which contributes more to the formation and making of a child, the sperm cell or egg cell?

Answer 1

the first abswer is wrong. Actually egg contributes more to the embryo because the cytoplasm in derived from maternal side because it grows in a female body.And there is also a phenomenon called as non-chromosomal gene inheritance which is because of female!!

Many of them dont know the intricacies of genetics so they are easily mislead.It's an amazing question.

Answer 2

They contribute equal amounts of chromosomes, but the egg is much larger and starts out contributing more material.

I understand sperm can be synthesized but the egg cannot.
http://www.guardian.co.uk/science/story/0,,1817401,00.html

Technically, then, the sperm may be irrelevant, ultimately.

Answer 3

they are equal

Answer 4

Gamete formation in females differs dramatically from the same process in males. The egg cells produced by meiosis in females are specialized to provide energy and materials for the developing embryo in its early stages. Meiosis in human females produces one large egg cell that has nearly all of the cytoplasm of the parent cell. The other cells produced by female meiosis are called "polar bodies". These are very small cells that have little more than the extra homologous chromosomes and chromatids not needed by the egg cell. The large amount of cytoplasm in the egg cell provides energy and stored materials for early cell divisions of the embryo before it attaches to the wall of the uterus and can acquire nutrients from the mother.

The female body itself is specialized to nourish the embryo through nine months of development and growth in the body and for some time afterwards. The cost of this to the female body is enormous. Unlike males, which produce millions of cheap sperm cells daily, human females can afford to allow only one or two eggs to mature at a time. Carrying more than one or two offspring at a time would very dangerous for mother and children alike, especially if time had elapsed between fertilizations and the fetuses were at different stages of development. Hormonal mechanisms in the female prevent this.

Shortly after birth, the human female has about 700,000 cells called "primary oocytes" in her ovaries. These are the cells that will give rise to eggs. They are stopped in Meiosis I. At puberty, about 250,000 primary oocytes remain in the ovaries. (The other 450,000 that were present shortly after birth have died for some reason.) During the next 40 years or so, over 400 of these primary oocytes will restart meiosis and become female gametes. Usually, only 1 gamete will be produced at a time on a monthly basis. At menopause, when production of female gametes stops, about 1,000 primary oocytes will remain. The majority of primary oocytes present at puberty never develop, for unknown reasons.

a. Hormones

Like sperm formation in males, the monthly maturation of a primary oocyte in females is under the control of chemical messages produced in the brain. GnRH (gonadotropin releasing hormone) is produced in the hypothalamus of the brain and triggers release of Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) from the anterior pituitary gland of the brain into the blood. These are the same brain hormones that cause testosterone secretion and sperm production in males. The big difference is that, while LH and FSH production in males is relatively stable, LH and FSH production rises and falls on a monthly cycle in females.

FSH (and LH) in the blood stimulate a follicle in one of the ovaries to begin cell division. Follicles consist of primary oocytes and additional cells around them. FSH and LH cause the primary oocyte to renew and complete Meiosis I while the other cells of the follicle divide by mitosis. As cell division proceeds and the follicle grows, it begins to produce estrogen.

Estrogen has several effects. It causes the inner lining of the uterus to thicken and develop many blood vessels, making it suitable for implantation of an embryo, should one happen along. Estrogen at relatively high levels also stimulates a burst of LH and FSH by the anterior pituitary. Finally, estrogen contributes to female characteristics such as breast development, distribution of body fat, and a hip structure appropriate for childbirth.

The burst of LH and FSH decribed in the preceeding paragraph drives a burst of cell division in the developing follicle. The follicle ruptures, releasing what is now a secondary oocyte that has completed Meiosis I. This is ovulation. Some of the follicle cells remain in the ovary to become the "corpus luteum", which continues to make estrogen and now also progesterone.

If the secondary oocyte is not fertilized after ovulation, it eventually dies, the corpus luteum in the ovary degenerates, and the thickened wall of the uterus sloughs off with some accompanying bleeding. The cycle will repeat in the next month.

If the secondary oocyte is fertilized, a different train of events follows. The nucleus of the secondary oocyte proceeds through Meiosis II and the resulting egg nucleus fuses with the nucleus of the fertilizing sperm. The now diploid zygote will initiate cell division by mitosis in 30 hours. It will also produce a chemical signal called Human Chorionic Gonadotropin (HCG) that is received by the corpus luteum and prevents its degeneration. (Early pregnancy test kits are very sensitive tests for HCG). The corpus luteum, and later the placenta of the developing fetus, will produce low levels of estrogen and progesterone throughout pregnancy.

The low levels of estrogen and progesterone produced by the corpus luteum and later by the placenta during pregnancy have the opposite effect of the high estrogen levels produced by the developing follicle close to ovulation. They inhibit monthly LH and FSH release by the anterior pituitary gland in the brain. This prevents additional ovulations from occurring during pregnancy. Fertilization of subsequent eggs during the months after a pregnancy has begun would be catastrophic for embryos and mother alike.

Figure 28.15 of your text provides further explanation of hormone cycles and ovulation in the human female



b. Female contraception

A variety of methods for female contraception have been developed. One of the most widely used and effective methods is the oral contraceptive pill, which manipulates the hormonal controls of ovulation. Hormonal contraceptives of this type are safe and effective. They contain synthetic estrogen and progesterone that suppress LH and FSH release from the anterior pituitary, just as estrogen and progesterone produced by the corpus luteum and placenta do during pregnancy. Hormonal birth control thus prevents ovulation by simulating pregnancy.

Hormonal birth control of this type was developed in the 1960s. The early formulations contained relatively high doses of hormones and were linked to strokes, blood clots, and other cardiovascular problems in a very few women. Modern formulations contain lower doses and have not been linked to any side effects. In fact, users of hormonal birth control show a significantly lower incidence of uterine and ovarian cancers.

A related topic is hormone replacement therapy after menopause. At this stage of a woman's life, the relatively few remaining primary oocytes lose their responsiveness to FSH and LH. Lack of regular follicle development leads to low estrogen levels and various symptoms related to low estrogen. This transition can be eased with hormone formulations similar to those used for birth control. It is now evident, however, that such hormone replacement increases the incidence of breast cancer over time (though it also reduces the risk of cardiovascular disease)

How can estrogen and progesterone reduce cancer risk in premenopasual women while promoting it in women after menopause? The present hypothesis is that any stimulation of cell division in a tissue increases the risk of cancer. Mutations to oncogenes or tumor suppressor genes can occur during the DNA replication phase of the cell division cycle. Faster cell division in tumors also works against the immune response to cancers. In premenopausal women, hormonal birth control decreases cell divisions in the ovary by preventing follicle development and in the uterus by reducing thickening of the inner lining that occurs with the menstrual cycle. In postmenopausal women, hormone replacement maintains cell division in breast tissue above the levels that it would normally exhibit. Thus, the influence of estrogen and progesterone on cancer risk is the result of their effect on cell division in different parts of the body at different times of life.