A.
Introduction a.
Types of cell division i.
Mitosis (2n

2n) for asexual reproduction, growth, development, repair ii.
Meiosis (2n  n) for sex b.
DNA is held in chromosomes . Chromosomes are made from chromatin (DNA + protein).
(Fig. 47.2) c.
Chromosome vocab: Homologs , sister chromatids , centromere , kinetochore, telomere . d.
The Mitotic Cell Cycle: G
1

S

G
2

M. DNA is replicated in S and separated in M.
(Fig. 32.3)
B.
Module 32: Mitosis (Fig. 4,5) 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.
C.
Module 33: Cell cycle control a.
Checkpoints regulate progression to next step of cell cycle (Fig. 2) b.
Signal transduction pathways allow proceeding to next phase. i.
E.g. MPF (mitosis promoting factor) is CDK + cyclin. (Fig. 3, 4) ii.
Forms active kinase that promotes mitosis by phosphorylation. This leads to events like nuclear breakdown, chromosome condensation, spindle formation. c.
Internal signals: e.g. Anaphase promoting complex (APC) breaks down metaphase cyclins only when all kinetochores are attached. Then anaphase can proceed. d.
External signals: growth factors trigger signal transduction leading to division.
D.
Module 36: Meiosis a.
Overview i.
Sexual life cycles (Fig. 35.3)
1.
Humans live as diploids and produce haploid gametes.
2.
Some plants and fungi can live as haploids adults. ii.
Comparison of mitosis and meiosis
1.
In mitosis, sister chromatids separate. Final cell is 2n.
2.
In meiosis, homologs separate then sisters separate. DNA exchanges by crossing-over, and random mixing of chromosomes in gamete to produce variation. Final cell is 1n. (Fig. 1) b.
Stages 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. 2). iii.
Metaphase I – homologs line up to separate (Fig. 3) iv.
Metaphase II – sisters line up to separate. (Fig. 8) c.
Variation

i.
Independent assortment of chromosomes: 2
23
= 8 million ii.
Random fertilization: 2
23
x 2
23
= 64 trillion iii.
Crossover (recombination): 2-3 crossovers/chromosome. (Fig. 13)
Lecture 13 – Genetics
A.
Module 37: Gregor Mendel a.
Experiments with peas i.
Traits that he used (Fig. 1) ii.
Mendel crossed peas by pollinating pistils. iii.
Crosses were done in generations (P, F1, F2 etc) (Fig. 3) b.
Mendel’s conclusions and some vocabulary (Fig. 4) 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 (Fig. 5) ii.
Law of Independent assortment – each gene will segregate alleles independently of other genes. (Fig. 6)
B.
Module 38: 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. 2) ii.
Each gamete possibility is placed on the side and top of the table and possible progeny are placed in squares of table. (Fig. 3) iii.
Genotypic ratios give you possible genotypes. iv.
Phenotypic ratios give you possible phenotypes. b.
Single Trait Crosses i.
E.g. BB X bb results in all Bb offspring(Fig. 4) ii.
Monohybrid cross – a cross between two heterozygotes. E.g. Aa X Aa iii.
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. 7) 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. 6) iii.
Test cross – cross to the double recessive and expect to find a 1:1:1:1 phenotypic and genotypic ratio. (Fig. 9) d.
Multiple trait crosses i.
Use probability – multiply out chance of each gene combination ii.
E.g. in AaBbCc X AaBbCc. Chance of getting AAbbCc is ¼ X ¼ X ½ = 1/32.
C.
Module 39: Non-Mendelian traits a.
Incomplete dominance – heterozygous has a new trait (pink flowers) (Fig. 1) b.
Multiple alleles – more than two e.g. blood typing: use I
A
, I
B
, I (Tab. 1) c.
Pleiotrophy – one gene controls gives more than one trait. e.g Tay-Sachs Disease, frizzle chickens (Fig. 3)

d.
Epistasis - one gene controls expression of another trait. E.g. labrador fur genes: B controls color, E determines pigment deposition (9:3:4) (Fig. 5) e.
Polygenic inheritance – multiple genes controlling one trait. E.g. skin color (Fig. 8) 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.
D.
Module 40, 43: Inheritance in Humans a.
Many human traits are Mendelian (Fig. 40.1) i.
Dominant: Huntington’s Disease ii.
Recessive: Sickle-Cell Anemia b.
Pedigree Analysis i.
Dominant and recessive disorders can be determined by analyzing family trees
(Fig. 43.1) ii.
“Dominant Pattern”: when parents both have trait but a child does not. (Fig. 43.2) iii.
“Recessive Pattern”: when parents both do not have trait but a child does. (Fig.
43.3) c.
Karyotype i.
Allows normal chromosome number and form to be analyzed. ii.
Blood cells taken, put on a slide, stained, and seen under a microscope (Fig. 40.6,
40.7) iii.
Down Syndrome can be found this way.
E.
Module 41-42: Chromosomes and Linkage a.
Chromosomal basis of Mendel’s Laws (Fig. 41.2) b.
Sex Linkage i.
Gene is on a sex chromosome ii.
Morgan studied fly eye color which is X-linked (Fig. 41.4)
1.
He found skewed results where traits followed sex
2.
Sex linked (X-linked) crosses (Fig. 42.3, 4) a.
Must use the designation X
N
, X n
, and Y b.
Must keep track of sex chromosome in Punnett Square. iii.
Sex determination in humans depends on presence of Y chromosome (Fig. 42.2).
Other animals use # of X, presence of Y, or ploidy. iv.
Barr bodies – inactivated X chromosome to compensate for dosage.
1.
Phenomenon of calico cats: only heterozygous female for orange and black fur color alleles. Have patches of each color because one X becomes a Barr early in development. Cells derived will maintain Barr.
(Fig. 42.5) c.
Two linked genes i.
If two genes are close together, there is less chance of crossing over between them. Ones that look like the parent are called parental. Ones that cross-over are called recombinants. (Fig. 42.6) ii.
BbVv x bbvv should give 1:1:1:1 ratio. But results give higher parental phenotypes (lower recombinant) = linkage. (Fig. 42.7) iii.
Sturtevant calculates map distance and creates linkage maps
1.
A map unit is the percentage of crossing over.
2.
Map unit = recombinants/total offspring.
3.
Partial genetic map of Dros. chrom 2 (Fig. 42.9)
F.
Module 43: Genetic Disorders a.
Change in ploidy

i.
Mechanism of nondisjunction (Fig. 6)
1.
Leads to some cells that are mono or trisomic for a chromosome.
2.
Down syndrome in trisomy 21
3.
Sex chromosome # changes (XO, XXX, XY, XYY) ii.
Whole set changes. Some plants and animals are triploid, tetraploid etc. b.
Change in chromosome structure i.
Deletion – part of chrom. missing. ii.
Duplication – part of chrom. repeated. Can cause overdosage iii.
Inversion – piece flipped around. can cause wrong expression iv.
Translocation – two pieces swapped. Gene in wrong location may be over or under-expressed (Fig. 7) c.
Imprinting i.
Even on an autosomal chromosome, a gene may be shut off maternally or paternally ii.
Example of Igf2 in mice.
1.
Mother always shuts off copy of Igf2 allele. Only paternal is expressed.
2.
Mechanism is methylation of cytosine by mother.
3.
Same mechanism for Prader-Willi Syndrome in humans (Fig. 5)