Instructors: Guo-Liang Wang and Eric Stockinger

Click below to download handouts and reference papers as PDF files

One slides/page lecture notes

Four slides/page lecture notes

Reference paper 1

Reference paper 2

Course video

Printed copies of handouts will not be provided in class. Please print out your own handouts.

Study questions

1. What do promoters do? What is a cis element? What is a trans-acting factor? What are enhancers? What do they do? Are enhancers always next to the gene they control, or can they be far away? Can promoters work without enhancers? Can enhancers work without promoters? What does co-regulation mean? If a set of genes exhibit co-regulation what might you hypothesize about the promoters of those genes?
2. How do reporter genes enable functional analyses of promoters? What information can be gained by creating a series of promoter deletions and transforming those back into the organism of interest? What is the purpose of making mutations in suspected cis elements? How have these types of studies aided in bioinformatic approaches that are now being used to find motifs?
3. In lining up two or more genomes, segments are often found that are highly conserved across all genomes yet they are in regions that do not encode protein. What might you hypothesize about these segments? Devise an experimental strategy to test your hypothesis.
4. How does Chromatin Immunoprecipitation (ChIP) work? How does ChIP differ from ChIP-chip? How does ChIP-chip differ from Chip-seq? What does ChIP-seq allow one to do that ChIP-chip does not?
5. What are the bait and target molecules of the yeast one hybrid system described in lecture 12? What are the bait and target molecules of the yeast one hybrid system described in lecture 13?
6. Finding important DNA sequence motifs using bioinformatic approaches can use pattern-driven algorithms or sequence-driven algorithms. What is the difference between these two types of motif finding strategies? Explain why gene-finding and promoter-prediction go hand in hand. How does CAP trapping aid in the identification of the +1 transcription start site (TSS)? If you do CAP trapping using two different tissues or two different environmental conditions and get two different results what might be a reasonable explanation?