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Chapter 10 – Cell Division
A. Introduction
a. Types of cell division (Fig 11.2)
i. Mitosis (2n2n) for asexual reproduction, growth, development, repair
ii. Meiosis (2nn) for creating gametes for sex
b. Chromosomes
i. DNA is held in chromosomes. Chromosomes are made from chromatin (DNA +
protein).
ii. Chromosomes condense and decondense throughout cell division. (Fig 10.5)
iii. Chromosome vocab: Homologs, sister chromatids, centromere, kinetochore,
telomere. (Fig 10.7)
c. The Mitotic Cell Cycle: G1  S  G2  M. DNA is replicated in S and separated in M.
(Fig 10.8)
B. Mitosis (The Cell Cycle) (Fig 10.11)
a. Interphase: DNA and centrioles (animals) duplicate.
b. Prophase: chromosomes condense, centrosomes form (centrioles migrate to poles),
nuclear components disappear, spindles appear and attach, chromosomes move to center
of cell.
c. Metaphase: Chromosomes line up on equatorial plane (metaphase plate)
d. Anaphase: Sister chromatids move apart. Mechanism of motor protein movement and
disassembly of microtubule at centromere end.
e. Telophase: Chromatids arrive at new pole, spindles detach and disassemble, nuclear
components appear, chromosomes decondense.
f. Cytokinesis: Cytoplasmic division. Cleavage furrow or cell plate appears. (Fig 10.14)
C. Cell cycle control
a. Checkpoints regulate progression to next step of cell cycle
b. Evidence that cytoplasmic factors act as regulators (Fig 10.16)
c. MPF (mitosis promoting factor)
i. Signal transduction pathways allow proceeding to next phase.
ii. MPF is CDK + cyclin. Is a kinase. Levels of CDK same, but activity cycles
because of partnership with cyclin (Fig 10.17)
iii. Kinase activity leads to events like nuclear breakdown, chromosome
condensation, spindle formation.
d. Anaphase promoting complex (APC) breaks down metaphase cyclins only when all
kinetochores are attached. Then anaphase can proceed.
e. External signals: growth factors trigger signal transduction leading to division. (Fig
10.22)
D. Cancer
a. Features
i. Over-proliferation – unregulated cell division
1. A cell division checkpoint can be defective
2. A growth factor can overstimulate division.
ii. Invasive – break through tissue barriers
iii. Angiogenesis – formation of blood vessels to feed the tumor
iv. Lose anchorage dependence
v. Lose contact inhibition
vi. No response to apoptosis signals
vii. Metastasis – invasion by secondary tumors
b. Genes in cancer
i. Oncogenes – cause cancer when overstimulated
1. Come from proto-oncogenes (normal form)
2. E.g. ras in growth stimulating pathway
a. 30% of cancers have ras mutation.
b. Is a G protein. Mutations cause overstimulation (even without
Tyr-kinase activation)
ii. Tumor-suppressor genes – cause cancer when understimulated/expressed (Fig
10.24)
1. Normally block proliferation, or other features of cancer
2. E.g. p53 in growth-inhibition pathway
a. 50% of cancers have p53 mutation
b. Is a txn factor for p21 that blocks cyclins
c. Turns on DNA repair genes.
d. Activates death signals for apoptosis
3. E.g. BRCA is involved in DNA repair.
a. If one allele mutated, woman has 60% chance of getting breast
cancer.
iii. Multiple mutations and development of cancer: e.g. Colorectal cancer
c. Treatments
i. Traditional treatments are nonspecific and harm normal cells
1. Chemotherapy are drugs that block cell division
2. Radiation therapy can cause other cancers.
ii. New targeted drugs
1. Success in Gleevec which help leukemia. Drug that specifically blocks
ATP binding site of Abl, a tyrosine kinase.
