Transcript 4.16.08 105 lecture

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EXAM II
Transcription and Translation
Regulation of Gene Expression
"Molecular" Genetics
"Classical" Genetics
DNA Replication
Genomics and Proteomics
EXAM III
Molecular Development
Molecular Development
Chapters 8-12, parts of 2, 3
Chapters 4, 15
Chapter 18
Chapter 16
Chapter 13
Chapter 14
Chapter 20
Chapters 4,13-16,18
Chapter 22
Cumulative Final Exam: Wednesday, May 7th, 10:45-12:45, room 303 Payson-Smith
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3/31
4/2
4/7
4/9
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4/14
4/16
4/21
4/23
4/28
4/30
EXAM II
Transcription and Translation
Regulation of Gene Expression
Molecular Genetics
"Classical" (Transmission) Genetics
DNA Replication
Genomics and Proteomics
EXAM III
Molecular Development
Molecular Development
Chapters 8-12, parts of 2, 3
Chapters 4, 15
Chapter 18
Chapter 16
Chapter 13
Chapter 14
Chapter 20
Chapters 4,13-16,18
Chapter 22
From your Mr. Spock handout:
You inherited one copy of each of your genes from your mom and one from your dad. The genes from
your mom and dad are similar but not identical. For example, you inherited two copies of the LDL
receptor gene. They may be identical but there is a very good chance that some of the nucleotide letters
are different between the two genes. Each version is called an allele. In a population of
organisms of the same species, there can be a variety of versions of each gene.
More from your Mr. Spock handout:
Different alleles of the LDL receptor gene can have differences in their coding region that lead to
differences in their primary amino acid sequence that lead to differences in their structure that lead to
differences in their function. The differences don’t change the basic function of the LDL receptor
but, for example, one allele might code for a receptor that is somewhat damaged and only works half
as well as the protein coded from a different allele. Wild-type is what we call the allele that has
The typical or “average” activity level for the gene. We could say wild-type is fully functional and
equivalent to 100% activity.
More from your Mr. Spock handout:
Any change in the DNA sequence within the gene is a mutation and produces a new allele and
a mutant genotype and that could affect the phenoptype. If the mutant allele causes a decrease in
gene function it is said to be a loss of function allele. Maybe the allele only works 50% as well as
wild-type, or maybe only 15%, or maybe it doesn’t work at all (0% this complete loss of function
is given a special name, a null allele). If the allele causes an increase above wild-type it is said to
be a gain of function allele.
More from your Mr. Spock handout:
Mutant alleles are fairly easy to understand when the mutation affects the coding region because
then an altered version of the protein get made. Mutations in the promoter can be more complex to
understand because they change where, when, or how much of the gene gets made. Consequently
they can have some very weird effects, like a fruit fly with an eye growing in the middle of its
wing, for example.
Mutations that occur in Nature are spontaneous and random. Scientists can design altered versions of
Genes in a test tube to create new alleles.
homozygous
heterozygous
These terms refer to the relationship
between heterozygous alleles:
Dominant
Recessive
Incomplete dominance
Codominance
Mendel’s Law of Segregation:
Punnet square
Mendel’s Law of Independent Assortment:
Some genes are “linked” because
they are on the same chromosome.
Crossing over (recombination) occurs randomly during meiosis I.
homozygous
heterozygous
These terms refer to the relationship
between heterozygous alleles:
Dominant
Recessive
Incomplete dominance
Codominance