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The retinoblastoma protein (RB) suppresses human cell division by arresting cells in the G? phase of the cell cycle and preventing progression to the next phase. It accomplishes this task by binding to another protein, E2F, a transcription factor needed for further progression through the cell cycle. Normal progression through the cell cycle is accomplished when cyclin-dependent kinases (CDKs) phosphorylate RB, preventing its binding to E2F. Many viruses can induce abnormal exit from G, using viral proteins that bind to RB at a motif at the N-terminal called LXCXE. An example is the E7 papilloma protein, which causes the excessive proliferation of cells in warts. The site at which LXCXE proteins bind is called the pocket domain and is highly conserved on RB and related proteins in plants and animals. The configuration of the pocket domain is well established. Mutant experimental RB proteins are available with alterations in the conserved amino acids of the pocket domain. A simple explanation for the ability of E7 to inactivate RB would be that both E7 and E2F bind to the pocket domain. To test this theory, wild-type (the naturally occurring or nonmutant variation) and pocket domain mutant RB were expressed in an RB-deficient cell line. Figure 1 shows the change in G, content of a population of cells transfected with wild-type or with three RB mutants (RB6, RB9, and RB10), or cotransfected with wild-type or the three RB mutants and E7. Figure 2 shows the percentage of G? cells following transfection with wild-type or mutant RB, and cotransfection of wild-type or mutant RB with the CDK4 kinase, which adds phosphate groups to RB. Change in percentage of cells in G? phase 120T 100 Percentage of cells in G? phase 80+ 60+ 40+ 20- 0 100- 90- 80- 70- 60- 50 40- WT 30- 20- Figure 1 Change in percentage of cells in G, after transfection with RB and after transfection with RB and E7. Note that a high number of cells in G, suggests that arrest has occurred. Change after transfection with wild-type RB is arbitrarily set at 100% in this analysis. (WT wild-type; other abbreviations designate the three different mutant RB proteins.) 10- 0 RB6 RB9 |||| RB6 WT RB10 RB9 RB10 Figure 2 Percentage of cells in G, after transfection with RB and after transfection with RB and CDK4 (WT = wild-type; other abbreviations designate the three different mutant RB proteins.) Comparing the bars for RB transfection with those of RB and CDK4 transfection in Figure 2 shows that: O A. mutant RB is better at arresting cells in G, than wild-type RB. O B. CDK4 transfection causes more mutant RB to be phosphorylated. O c. more cells are G, arrested in CDK4-transfected cells. O D. CDK4 transfection results in fewer cells being G? arrested. O A. vital to an organism’s survival. OB. chemically incapable of mutation. O c. stored in vesicles for later secretion. RB ORB IRB ?RB + ( The LXCXE motif is described as being “highly conserved.” Certain parts of the genome, such as that encoding the LXCXE motif, are highly conserved because they are: OD. stored in cell compartments where they are unlikely to be secreted. O A. bind to E7. O B. bind to E2F. O C. arrest cells in G?. O D. permit exit from G?.