2. Gene therapy: introduce a functional tumor suppressor gene.
Chapter 11 – Meiosis
A. Overview
a. Gametes are haploid (one set of chromosomes), zygote is diploid (two sets) (Fig 11.1)
b. Sexual life cycle (Fig 11.2)
c. Comparison of mitosis and meiosis (Fig 11.7)
i. In mitosis, sister chromatids separate. Final cell is 2n.
ii. In meiosis, homologs separate then sisters separate. DNA exchanges by crossingover, and random mixing of chromosomes in gamete to produce variation. Final
cell is 1n.
d. Stages (Fig 11.6)
i. Interphase  meiosis I (homologs separate)  meiosis II (sisters separate)
ii. Prophase I – homologs pair up (synapses) and crossing over. Chiasmata are sites
of crossing-over (Fig 11.3).
iii. Metaphase I – homologs line up to separate (Fig 11.4)
iv. Metaphase II – sisters line up to separate.
e. Variation
i. Independent assortment of chromosomes: 223 = 8 million
ii. Random fertilization: 223 x 223 = 64 trillion
iii. Crossover (recombination): 2-3 crossovers/chromosome.
Chapter 12 – Mendelian Genetics
A. Gregor Mendel
a. Experiments with peas
i. Mendel crossed peas by pollinating pistils. (Fig 12.3)
ii. Traits that he used (Fig 12.4)
iii. Crosses were done in generations (P, F1, F2 etc) (Fig 12.5)
b. Mendel’s conclusions and some vocabulary
i. Gene (location of trait/alleles) and alleles (form of the gene)
ii. Dominant (masking trait/allele) vs. recessive (masked trait/allele)
iii. Homozygous (same alleles) vs. heterozygous (different alleles)
iv. Phenotype (trait) vs. genotype (genetic make up)
c. Mendel’s Laws
i. Law of Segregation – each allele will separate independently
ii. Law of Independent assortment – each gene will segregate alleles independently
of other genes.
B. Mendelian Inheritance
a. Punnett Squares are tools for calculating probability of crosses
i. Each parent produces gametes that randomly contain one of the alleles for each
gene. This is like a coin flip (Fig 12.6)
ii. Each gamete possibility is placed on the side and top of the table and possible
progeny are placed in squares of table.
iii. Genotypic ratios give you possible genotypes.
iv. Phenotypic ratios give you possible phenotypes.
b. Single Trait Crosses
i. Monohybrid cross – a cross between two heterozygotes. E.g. Aa X Aa
ii. Test cross – cross a dominant with unknown genotype to the recessive to figure
out genotype. If all offspring are dominant, then original parent was
homozygous. If half of the offspring are dominant, then original parent was
heterozygous. (Fig 12.10)
c. Two trait crosses
i. AABB X aabb. Each gamete must have an A allele and a B allele. E.g. gametes
from above cross are AB and ab.
ii. Dihybrid cross – a cross between two heterozygotes for two genes. AaBb X
AaBb (Fig 12.9). Gives you 9:3:3:1 phenotypic ratio.
iii. Test cross – cross to the double recessive and expect to find a 1:1:1:1 phenotypic
and genotypic ratio.
d. Use probability – multiply out chance of each gene combination
i. Useful for multiple trait crosses
ii. E.g. in AaBbCc X AaBbCc. Chance of getting AAbbCc is ¼ X ¼ X ½ = 1/32.
e. Pedigree Analysis
i. Dominant and recessive disorders can be determined by analyzing family trees
(Fig 12.7)
ii. “Dominant Pattern”: when parents both have trait but a child does not.
iii. “Recessive Pattern”: when parents both do not have trait but a child does.
C. Non-Mendelian traits
a. Incomplete dominance – heterozygous has a new trait (pink flowers) (Fig 12.12)
b. Multiple alleles – more than two e.g. blood typing: use IA, IB, I (Fig 12.13)
c. Polygenic inheritance – multiple genes controlling one trait. E.g. skin color (Fig 12.11)
d. Pleiotropy – one gene controls gives more than one trait. e.g Tay-Sachs Disease, frizzle
chickens
e. Epistasis - one gene controls expression of another trait. E.g. one gene controls color,
other determines pigment deposition. A dihybrid cross gives you a 9:3:4 phenotypic ratio
(Fig 12.15)
f. Environment
i. May cause change in phenotype. E.g. hydrangea is pink in high pH and purple in
low pH.
ii. Gene expression can be influence by environment. E.g. methylation shuts down
embryonic genes.