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Chapter 20
20.2 and 20.3 only
Biology
Sixth Edition
Raven/Johnson
(c) The McGraw-Hill Companies, Inc.
Mutations are rare (a
particular gene typically
mutates in about 1 in a million
gametes) but important.
One method of evolution.
More important (in terms of
evolution) in germ-line cells
than in somatic cells. Why?
Mutation in the bithorax – a gene
important in a critical stage of
development.
Change in the content of a genetic message
I love Biology 155 so much, I wish I could take it again.
Point mutation
I live Biology 155 so much, I wish I could take it again.
I take Biology 155 so much, I wish I could love it again.
Genetic Recombination
Genetic recombination – alters gene location and
can occur by gene transfer or reciprocal
recombination
DNA Alteration by Mutation
• Base substitution – Spontaneous pairing errors
• Chemical modification – a base is chemically altered by
a mutagenic chemical
• DNA breaks – Ionization radiation can cause double
strand breaks in DNA
• Slipped mispairing – frameshift mutation
• Triplet expansion – 3-base sequence repeated several
times
Changes in gene position:
Chromosomal rearrangements
-translocations
-inversions
Insertional inactivation
-transposons
Cancer is unregulated cell
growth and results in a
tumor – caused by
damaged genes.
Cells that leave a tumor
and form new tumors at
distant sites are called
metastses.
Sarcoma – tumors arising from connective tissue, bone,
or muscle.
Carcinoma – tumors arising from epithelial tissue such
as skin.
Mutagen (mutagenic) – an agent responsible for causing
a mutation in DNA.
Carcinogen (carcinogenesis theory) – an agent thought
to cause cancer.
The more colonies – the more
potent the carcinogen
- Has enzymes that can convert
carcinogens to mutagens
Cancer Alley??
Many cancers can be
avoided just by altering
our behavior!
Some Tumors are Caused by Chemicals
- and many of these chemicals are common (see
table 20.3): Benzene, diesel exhaust, mineral oils,
pesticides, cigarette smoke!
Mutations in proto-oncogenes genes
Proto-oncogenes are responsible for initiating
cell division when the correct external signal is
received (‘Simon says’).
When they mutate to oncogenes, they initiate cell
division without receiving external signals. Thus,
this cell continues to divide without regulation
(doesn’t wait for ‘Simon says’).
Mutations in tumor-suppressor genes
Tumor-suppressor genes are responsible for
blocking cell division (‘Simon didn’t say’).
When they mutate to, they are no longer able to
block cell division. Thus, this cell continues to
divide without regulation (doesn’t wait for ‘Simon
says’).
Mutations in tumor-suppressor genes
Phosphorylation
of Rb releases
E2F and
stimulates cells
division
p16 binds with
Cdk, blocking
cyclins, so E2F
is never
released,
reinforcing the
G1 checkpoint.
Damage to p53 stops
this process.
It usually takes about
four mutations within
a cell to initiate
cancerous growth.
That is why cancer is
more prevalent among
the elderly.
Exposure to
carcinogens can
greatly speed this
process!
1) Receiving the signal to divide. 2) Relay switch.
3) Amplifying the signal. 4) Releasing the brake. 5) Checking
that everything is ready. 6) Telomerase
Also - Preventing Angiogenesis and Metastasis
The End.
Plasmid –
extrachromosomal
DNA segments
Conjugation
When chickens are infected with this virus, the src
viral gene doesn’t need the chicken promoters to
initiate cell division.