Gametogenesis and Fertilization

Oogenesis Primary Oogenesis: formation of the primary oocyte in the ovary Occurs during embryological development Oogonia (sex cells) divide and undergo meiosis until prophase I  primary oocyte stop and are quiescent (silent) and housed in protective cells called the follicle

At puberty, FSH stimulates the follicle to reinitiate meiosis (FSH = Follicle Stimulating Hormone) Cell divides unequally giving one cell a greater amount of cytoplasm than the other Larger cell  secondary oocyte Smaller cell  polar body  dies Secondary Oocyte proceeds until it reaches Metaphase II Remains in this stage until it is fertilized When fertilized it rapidly undergoes the second division removing a second polar body and forming a haploid nucleus for fusion with the sperm nucleus

Primary germ cell in embryo Ovary Primary germ cell in embryo Differentiation Oogonium in ovary Mitotic division Primary oocyte, arrested in prophase of meiosis I (present at birth) Completion of meiosis I and onset of meiosis II Primary oocyte within follicle Secondary oocyte, arrested at meta- phase of meiosis II First polar body Ovulation Entry of sperm triggers completion of meiosis II Ovum Growing Mature follicle Ruptured Ovulated secondary oocyte Corpus luteum Degenerating corpus luteum 2n n Figure 46.11

Menstrual and Ovarian Cycles – balance of hormonal regulation 1. Release of GnRH (gonadotropin releasing hormone) from the hypothalamus 2. stimulate the release of FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone) from the anterior pituitary 3. FSH – causes the development of an egg cell in a follicle

Figure 45.7 Hypothalamus Neurosecretory cells of the hypothalamus Axon Anterior pituitary Posterior HORMONE ADH Oxytocin TARGET Kidney tubules Mammary glands, uterine muscles

Figure 45.8 Tropic Effects Only FSH, follicle-stimulating hormone LH, luteinizing hormone TSH, thyroid-stimulating hormone ACTH, adrenocorticotropic hormone Nontropic Effects Only Prolactin MSH, melanocyte-stimulating hormone Endorphin Nontropic and Tropic Effects Growth hormone Neurosecretory cells of the hypothalamus Portal vessels Endocrine cells of the anterior pituitary Hypothalamic releasing hormones (red dots) HORMONE FSH and LH TSH ACTH MSH TARGET Testes or ovaries Thyroid Adrenal cortex Mammary glands Melanocytes Pain receptors in the brain Liver Bones Pituitary hormones (blue dots) Figure 45.8

4. Developing follicle releases estrogen Estrogen causes the lining of the uterus (endometrium) to thicken and become highly vascularized – prepping for implantation of embryo

Increased levels of estrogens cause the amount of FSH and LH to eventually spike (initially inhibited until levels of estrogens are high) – positive feedback – LH causes for more estrogen to be released

Control by hypothalamus Uterine (menstrual) cycle Figure 46.13a–e Control by hypothalamus Inhibited by combination of estrogen and progesterone Stimulated by high levels of estrogen Inhibited by low levels of estrogen Hypothalamus Anterior pituitary GnRH FSH LH Pituitary gonadotropins in blood FSH and LH stimulate follicle to grow LH surge triggers ovulation Ovarian cycle Growing follicle Mature follicle Corpus luteum Degenerating corpus luteum Estrogen secreted by growing follicle in increasing amounts Progesterone and estrogen secreted by corpus luteum Follicular phase Luteal phase Ovulation Ovarian hormones Peak causes LH surge Estrogen Progesterone Estrogen level very low Progesterone and estro- gen promote thickening of endometrium Uterine (menstrual) cycle Endometrium Menstrual flow phase Proliferative phase Secretory phase 5 10 14 15 20 25 28 Days 1 (a) (b) (c) (d) (e) 3 6 7 8 4 2 9

5. High levels of LH cause the follicle to mature and burst and the secondary oocyte ruptures from the ovary (ovulation) for possible fertilization in the fallopian tube

