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Spermiogenesis is the final stage of spermatogenesis, which sees the

maturation of spermatids into mature, motile spermatozoa. The spermatid
is a more or less circular cell containing a nucleus, Golgi apparatus,
centriole and mitochondria. All these components take part in forming the
Spermiogenesis is the process by which haploid round spermatids complete an
extraordinary series of events to become streamlined spermatozoa capable of
motility. Spermiogenesis begins after spermatocytes complete 2 quick successive
meiotic reductive divisions to produce haploid round spermatids. No further cell
division occurs as spermatids undergo their complex cytodifferentiation, over a
period of 2–3 weeks in mice and rats, to form mature elongated spermatids that
will ultimately be released from the seminiferous epithelium via a process known
as spermiation.
The different steps, or phases, of spermiogenesis are distinguished by the
morphological appearance of the developing acrosome and the changing shape of
the nucleus.1 During steps 1–7 of rat and mouse spermiogenesis, round spermatids
have a spherical, central nucleus, and begin to assemble the acrosome and the
axoneme, structures needed for fertilization and motility, respectively. During step
8, the nucleus and acrosome polarize to one side of the cell, signaling the
beginning of the elongation phase of spermiogenesis. At this time, the spermatid
forms a unique intercellular junction with the supporting Sertoli cell2 and the
nucleus starts to change shape and compact, to achieve the dense, species-specific
head shape that is important for motility. These changes involve nuclear
compaction and chromatin condensation, as well as sculpting of the sperm head by
a microtubule-based structure known as the manchette.3
As the spermatid nucleus compacts, nucleosomal chromatin is transformed into
compacted chromatin fibers by the replacement of histones with transition proteins,
which are subsequently replaced by protamines. The spermatid ceases active gene
transcription as nucleosomes disappear and the chromatin is remodelled and
compacted.4,5 Accordingly, earlier round spermatids in steps 1–7 actively
transcribe many mRNAs that are necessary for spermiogenesis,6 however many of
those mRNAs are subjected to translational delays until the protein is required later
in spermiogenesis.4,5
Another major event occurring during spermiogenesis is the assembly of the sperm
flagellum, reviewed in.7-9 The central component of the flagellum, the microtubule-
based axoneme, is assembled soon after the completion of meiosis. As spermatids
elongate, the accessory structures needed for flagella function (outer dense fibers,
fibrous sheath, mitochondrial sheath) are assembled around the central axoneme.
The final stage of spermiogenesis is known as spermiation, and is the process by
which the elongated spermatids undergo their final remodelling and release from
the seminiferous epithelium. Spermiation is a complex, multi-step process, which
is particularly vulnerable to disruption.10
The following chapter gives a broad overview of the mechanisms governing the
major events in spermiogenesis and spermiation. Wherever possible, recent review
articles have been cited; the reader is encouraged to consult these reviews for a
more detailed description of, and original references pertaining to, the mechanism
of interest. To aid in the understanding of reproductive toxicant effects or
phenotypic changes, the chapter is arranged according to the major morphological
defects that are observed in these processes during reproductive toxicant
administration, as well as those often observed in transgenic mouse models of male

The spermatid is the haploid male gametid that results from division of
secondary spermatocytes. As a result of meiosis, each spermatid contains
only half of the genetic material present in the original primary
Spermatids are connected by cytoplasmic material and have superfluous
cytoplasmic material around their nuclei.
When formed, early round spermatids must undergo further maturational
events to develop into spermatozoa, a process
termed spermiogenesis (also termed spermeteliosis).
The spermatids begin to grow a living thread, develop a thickened mid-
piece where the mitochondria become localised, and form an acrosome.
Spermatid DNA also undergoes packaging, becoming highly condensed.
The DNA is packaged firstly with specific nuclear basic proteins, which are
subsequently replaced with protamines during spermatid elongation. The
resultant tightly packed chromatin is transcriptionally inactive.
A spermatozoon is a motile sperm cell, or moving form of
the haploid cell that is the male gamete. A spermatozoon joins an ovum to
form a zygote. (A zygote is a single cell, with a complete set
of chromosomes, that normally develops into an embryo.)
Sperm cells contribute approximately half of the nuclear genetic
information to the diploid offspring (excluding, in most cases, mitochondrial
DNA). In mammals, the sex of the offspring is determined by the sperm
cell: a spermatozoon bearing a X chromosome will lead to a female (XX)
offspring, while one bearing a Y chromosome will lead to a male (XY)
offspring. Sperm cells were first observed by Anton van Leeuwenhoek in

The process of spermiogenesis is traditionally divided into four stages: the
Golgi phase, the cap phase, formation of tail, and the maturation stage
Golgi phase
Cap/Acrosome phase
Formation of Tail
Maturation phase

The acrosome is an organelle that develops over the anterior half of the
head in the spermatozoa (sperm cells) of many animals including humans.
It is a cap-like structure derived from the Golgi apparatus.

The mature spermatozoa are released from the protective Sertoli cells into
the lumen of the seminiferous tubule and a process called spermiation then
takes place, which removes the remaining
unnecessary cytoplasm and organelles.[2]
The resulting spermatozoa are now mature but lack motility, rendering
them sterile. The non-motile spermatozoa are transported to
the epididymis in testicular fluid secreted by the Sertoli cells, with the aid
of peristaltic contraction.
Whilst in the epididymis, they acquire motility. However, transport of the
mature spermatozoa through the remainder of the male reproductive
system is achieved via muscle contraction rather than the spermatozoon's
motility. A glycoprotein coat over the acrosome prevents the sperm from
fertilizing the egg prior to traveling through the male and female
reproductive tracts. Capacitation of the sperm by the enzymes FPP
(fertilization promoting peptide, produced in the epididymis) and heparin (in
the female reproductive tract) removes this coat and allows sperm to bind
to the egg.

Spermiation is the process by which mature spermatids are released from the
supporting somatic Sertoli cells into the lumen of the seminiferous tubule. It is a
critical determinant of the number of sperm entering the epididymis, and thus the
sperm content of the ejaculate. Spermiation is a protracted, complex process
occurring over several days (∼82 hrs in the rat, see below), commencing at the
beginning of stage VII in the rat and mouse1 with the alignment of elongated
spermatids along the luminal edge of the seminiferous epithelium. Spermiation is
completed towards the end of stage VIII, when spermatids are released into the
tubule lumen, and the remainder of the spermatid cytoplasm, known as the residual
body, is phagocytosed by the Sertoli cell. Although the primary goal of
spermiation is to release the spermatid from the Sertoli cell, this process also leads
to extensive restructuring and remodelling of the spermatid to produce a
streamlined spermatozoan. Spermiation is a known target for hormone-based male
contraceptives2 and, by virtue of its role in spermatid restructuring and release, is
important for optimal fertility. The morphological and ultra-structural events
associated with spermiation have been well described and appear conserved among
rodents, monkeys and humans,1,3 however, the molecular control of spermiation is
less understood.
The purpose of this review is to examine the morphological and molecular events
involved in mammalian spermiation, together with their likely proteomic
composition, in order to provide a better understanding of the spermiation
machinery, i.e., the cellular processes and structures required for the successful
completion of spermiation. Much of this information will necessarily come from
studies in rodents, but will be applied to human spermiation where possible. The
causes of spermiation failure and their impact on sperm morphology and function
will also be examined in an effort to understand how this process may impact on
male fertility.