Genetic analysis of adenovirus E1A: Induction of genetic instability and altered cell morphologic and growth characteristics are segregatable functions

Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis

Volumn 421, Issue 1, 1998, Pages 9-25

  Drews, Reed ^a,b   Kolker, Mitchell ^a,b   Moran, Colin ^a,b   Sachar, David ^a,b   Chan, Victor ^a,b,c   Schnipper, Lowell ^a,b  

^a BETH ISRAEL DEACONESS MEDICAL CENTER   (United States)

^b HARVARD MEDICAL SCHOOL   (United States)

^c THE OHIO STATE UNIVERSITY COLLEGE OF MEDICINE   (United States)

Author keywords

Adenovirus E1A; Cell transformation; Genomic instability; p107; p300; pRb

Indexed keywords

GENE PRODUCT; KANAMYCIN KINASE; VIRUS PROTEIN;

ADENOVIRUS; ANIMAL CELL; ARTICLE; CELL STRAIN 3T3; CELL STRUCTURE; CELL TRANSFORMATION; GENETIC ANALYSIS; GENETIC STABILITY; GENETIC TRANSFECTION; NONHUMAN; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; VIRUS MUTANT;

3T3 CELLS; ADENOVIRIDAE; ADENOVIRUS E1A PROTEINS; ANIMALS; ANTI-BACTERIAL AGENTS; CELL DIVISION; CELL SIZE; GENE EXPRESSION; GENE REARRANGEMENT; GENETIC COMPLEMENTATION TEST; GENTAMICINS; KANAMYCIN KINASE; MICE; MUTATION; RNA SPLICING; RNA, MESSENGER; SEQUENCE DELETION; TRANS-ACTIVATION (GENETICS); TRANSFECTION;

ADENOVIRIDAE;

EID: 0032511835     PISSN: 00275107     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0027-5107(98)00149-3     Document Type: Article

References (58)

1. [1] T.D. Tlsty, Normal diploid human and rodent cells lack a detectable frequency of gene amplification, Proc. Natl. Acad. Sci. U.S.A. 87 (1990) 3132-3136.
2. [2] J.A. Wright, H.S. Smith, F.M. Watt, M.C. Hancock, D.L. Hudson, G.R. Stark, DNA amplification is rare in normal human cells, Proc. Natl. Acad. Sci. U.S.A. 87 (1990) 1791-1795.
3. [3] L.A. Loeb, Mutator phenotype may be required for multi-stage carcinogenesis, Cancer Res. 51 (1991) 3075-3079.
4. [4] L.H. Hartwell, M.B. Kastan, Cell cycle control and cancer, Science 266 (1994) 1821-1828.
5. [5] P. Modrich, Mismatch repair, genetic stability, and cancer, Science 266 (1994) 1959-1960.
6. [6] N.C. Denko, A.J. Giaccia, J.R. Stringer, P.J. Stambrook, The human Ha-ras oncogene induces genomic instability in murine fibroblasts within one cell cycle, Proc. Natl. Acad. Sci. U.S.A. 91 (1994) 5124-5128.
7. [7] K.J. Pienta, A.W. Partin, D.S. Coffey, Cancer as a disease of DNA organization and dynamic cell structure, Cancer Res. 49 (1989) 2525-2532.
8. [8] L.R. Livingstone, A. White, J. Sprouse, E. Livanos, T. Jacks, T.D. Tlsty, Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53, Cell 70 (1992) 923-935.
9. [9] Y. Yin, M.A. Tainsky, F.Z. Bischoff, L.C. Strong, G.M. Wahl, Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles, Cell 70 (1992) 937-948.
10. [10] L.E. Schnipper, V. Chan, J. Sedivy, P. Jat, P.A. Sharp, Gene activation by induced DNA rearrangements, Cancer Res. 49 (1989) 6640-6644.
11. [11] R.E. Drews, V.T.-W. Chan, L.E. Schnipper, Oncogenes result in genomic alterations that activate a transcriptionally silent, dominantly selectable reporter gene (neo), Mol. Cell. Biol. 12 (1992) 198-206.
12. [12] B. Vogelstein, K.W. Kinzler, p53 function and dysfunction, Cell 70 (1992) 523-526.
13. [13] M.B. Kastan, Q. Zhan, W.S. El-Deiry, F. Carrier, T. Jacks, W.V. Walsh, B.S. Plunkett, B. Vogelstein, A.J. Fornace, A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia telangiectasia, Cell 71 (1992) 587-597.
14. [14] S.M. Cross, C.A. Sanchez, C.A. Morgan, M.K. Schimke, S. Ramel, R.L. Idzerda, W.H. