Biology 2

Chapter 18 OBJECTIVE

1. Compare the organization of prokaryotic and eukaryotic genomes.

1. Describe the current model for progressive levels of DNA packing.

2. Explain how histones influence folding in eukaryotic DNA.

3. Distinguish between heterochromatin and euchromatin.

4. Using the Barr body as an example, describe the function of heterochromatin in interphase cells.

5. Describe where satellite DNA is found and what role it may play in the cell.

6. Describe the role of telomeres in solving the end-replication problem with the lagging DNA strand.

7. Using the genes for rRNA as an example, explain how multigene families of identical genes can be advantageous for a cell.

8. Using a-globin and b-globin genes as an examples, describe how multigene families of nonidentical genes probably evolve, including the role of transposition

9. Explain the potential role that promoters and enhancers play in transcriptional control.

10. Explain why the nuclear envelope in eukaryotes offers a level of post-transcriptional control beyond that found in prokaryotes.

11. Explain why the ability to rapidly degrade mRNA can be an adaptive advantage for prokaryotes.

12. Describe the importance of mRNA degradation in eukaryotes, describe how it can be prevented.

13. Explain how gene expression may be controlled at the translation and post-translation level.

14. Compare the arrangement of coordinately controlled genes in prokaryotes and eukaryotes.

15. Explain how eukaryotic genes can be coordinately expressed and give some examples of coordinate gene expression in eukaryotes.

16. Provide evidence from studies of polytene chromosomes, that eukaryotic gene expression is controlled at transcription and that gene regulation responds to chemical signals such as steroid hormones.

17. Describe the key steps of steroid hormone action on gene expression in vertebrates,

18. In general terms, explain how genome plasticity can influence gene expression.

19. Describe the effects of fen amplification, selective gene loss and DNA methylation.

20. Explain how rearrangements in the genome can activate or inactive genes.

21. Explain the genetic basis for antibody diversity.

22. Explain how DNA methylation may be a cellular mechanism for long-term control of gene expression and how it can influence early development.

23. Describe the normal control mechanisms that limit cell growth and division.

24. Briefly describe the four mechanisms than can convert proto-oncogenes to oncogenes.

25. Explain how changes in tumor-supressor genes can be involved in transforming normal cells into cancerous cells.

26. Explain how oncogenes are involved in virus-induced cancers.