M 3/31 EXAM II Chapters 8-12, parts of 2, 3

1. M 3/31 EXAM II Chapters 8-12, parts of 2, 3 • W 4/2 Transcription and Translation Chapters 4, 15 • M 4/7 Regulation of Gene Expression Chapter 18 • W 4/9 "Molecular" Genetics Chapter 16 • M 4/14 "Classical" Genetics Chapter 13 • W 4/16 DNA Replication Chapter 14 • M 4/21 Genomics and Proteomics Chapter 20 • W 4/23 EXAM III Chapters 4,13-16,18 • M 4/28 Molecular Development Chapter 22 • W 4/30 Molecular Development • Cumulative Final Exam: Wednesday, May 7th, 10:45-12:45, room 303 Payson-Smith

2. M 3/31 EXAM II Chapters 8-12, parts of 2, 3 • W 4/2 Transcription and Translation Chapters 4, 15 • M 4/7 Regulation of Gene Expression Chapter 18 • W 4/9 Molecular Genetics Chapter 16 • M 4/14 "Classical" (Transmission) Genetics Chapter 13 • W 4/16 DNA Replication Chapter 14 • M 4/21 Genomics and Proteomics Chapter 20 • W 4/23 EXAM III Chapters 4,13-16,18 • M 4/28 Molecular Development Chapter 22 • W 4/30 Molecular Development

3. 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.

4. 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.

5. 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.

6. 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.

7. homozygous heterozygous These terms refer to the relationship between heterozygous alleles: Dominant Recessive Incomplete dominance Codominance

10. Mendel’s Law of Segregation: Punnet square

12. Mendel’s Law of Independent Assortment:

13. Some genes are “linked” because they are on the same chromosome.

14. Crossing over (recombination) occurs randomly during meiosis I.

15. homozygous heterozygous These terms refer to the relationship between heterozygous alleles: Dominant Recessive Incomplete dominance Codominance