Download Ch 7 Genetic Variety

GENETIC VARIATION
& CELL DEATH
FUN FACT

Mitosis usually occurs within 1-2 hours
MALE (testis)

Meiosis takes 1 month (Prophase1 = 1 week)
FEMALE (ovaries)

Meiosis takes decades (Prophase1 = before female
is born)
GENETIC
MIXING
*Only in Meiosis
1. CROSSING OVER
During Synapsis (during Prophase1 to
Metaphase1)
 4 chromosomes form a tetrad
 Genetic material is exchanged by “non-sister”
chromatid on homologous chromosomes

2. INDEPENDENT ASSORTMENT
It is random how the homologs split up in
Anaphase1
 Can be different at every Meiosis
 More chromosomes = greater genetic variety

Ex. Humans (23 chromosomes)
223 = 8,388,608 different combinations of
maternal and paternal DNA
3. MUTATIONS
A. Nondisjunction

Homologous chromosomes don’t separate (disjoin) during
Anaphase1 or pairs don’t separate in Anaphase2
Aneuploidy- organism with extra or missing chromosome


10-30% zygotes show aneuploidy, but most don’t develop
into fetus
Chromosome #21 Trisomy = Down Syndrome
HUMAN NONDISJUNCTION CAUSING ANEUPLOIDY
Ex. Homologs of Chromosme#21 don’t separate
MEIOSIS: oogenesis
#21
#21
No
#21
#21
#21
24 chromosomes
(1 extra)
No
#21
Fertilization
22 chromosomes
(1 less)
Down
Syndrome
#21
#21
#21
Egg
Sperm
#21
#21
#21
Zygote has
Trisomy of
Chromosome #21
OR
MEIOSIS: oogenesis
#21
#21
#21
#21
24 chromosomes
(1 extra)
No
#21
No
#21
22 chromosomes
(1 less)
Fertilization
No
#21
#21
Egg
Sperm
#21
Zygote has
Monosomy of
Chromosome #21
B. Polyploidy: many chromosome sets
Most living are diploid (2n, animals) or haploid (1n, fungi)
 Sometimes Triploid (3n) or Tetraploid (4n) occurs


Caused by extra round of DNA replication or if spindle doesn’t
form
*Can create new species
 Triploid can’t do meiosis, but even sets, like Tetraploid
can do meiosis

C. Translocation- Crossing Over occurs with
NON-homologous pairs
 Common
 Loci (gene location) is important so
Translocation can greatly change genetics
Ex. Translocation of
Chromosome #9 (gene abl)
& #22 (gene bcr) = form of
Leukemia, white blood cell
cancer
END OF CELL CYCLE:
CELL DEATH
PROGRAMMED CELL DEATH
1.
Necrosis- cells are damaged
mechanically, by toxins, or lack of
oxygen/nutrients
Swell and burst
Release their contents into extracellular space
Causes inflammation




Ex. Diabetes or Frostbite
Tissue Necrosis *if you
get grossed out easily,
do not look*
2. Apoptosis- planned cell suicide
Because cell type is no longer needed (webbed
connective tissue between human fetal fingers)
2. Cell is old (prone to genetic problems like
cancer)
1.
Cell detaches from neighbors & hydrolyzes DNA into small
“blebs”
Cell remains are digested by other cells’ phagocytosis (by
lysosomes)


Controlled by Signal Transduction pathways


Activates Caspase (enzymes) hydrolyzes cell
TUMOR
PROTEINS
1. ONCOGENE
Positive Regulator- makes cell division
 Proteins that became mutated or overactive
 Cause cancer cells to divide more

Ex. “HER2” (Growth cancer receptor in Breast
Cancer Cells)

Excess HER2 in 25% of Breast Cancer tumors
2. TUMOR SUPRESSORS
Negative Regulator- stops cell division
 Inactive in Cancer cells

Ex. Retinoblastoma (RB protein)- stops G1 from
continuing into cell cycle.

HPV (human papoloma virus) makes protein E7
E7 fits perfectly into RB protein and inactivates it from working
 Causes Cervical Cancer
