis that are lacking
on the Y chromosome.
Spermiogenesis The final stage of spermatogenesis, called spermiogenesis,
involves the maturation of spermatids into spermatozoa. Each spermatid develops a
head with an acrosome (enzyme-containing granule) and a flagellum (tail). Since there
is no cell division in spermiogenesis, each spermatid develops into a single
spermatozoon (sperm cell or sperm). The release of a spermatozoon from its
sustentacular cell is known as spermiation.
Sperm enter the lumen of the seminiferous tubule and migrate to the ductus
epididymis. There, they complete their maturation in 10 to 14 days and become
capable of fertilizing an ovum. Spermatozoa are also stored in the ductus (vas)
deferens. Here, they can retain their fertility for up to several months.