rep
REPRODUCTION
DIPLOID- autosomal cells, 2n: have 2 copies of each chromosome
GERM- cells that are haploid (n), only 1 copy of each chromosome
THE CELL CYCLE
CONTROLS OF THE CELL CYCLE:
Cell cycle controlled by cyclins and cyclin dependent kinases(CDK)
CDKs must have the right cyclins in order to be activated
When activated the CDKs are active during the cell cycle and increase/ decrease at certain stages
The cyclins bind to the CDK: CDK-cyclin complex which can phosphorylate transcription factors
Transcription factors promote transcription of genes required for the next stage in the cell cycle
P53 protein also serves as a checkpoint at the G1/S and S/G2 phase to make sure there are no defects in the replicated DNA
WHEN CELL CYCLE DAMAGED:
Cancer occur because damaged cells are allowed to undergo MITOSIS
Common mutation is when p53 gene(TP53) is mutated which allows mutated genes to continue through cell cycle without quality control
Tumors result and metastasis
ACTUAL STAGES:
Interphase: G1,S and G2
Longest part that works to divide cells 90% of the time i
Cells that don't divide spend their entire life in G0 stage- simply living and carrying out functions without any preparation for division
During interphase: individual chromosomes not visible because they are instead in a less condensed form called chromatin
- in a chromatin form because DNA must be available tp RNA polymerase so that genes can be transcribes
G1:Pre Synthetic cap (‘growing’)
Cells create organelles for energy and protein(enzyme) production while also increasing their size.
To get into the S stage: there is a restriction point, which checks for any damaged DNA
** p53 protein plays a key role in quality control.
S stage: synthesis of DNA
Cell replicated DNA using the enzymes made in G1 so each daughter has identical copies
Now each chromosome has identical chromatids bound at the centromere
Ploidy remains the same (2N), but the amount of DNA has doubled.
Now cells entering G2 have 2x as much DNA as cells in G1
p53 protein also serves as a checkpoint
G2: Postsynthetic Gap (more growing)
Grows even more
Anther checkpoint to make sure that
there are enough organelles and cytoplasm for 2 daughter cells
DNA replication was done correctly
M stage: MITOSIS
2 identical daughter cells created from a single cell in somatic tissue
4 phases:(PMAT + cytokinesis)
Prophase
Chromatin condenses into chromosomes.
Nuclear membrane dissolves.
Centrioles migrate to opposite poles and form the mitotic spindle.
Kinetochores( protein structures that attach chromosomes to spindle fibers) appear at the centromere.
Metaphase
Chromosomes align at the metaphase plate (equatorial plane).
Spindle fibers attach to kinetochores.
Anaphase
Sister chromatids separate and are pulled toward opposite poles by spindle fibers.
Telophase
Nuclear membranes reform, chromosomes decondense back into chromatin.
Spindle apparatus dissolves.
Cytokinesis
Cytoplasm and organelles divide, forming two genetically identical daughter cells.
MEIOSIS
Unlike mitosis: it occurs in gametophytes: germ cells resulting in 4 identical gametes(sex cell)
1. Meiosis I ("Reductional Division")
Homologous chromosomes separate, reducing chromosome number from diploid (2N) → haploid (N).
Genetic recombination occurs, increasing genetic diversity.
Prophase I
Chromatin condenses into chromosomes.
Nuclear membrane dissolves.
Homologous chromosomes pair up in a process called synapsis, forming a tetrad (4 chromatids total).
Crossing over occurs at the chiasmata, leading to genetic recombination.
Mendel’s Law of Independent Assortment applies.
Metaphase I
Homologous pairs(tetrad) align at the metaphase plate.
Each homolog attaches to spindle fibers from opposite poles (random orientation).
Anaphase I
Homologous chromosomes separate and are pulled to opposite poles.
This is called disjunction, following Mendel’s Law of Segregation.
The paternal chromosome separates from its homologous maternal which results in a random effect of what the daughter cell will have
Sister chromatids remain attached at the centromere.
