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The mammalian egg is cloaked by follicle cells released along with the egg during ovulation. A
sperm cell must migrate through this layer of follicle cells before it reaches the   , the
extracellular matrix of the egg. One component of the zonapellucida functions as a sperm receptor,
binding to a complementary molecule on the surface of the sperm head. Binding of the sperm head
to receptor molecules induces an acrosomal reaction similar to that of sea urchin sperm. Hydrolytic
enzymes spilled from the acrosome enable the sperm cell to penetrate the zonapellucida and
reach the plasma membrane of the egg. The acrosomal reaction also exposes a protein in the
sperm membrane that binds with the eggƍs plasma membrane.

As in sea urchin fertilization, the binding of a sperm cell to the egg triggers changes within the egg
leading to a cortical reaction, the release of enzymes from cortical granules to the outside of the
cell via exocytosis. The released enzymes catalyze alterations of the zonapellucida, which then
functions as the slow block to polyspermy. (There is no known fast block to polyspermy in
mammals.)

After the egg and sperm membranes fuse, the whole sperm, tail and all, is taken into the egg,
which lacks a centrosome. A centrosome forms around the centriole that acted as the basal body
of the spermƍs flagellum. This centrosome, which now includes a second centriole, duplicates to
form two centrosomes in the zygote. These will generate the mitotic spindle for the first cell
division. The haploid nuclei of mammalian sperm and egg do not fuse immediately as in sea urchin
fertilization. Instead, the envelopes of both nuclei disperse, and the two sets of chromosomes (one
set from each gamete) share a common spindle apparatus during the first mitotic division of the
zygote. Thus, only after this first division, as diploid nuclei form in the two daughter cells, do the
chromosomes from the two parents come together in a common nucleus. Fertilization is much
slower in mammals than in the sea urchin; the first cell division occurs 12±36 hours after sperm
binding in mammals, compared with about 90 minutes in sea urchins.

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Organisms that reproduce through asexual reproduction tend to grow in number
exponentially. However, because they rely on mutation for variations in their
DNA, all members of the species have similar vulnerabilities. Organisms that
reproduce sexually yield a smaller number of offspring, but the large amount of
variation in their genes makes them less susceptible to disease.
Many organisms can reproduce sexually as well as asexually. Aphids, slime
molds, sea anemones, some species of starfish (by fragmentation), and many
plants are examples. When environmental factors are favorable, asexual
reproduction is employed to exploit suitable conditions for survival such as an
abundant food supply, adequate shelter, favorable climate, disease, optimum pH
or a proper mix of other lifestyle requirements. Populations of these organisms
increase exponentially via asexual reproductive strategies to take full advantage
of the rich supply resources.
When food sources have been depleted, the climate becomes hostile, or
individual survival is jeopardized by some other adverse change in living
conditions, these organisms switch to sexual forms of reproduction. Sexual
reproduction ensures a mixing of the gene pool of the species. The variations
found in offspring of sexual reproduction allow some individuals to be better
suited for survival and provide a mechanism for selective adaptation to occur. In
addition, sexual reproduction usually results in the formation of a life stage that is
able to endure the conditions that threaten the offspring of an asexual parent.
Thus, seeds, spores, eggs, pupae, cysts or other "over-wintering" stages of
sexual reproduction ensure the survival during unfavorable times and the
organism can "wait out" adverse situations until a swing back to suitability occurs.
Sexual reproduction has many drawbacks, since it requires far more energy than
asexual reproduction and diverts the organisms from other pursuits, and there is
some argument about why so many species use it.
George C. Williams used lottery tickets as an analogy in one explanation for the
widespread use of sexual reproduction.He argued that asexual reproduction,
which produces little or no genetic variety in offspring, was like buying many
tickets that all have the same number, limiting the chance of "winning" - that is,
producing surviving offspring. Sexual reproduction, he argued, was like
purchasing fewer tickets but with a greater variety of numbers and therefore a
greater chance of success.
The point of this analogy is that since asexual reproduction does not produce
genetic variations, there is little ability to quickly adapt to a changing
environment. The lottery principle is less accepted these days because of
evidence that asexual reproduction is more prevalent in unstable environments,
the opposite of what it predicts.
 