Figure 46.13a–e Control by hypothalamus Inhibited by combination of estrogen and progesterone Stimulated by high levels of estrogen Inhibited by low levels of estrogen Hypothalamus Anterior pituitary GnRH FSH LH Pituitary gonadotropins in blood FSH and LH stimulate follicle to grow LH surge triggers ovulation Ovarian cycle Growing follicle Mature follicle Corpus luteum Degenerating corpus luteum Estrogen secreted by growing follicle in increasing amounts Progesterone and estrogen secreted by corpus luteum Follicular phase Luteal phase Ovulation Ovarian hormones Peak causes LH surge Estrogen Progesterone Estrogen level very low Progesterone and estro- gen promote thickening of endometrium Uterine (menstrual) cycle Endometrium Menstrual flow phase Proliferative phase Secretory phase 5 10 14 15 20 25 28 Days 1 (a) (b) (c) (d) (e) 3 6 7 8 4 2 9

6. LH then causes the follicle tissue to thicken and form the corpus luteum Corpus luteum releases progesterone and estrogen Shut down secretion of FSH and LH – negative feedback

Figure 46.13a–e Control by hypothalamus Inhibited by combination of estrogen and progesterone Stimulated by high levels of estrogen Inhibited by low levels of estrogen Hypothalamus Anterior pituitary GnRH FSH LH Pituitary gonadotropins in blood FSH and LH stimulate follicle to grow LH surge triggers ovulation Ovarian cycle Growing follicle Mature follicle Corpus luteum Degenerating corpus luteum Estrogen secreted by growing follicle in increasing amounts Progesterone and estrogen secreted by corpus luteum Follicular phase Luteal phase Ovulation Ovarian hormones Peak causes LH surge Estrogen Progesterone Estrogen level very low Progesterone and estro- gen promote thickening of endometrium Uterine (menstrual) cycle Endometrium Menstrual flow phase Proliferative phase Secretory phase 5 10 14 15 20 25 28 Days 1 (a) (b) (c) (d) (e) 3 6 7 8 4 2 9

7. degeneration of corpus luteum causes the levels of estrogen and progesterone to fall and results in the shedding of the thickened endometrium (menstruation) allows for renewed secretion of FSH and LH to allow a new follicle to form

Control by hypothalamus Uterine (menstrual) cycle Figure 46.13a–e Control by hypothalamus Inhibited by combination of estrogen and progesterone Stimulated by high levels of estrogen Inhibited by low levels of estrogen Hypothalamus Anterior pituitary GnRH FSH LH Pituitary gonadotropins in blood FSH and LH stimulate follicle to grow LH surge triggers ovulation Ovarian cycle Growing follicle Mature follicle Corpus luteum Degenerating corpus luteum Estrogen secreted by growing follicle in increasing amounts Progesterone and estrogen secreted by corpus luteum Follicular phase Luteal phase Ovulation Ovarian hormones Peak causes LH surge Estrogen Progesterone Estrogen level very low Progesterone and estro- gen promote thickening of endometrium Uterine (menstrual) cycle Endometrium Menstrual flow phase Proliferative phase Secretory phase 5 10 14 15 20 25 28 Days 1 (a) (b) (c) (d) (e) 3 6 7 8 4 2 9

Effects of Pregnancy Embryo implants in endometrium and secretes human chorionic gonadotropin – simulates release of progesterone and estrogen from the corpus luteum to maintain the endometrium and prevents menstruation Embryo is at first nourished by the endometrium, but then tissue grows out of the embryo and intermingles with the endometrium to form the placenta

Menopause Cessation of ovulation and menstruation Ovaries lose responsiveness to FSH and LH

Gametogenesis in Males – Page 975 GnRH causes release of FSH and LH LH causes the release of testosterone from the Leydig cells which causes spermatogenesis (meiosis) FSH stimulates Sertoli cells which produce nutrients for developing sperm in the seminiferous tubules of the testicles

Secondary spermatocyte Epididymis Seminiferous tubule Testis Cross section of seminiferous tubule 2n Spermatogonium Mitotic division, producing large numbers of spermatogonia Sertoli cell nucleus Differentiation and onset of meiosis I 2n Primary spermatocyte (in prophase of meiosis I) Meiosis I completed n n Secondary spermatocyte Meiosis II Lumen of Seminiferous tubule n n n n Early spermatids Spermatids (at two stages of differentiation) Differentiation (Sertoli cells provide nutrients) n n n Sperm cells n Neck Head Midpiece Tail Plasma membrane Mitochondria Nucleus Figure 46.12 Acrosome