Telophase I & Cytokinesis
Nuclear membrane reforms around haploid nuclei.
Each daughter cell contains haploid (N) chromosomes, but each still has two sister chromatids.
Interkinesis may occur (a short rest phase before Meiosis II).
2. Meiosis II ("Equational Division")
Similar to mitosis, but results in four haploid (N) daughter cells.
Prophase II
Nuclear envelope dissolves, spindle fibers form.
No crossing over occurs.
Metaphase II
Sister chromatids align at the metaphase plate.
Anaphase II
Sister chromatids separate and are pulled to opposite poles.
Telophase II & Cytokinesis
Nuclear membranes reform around each nucleus.
Cytoplasm divides, forming four haploid gametes.
Key Points & High-Yield Annotations
1. Biological Sex & Determination
Sex is determined by the 23rd chromosome pair.
XX → Female, XY → Male
Mutations of the X chromosome can cause sex linked disorders because the X chromosome carries a sizeable amount of genetic info
Males are hemizygous to X chromosome genes because they only have one copy
Females don't have to express the gene always because they have 2 copies and if they don't express it they are called carriers
Y chromosome contains very little genetic information
One gene that it does carry is the SRY (Sex-determining Region Y) gene on the Y chromosome
This triggers male differentiation by initiating testis formation.
Without SRY, female reproductive structures develop by default.
2. Male Reproductive System
Testes (dual function)
Developed formed gonads-(responsible for sex organ creation) and located in the scrotum- external pouch hanging outside of the penis
- it is positioned this way to allow it to have a temperature 2-4 degrees lower than the body
2 functional components of the testes:
Seminiferous tubules →highly coiled tubes responsible for sperm production, nourished by Sertoli cells
Interstitial cells of Leydig → secrete testosterone & androgens
Sperm Pathway (SEVEN UP):
Seminiferous tubules: produces sperm
Passes on to the->epididymis
Epididymis → sperm gain motility and stored here until ejaculation
Passes on to the->vandeferes
Vas deferens:A coiled tube that carries the sperm out of the testes.
Passes on to the->ejactutalory duct
Ejaculatory duct(2) : at the posterior edge of the prostate gland, fuse to carry out sperm to urethra
Passes on to the->urethra
Nothing (mnemonic filler)
Urethra- carries sperm to exit the body
Penis
As sperm passes through the reproductive tract it is mixed with Seminal fluid production which nourishes sperm
This is done by:
Seminal vesicles → the seminal fluid produces has fructose (energy source for sperm)
Prostate gland → the seminal fluid produced gives sperm alkaline fluid so sperm can survive the acidity of female tract
Bulbourethral (Cowper’s) glands → the seminal fluid is a thick fluid (precum) which lubricates and cleans out urethra from pee
- seminal fluid combines with sperm later to ejaculate semen
3. Spermatogenesis (Sperm Development)
Semen produces in the walls seminiferous tubules
Spermatogonia(2n) is diploid and undergoes mitosis with one going to sperm cell and another going further into the next generation of sperm: overall results in a primary spermatocyte(2n)
Primary spermatocyte (2n) turns into a secondary spermatocyte (n)in meiosis 1
Secondary spermatocyte(n) undergoes meiosis 2 and turns into 4 spermatid(n) cells
The spermatid reaches lumen of the tubule maturing by growing a flagellum making it a spermatozoa (n)
RESULT: 1 cell of 2n spermatogonia-> 4 cells of spermatozoa (n)
Mature Sperm structure:
Very compact
Head → contains acrosome cap- has enzymes to penetrate the ovum
Midpiece → packed with mitochondria (ATP to reach the female reproductive tract)
Tail → flagellum (mobility)
Female Reproductive System
Ovaries(female gonads) → produce ova(eggs), estrogen, progesterone
Located in the pelvic cavity:has a lot of follicles- multilayered sacs that nourish the eggs
Pathway of an egg (monthly cycle): happens between puberty and menopause