‡ all potential gametes produced before birth
‡ Meiotic divisions unequal, leading to the formation of polar bodies (eventually destroyed)
‡ puberty releases the "arrested state" of primary oocytes, leading to ovulation
‡ Meiosis II does not occur until fertilization of the secondary oocyte by mature sperm
‡ ovulation and reproduction naturally end during menopause



‡ spermatogenesis from spermatogenic cells starts at puberty and continues through life
‡ Meiotic divisions are equal, leading to 4 spermatozoa from original spermatogenic cell
Meiosis II completed before the sperm leads to fertilization

„  
„
  
! "
Pregnancy is an immunological enigma. Half of the embryoƍs genes are inherited
from the father; thus, many of the chemical markers present on the surface of the
embryo will be foreign to the mother. Why, then, does the mother not reject the
embryo as a foreign body, as she would a tissue or organ graft bearing antigens
from another person? Reproductive immunologists are working to solve this
puzzle.

A major key to the puzzle may be the tissue called the trophoblast (see Figures
46.15 and 47.18). Originally the outermost layer of the blastocyst, the trophoblast
brings about implantation by growing into the endometrium and later develops
into the fetal part of the placenta (see Figures 46.15 and 46.16). How might the
trophoblast, and later the placenta, protect the embryo from rejection? Some
possibilities follow and are most prone to sexual activity right before
ovulation.
During early pregnancy, the trophoblast seems to prevent the motherƍs immune
system from rejecting the blastocyst by releasing signal molecules with
immunosuppressive effects. These include HCG, a variety of protein ³factors,´ a
prostaglandin, several interleukins, and an interferon. Several lines of research
suggest that some combination of these substances interferes with immune
rejection by acting on the motherƍs T lymphocytes, important players in the
immune system (see Chapter 43).

A very different hypothesis is that the trophoblast and later the placenta secrete
an enzyme that rapidly breaks down local supplies of tryptophan, an amino acid
necessary for T cell survival and function. At least in mice, this enzyme seems to
be essential for maintaining pregnancy.

Another possibility is the absence of certain histocompatibility antigens on

placental cells and the secretion of a hormone that induces synthesis of a ³death
activator´ membrane protein (FasL) on placental cells. Activated T cells have a
complementary ³death receptor´ (Fas), and the binding of FasL to Fas would
cause the T cells to self±destruct by apoptosis.




! 
The estrous cycle comprises the recurring physiologic changes that are induced
by reproductive hormones in most mammalian placental females. Humans and
great apes undergo a menstrual cycle instead. Estrous cycles start after puberty
in sexually mature females and are interrupted by anestrous phases. Typically
estrous cycles continue until death. Some animals may display bloody vaginal
discharge, often mistaken for menstruation.

Mammals share the same reproductive system, including the regulatory

hypothalamic system that releases gonadotropin releasing hormone in pulses,
the pituitary that secretes follicle stimulating hormone and luteinizing hormone,
and the sex hormones including estrogens and progesterone. However, species
vary significantly in the detailed functioning. One difference is that animals that
have estrous cycles reabsorb the endometrium if conception does not occur
during that cycle. Animals that have menstrual cycles shed the endometrium
through menstruation instead. Another difference is sexual activity. In species
with estrous cycles, females are generally only sexually active during the estrous
phase of their cycle (see below for an explanation of the different phases in an
estrous cycle). This is also referred to as being "in heat." In contrast, females of
species with menstrual cycles can be sexually active at any time in their cycle,
even when they are not about to ovulate. Humans, unlike some other species, do
not have any obvious external signs to signal receptivity at ovulation (concealed
ovulation). Research has shown however, that women tend to have more sexual
thoughts and are most prone to sexual activity right before ovulation.

" 
  

! 
?ou should know:
1) Gonadotropic hormone cycle =
Pituitary gland produces LH
and FSH, which stimulates the
ovaries to mature the ova from
the oocyte and triggers the
production of estrogen.
Hormone levels then drop
once ovulation has occurred. If
the egg isn¶t fertilized, cycle
starts again.
2) Ovarian cycle = @ the start of
the follicular phase, estrogen
(& progesterone) levels are
low, but rise as phase
continues. The egg starts to
develop ƒ ovulation occurs.
Corpus luteum produces
progesterone at its highest
level; if fertilization hasn¶t
occurred, corpus luteum
breaks down ƒ cycle starts
again
3) Endometrial cycle = starts with
menstrual phase (shedding of
lining), then it begins to
rebuild. An egg will then
attach, and if not fertilized,
cycle starts again.