Figure 46.14 Stimuli from other areas in the brain Hypothalamus GnRH from the hypothalamus reg- ulates FSH and LH release from the anterior pituitary. FSH acts on the Sertoli cells of the seminiferous tubules, promoting spermatogenesis. LH stimulates the Leydig cells to make testosterone, which in turn stimulates sperm production. Anterior pituitary Negative feedback Leydig cells make testosterone Primary and secondary sex characteristics Sertoli cells Spermatogenesis Testis Figure 46.14

Sperm anatomy Head – - acrosome - Contains digestive enzymes - actin – forms acrosomal process - nucleus – haploid DNA Collar – filled with mitochondria Tail - flagellum

Fertilization Process Sperm hit outer layer (jelly coat) of the egg cell and releases digestive enzymes that start to digest the outer layer away Actin filaments grow forming the acrosomal process Actin filaments fuse with the surface proteins of the egg – this ensures the correct type of sperm (species) is fertilizing the egg Sperm membrane unites with the membrane of the egg cell

Figure 47.3 Sperm nucleus Sperm plasma membrane Hydrolytic enzymes Cortical granule Cortical granule EGG CYTOPLASM Basal body (centriole) head Acrosomal process Actin Acrosome Jelly coat Egg plasma Vitelline layer Fused plasma membranes Perivitelline space Fertilization envelope Cortical reaction. Fusion of the gamete membranes triggers an increase of Ca2+ in the egg’s cytosol, causing cortical granules in the egg to fuse with the plasma membrane and discharge their contents. This leads to swelling of the perivitelline space, hardening of the vitelline layer, and clipping of sperm-binding receptors. The resulting fertilization envelope is the slow block to polyspermy. 5 Contact and fusion of sperm and egg membranes. A hole is made in the vitelline layer, allowing contact and fusion of the gamete plasma membranes. The membrane becomes depolarized, resulting in the fast block to polyspermy. 3 Acrosomal reaction. Hydrolytic enzymes released from the acrosome make a hole in the jelly coat, while growing actin filaments form the acrosomal process. This structure protrudes from the sperm head and penetrates the jelly coat, binding to receptors in the egg cell membrane that extend through the vitelline layer. 2 Contact. The sperm cell contacts the egg’s jelly coat, triggering exocytosis from the sperm’s acrosome. 1 Sperm-binding receptors Entry of sperm nucleus. 4 Figure 47.3

Fusion of the gamete membranes causes the egg cell to depolarize by the release of Ca2+ Depolarization initiates the release of cortical granules = Cortical Reaction – this causes the membrane of the egg to change preventing other sperm from fertilizing the egg. This also activates the egg cell and the second phase of meiosis is completed

Figure 47.3 Sperm nucleus Sperm plasma membrane Hydrolytic enzymes Cortical granule Cortical granule EGG CYTOPLASM Basal body (centriole) head Acrosomal process Actin Acrosome Jelly coat Egg plasma Vitelline layer Fused plasma membranes Perivitelline space Fertilization envelope Cortical reaction. Fusion of the gamete membranes triggers an increase of Ca2+ in the egg’s cytosol, causing cortical granules in the egg to fuse with the plasma membrane and discharge their contents. This leads to swelling of the perivitelline space, hardening of the vitelline layer, and clipping of sperm-binding receptors. The resulting fertilization envelope is the slow block to polyspermy. 5 Contact and fusion of sperm and egg membranes. A hole is made in the vitelline layer, allowing contact and fusion of the gamete plasma membranes. The membrane becomes depolarized, resulting in the fast block to polyspermy. 3 Acrosomal reaction. Hydrolytic enzymes released from the acrosome make a hole in the jelly coat, while growing actin filaments form the acrosomal process. This structure protrudes from the sperm head and penetrates the jelly coat, binding to receptors in the egg cell membrane that extend through the vitelline layer. 2 Contact. The sperm cell contacts the egg’s jelly coat, triggering exocytosis from the sperm’s acrosome. 1 Sperm-binding receptors Entry of sperm nucleus. 4 Figure 47.3

Basic Development - Zygote - Cleavage: cell division - Blastula: Hollow ball of cells

Gastrulation: infolding of ball (deflated ball) - forms gastrula - point of infolding = blastopore infolding results in tissue layers Video Ectoderm: outer layer Endoderm: inner layer Archenteron: space formed by the infolding of gastrula – becomes the digestive tract

Blastula, Gastrulation, Gastrula