Ovary → releases egg during ovulation into the peritoneal sac
Fallopian tube- egg drawn here to fertilize it
The fallopian tube is lined with cilia in order to propel the egg forward into the uterus
Uterus- site of fetal development (implantation or shedding)
Cervix (lower part of the uterus) → Vaginal canal
Oogenesis (Egg Development):
Different from the spermatogenesis because
Supply of eggs is constant and not ever ending
By birth all oogonia have already replicated and are already considered primary oocytes(2n)
Primary oocytes (2n) are stuck in prophase I until first period(menarche)
After menarche, one primary oocyte will complete meiosis 1 producing Secondary oocyte (n)
Fertilization of egg by sperm→ completes meiosis II → ovum (n)
Oocytes surrounded by:
Zona pellucida (glycoproteins, protects oocyte, sperm binding nutrients )
Corona radiata (outer layer, support, adherence to the oocyte during ovulation)
SPERM contributes only ½ of DNA during fertilization while ovum passes almost everythings it has: haploid pronuclei of sperm and ovum jon creating zygote
Hormonal Control of Reproduction
Prior to puberty hypothalamus restricts the products GnRH (Gonadotropin-releasing hormone)
At the start of puberty, thai restriction is lifted:
Hypothalamus releases GnRH (Gonadotropin-releasing hormone) → Stimulates anterior pituitary to synthesize
Follicle Stimulating Hormone & Luteinizing Hormone which drive reproductive processes
In males:
FSH → stimulates Sertoli cells → spermatogenesis
LH → stimulates Leydig cells → testosterone production
In females:
FSH → stimulates follicle development(maturation of single ovum) & estrogen secretion
LH surge → triggers ovulation and corpus luteum formation → secretes progesterone(thickens and nominations the endometrium(thick lining of the uterus))
MALE SEXUAL DEVELOPMENT:
Fetal period: presence of Y chromosome lead to production of androgens resulting in male differentiation
Puberty: testosterone increases and sperm production begins
Done by the FSH (sertoli cells for spermatogenesis) and LH(Leydig cells for testosterone production)
Also results in secondary sexual characteristics such as deep voice and facial hair
FEMALE SEXUAL DEVELOPMENT
FSH stimulates estrogen secretion: grows boobs, widens hips ect
Estrogen:
Embryo: stimulates development of female reproductive tract
In adults: estrogen thicken the uterus lining: endometrium, which prepares body for zygote implantation
Progesterone: in response to the LTH
Thickens and maintenance of the endometrium
Menstrual Cycle Phases (28 Days)
Follicular Phase (Day 1-13)
When menstrual cycle begins
Progesterone and estrogen rates drop which causes GnRH to secrete more of it
FSH stimulates follicle growth → estrogen rises
Estrogen → endometrial thickening
Ovulation (Day 14)
LH surge(peak of estrogen) triggers ovulation
Releases the ovum from ovary to the peritoneal cavity
Luteal Phase (Day 15-28)
Corpus luteum secretes progesterone → maintains endometrium
Progesterone high levels aids negative feedback on GnRH reducing FSH and LH levels and preventing ovulation of multiple eggs
Menstruation (if no fertilization)
Estrogen & progesterone drop → shedding of endometrial lining
7. Pregnancy & Fertilization
Fertilization → zygote → blastocyst → implants in endometrium
hCG (human chorionic gonadotropin) will be secreted in zygote develops
Very similar to LH and can stimulate LH receptors
Maintains corpus luteum to sustain progesterone and estrogen levels in the FIRST TRIMESTER
SECOND TRIMESTER: hGG levels decline because Placenta can take over hormone production of estrogen and progesterone
Birth control pills mimic high estrogen & progesterone → inhibits FSH/LH (no ovulation)
8. Menopause
Ovaries become less sensitive to FSH and LH which results in:
Ovarian atrophy, ↓ estrogen & progesterone: stopping menstruation
FSH & LH increase drastically to try to make up for (loss of negative feedback)
But no response which can contribute to the side effects such as hot flashes