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CAMPBELL BIOL 111 - Biology 111 EXAM

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DirectionsTerminologyBiology 111 NAME:_______________________ Directions Read the portion of the article (Role of Genotype in the Cycle of Violence in Maltreated Children, Science, August 2, 2002) provided. The questions below will be addressed during the following class period. You will submit your responses at the end of the next class period.  The word “genotype” appears in the title of the article. What is meant by genotype? What genotype(s) are being investigated in this research article?  Violent behavior seems to be more attributed to male children than to female children. Is there any information provided in this article that might suggest a reason why boys may be more likely to become violent than girls?  In your own words, explain the hypothesis of the investigators of this study.  Does the data in Figure 2 support or refute the hypothesis? Explain. Terminology Functional polymorphism = genetic variation (often as a result of a point mutation) that results in an altered function of the gene product (i.e. protein) Null allele = An allele whose effect is either an absence of normal gene product at the molecular level or an absence of normal function at the phenotypic level.14. A. Streit et al., Development 125, 507 (1998).15. T. C. Dale, Biochem. J. 329 (Part 2), 209 (1998).16. J. R. Miller, Genome Biol. 3, REVIEWS3001 (2002).17. M. Ikeya, S. M. Lee, J. E. Johnson, A. P. McMahon, S.Takada, Nature 389, 966 (1997).18. J. P. Saint-Jeannet, X. He, H. E. Varmus, I. B. Dawid,Proc. Natl. Acad. Sci. U.S.A. 94, 13713 (1997).19. C. Chang, A. Hemmati-Brivanlou, Dev. Biol. 194, 129(1998).20. C. LaBonne, M. Bronner-Fraser, Development 125,2403 (1998).21. M. A. Deardorff, C. Tan, J. P. Saint-Jeannet, P. S. Klein,Development 128, 3655 (2001).22. C. Tan et al., Development 128, 3665 (2001).23. C. A. Cauthen, E. Berdougo, J. Sandler, L. W. Burrus,Mech. Dev. 104, 133 (2001).24. S. Hoppler, J. D. Brown, R. T. Moon, Genes Dev. 10,2805 (1996).25. A. G. Bang, N. Papalopulu, M. D. Goulding, C. Kintner,Dev. Biol. 212, 366 (1999).26. L. L. McGrew, S. Hoppler, R. T. Moon, Mech. Dev. 69,105 (1997).27. M. A. Nieto, M. G. Sargent, D. G. Wilkinson, J. Cooke,Science 264, 835 (1994).28. M. I. Garcı´a-Castro, C. Marcelle, M. Bronner-Fraser,data not shown.29. G. C. Tucker, H. Aoyama, M. Lipinski, T. Tursz, J. P.Thiery, Cell Differ. 14, 223 (1984).30. A. Chakrabarti, G. Matthews, A. Colman, L. Dale,Development 115, 355 (1992).31. N. R. Ramakrishna, A. M. Brown, Development (Suppl)95 (1993).32. P. Bhanot et al., Nature 382, 225 (1996).33. Q. Xu, P. A. D’Amore, S. Y. Sokol, Development 125,4767 (1998).34. J. C. Hsieh et al., Nature 398, 431 (1999).35. D. Cook et al., EMBO J. 15, 4526 (1996).36. T. Yamada, S. L. Pfaff, T. Edlund, T. M. Jessell, Cell 73,673 (1993).37. M. Hammerschmidt et al., Development 123, 95 (1996).38. B. Neave, N. Holder, R. Patient, Mech. Dev. 62, 183 (1997).39. V. H. Nguyen et al., Dev. Biol. 199, 93 (1998).40. V. H. Nguyen et al., Development 127, 1209 (2000).41. D. J. Connolly, K. Patel, J. Cooke, Int. J. Dev. Biol. 41,389 (1997).42. J. A. McMahon et al., Genes Dev. 12, 1438 (1998).43. G. Winnier, M. Blessing, P. A. Labosky, B. L. Hogan,Genes Dev. 9, 2105 (1995).44. T. M. Schultheiss, J. B. Burch, A. B. Lassar, Genes Dev.11, 451 (1997).45. D. Henrique et al., Nature 375, 787 (1995). Thefollowing probes were used: Slug [from A. Nieto (16)];Wnts1, 3a, 4, 5a, 5b, and 6 (from A. McMahon);Wnt8c (from J. Dodd); BMP-4 (from D. Wu and P.Brickell); and BMP-7 (from M. Dickinson).46. Intermediate neural plates from stage 10 [as de-scribed by V. Hamburger, H. L. Hamilton, J. Morphol.88, 49 (1951)] White Leghorn chicken embryos weredissected and cultured [as described in (5, 10, 11),and also based on (6–8, 35)].47. S2and S2-Wg cells (gift of R. Nusse) were grown [asrecommended in F. van Leeuwen, C. H. Samos, R.Nusse, Nature 368, 342 (1994)], and DMEM, pen/strep control-CM, and Wg-CM were collected in 1/10original volume. Wg (54 kD) was identified by West-ern blot analysis.48. E. Pera, S. Stein, M. Kessel, Development 126, 63 (1999).49. A Hind III–Snc B1 fragment from mouse DnWnt1 [giftof R. Moon (23)] was cloned into a Hind III–Smafragment of pC1 Neo (Promega, Madison, WI); per-manently transfected 3T3 cells were selected after 3months. Cell labeling and injections were performed[as described in (10, 11)]. Expression of mRNA fromDnWnt1 was detected after injection. Wnt1-cell lineswere kindly provided by N. Brown and A. Kiespert.50. Supported by NIH grant number NS36585. We thankC. Baker, A. Groves, and A. Knecht for helpful com-ments on this work.Supporting Online Materialwww.sciencemag.org/cgi/content/full/1070824/DC1Figs. S1 and S212 February 2002; accepted 28 May 2002Published online 13 June 2002;10.1126/science.1070824Include this information when citing this paper.Role of Genotype in the Cycleof Violence in MaltreatedChildrenAvshalom Caspi,1,2Joseph McClay,1Terrie E. Moffitt,1,2*Jonathan Mill,1Judy Martin,3Ian W. Craig,1Alan Taylor,1Richie Poulton3We studied a large sample of male children from birth to adulthood to deter-mine why some children who are maltreated grow up to develop antisocialbehavior, whereas others do not. A functional polymorphism in the gene en-coding the neurotransmitter-metabolizing enzyme monoamine oxidase A(MAOA) was found to moderate the effect of maltreatment. Maltreated childrenwith a genotype conferring high levels of MAOA expression were less likely todevelop antisocial problems. These findings may partly explain why not allvictims of maltreatment grow up to victimize others, and they provide epi-demiological evidence that genotypes can moderate children’s sensitivity toenvironmental insults.Childhood maltreatment is a universal risk fac-tor for antisocial behavior. Boys who experi-ence abuse—and, more generally, those ex-posed to erratic, coercive, and punitive parent-ing—are at risk of developing conduct disorder,antisocial personality symptoms, and of becom-ing violent offenders (1, 2). The earlier childrenexperience maltreatment, the more likely theyare to develop these problems (3). But there arelarge differences between children in their re-sponse to maltreatment. Although maltreatmentincreases the risk of later criminality by about50%, most maltreated children do not becomedelinquents or adult criminals (4). The reasonfor this variability in response is largely un-known, but it


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