MCDB 2150 Fall 1998 Review Questions

Revised November 29, 1998

Lecture 31: RFLPs, DNA fingerprinting, polymerase chain reaction

1. What is meant by the term "restriction map"? What is the value of using partial digests in such mapping?

2. What is the advantage of preparing a restriction map with more than one restriction endonuclease?

3. Define restriction fragment length polymorphism (RFLP) and describe the procedures that are used to detect RFLPs.

4. RFLP's are usually described in terms of a specific probe and a specific restriction endonuclease. Would you expect to be able to detect RFLPs with the same probe but different restriction endonucleases? Explain your answer.

5. What type of probe would you use to detect an RFLP that is not located within the coding sequence of a gene? What are such probes called and why are they considered to be so valuable in studies seeking to identify human disease genes? of RFLPs?

6. What is an RFLP haplotype? What special value does it have in human genetic analysis?

7. How do RFLP haplotypes contribute to the identification of the genes responsible for specific human genetic diseases?

8. Describe three distinctly different types of genetic changes that could alter the pattern of restriction fragment lengths observed with Bam HI (G^GATCC) and a 5 kb probe. (^ = cut site)

9. How can the length of a restriction fragment be altered by a polymorphic cut site that lies outside of the region that hybridizes to the probe?

10. Probe X detects an RFLP that involves two polymorphic HindIII sites.

a. How many different haplotypes would be seen in a survey of a population that includes polymorphisms at both cut sites?

b. How many different haplotypes would you expect to see in any one individual and why?

c. How would you interpret an individual that exhibited only one haplotype?

d. Would you expect Hin dIII to cut probe X into smaller pieces? Explain the reasoning behind your answer.

e. What results would you expect in part a if you were using a probe based on the first 50 nucleotides at the 5'-end of probe X? Explain your answer.

11. Probe Z is 4.0 kb in length. Use diagrams to explain how each of the following RFLP patterns might be obtained with probe Z and appropriate restriction endonucleases with six nucleotide recognition sites.

a. a haplotype consisting of a single fragment 5.7 kb in length vs. a haplotype consiting of fragments 3.0 and 2.7 kb in length.

b. a single fragment 4.2 kb in length vs. a fragment 7.3 kb in length.

c. A haplotype consisting of fragments 4.7 and 5.1 kb in length vs a haplotype consisting of fragments 2.5 and 4.7 kb in length.

d. A haplotype consisting of fragments 2.5, 4.7 and 5.1 kb in length vs. a haplotype consisting of fragments 3.6 and 5.1 kb in length. (Hint: think in terms of sampling the general population and do not assume that the difference necessarily arises from a single mutational event.)

e. What general pattern of fragments would you expect to see if you used the same probe with a restriction endonuclease that has a four nucleotide recognition site.

12. Using the table of codons in the textbook, identify all possible amino acid sequences whose genomic coding sequences could generate a cut site for EcoRI (G|AATTC). (Be sure to examine all possible reading frames and exclude all nucleotide sequences that could not be found in the coding sequences for proteins.)

13. In an organism whose DNA is 50% AT, how long would a protein have to be to have a 50% chance of containing a cut site for EcoRI within its coding sequence?

14. Describe the genetic defect that is responsible for Huntington disease.

15. Discuss the psychological problems that must be considered before deciding whether or not the child of a known Huntington disease parent should be screened to determine whether he or she has inherited the disease. Also answer for a young adult whose father has just begun to develop the symptoms of Huntington disease.

16. What feature makes genetic screening for Huntington disease unusually easy?

17. How can Huntington disease patients with two normal parents be explained? What types of tests would you perform if the husband of the mother of the patient demanded proof that he was actually the father of the patient?

18. The gene that becomes altered in Huntington disease and the nature of the changes that lead to the disease have been identified precisely. Describe the additional problems that stand in the way of finding a cure for the disease.

19. "Annonymous" probes are now widely used in human genetic studies.

a. What is an annonymous probe and why is it so named?

b. What is the advantage of using annonymous probes rather than known genes?

c. Describe the role played by an annonymous probe in the identification of the gene that is altered in Huntington disease.

d. What special feature was possessed by the G8 annonymous probe used in the study of Huntington disease that made it potentially more valuable than a simpler annonymous probe might have been?

e. Would you expect the same G8 haplotype to be associated with Huntington disease in all disease-prone families? Explain your answer.

20. Explain how "exon-trapping" is used to identify genes within an uncharacterized segment of chromosomal DNA.

21. Briefly summarize techniques that can be used to identify active genes within a chromosomal segment that has been shown by linkage analysis to contain the gene responsible for a human inherited disease.

22. How would you determine which of the active genes identified in question 21 was the one responsible for the genetic disease under study?

23. What characteristic of the restriction endonuclease Hpa II causes it to yield "tiny" fragments (as well as unusually large fragments) when compared to most of the commonly used restriction endonucleases? How were these properties exploited in the search for the cystic fibrosis gene?

24. Explain how detailed genetic analysis of female patients with Duchenne muscular dystrophy (DMD) made it possible to identify the chromosomal region that carried the gene that is defective in DMD.

25. Mutations in gene BRCA1 are responsible for much of human hereditary breast cancer. What practical problems stand in the way of developing an effective genetic screening program for carriers of the defective genes?

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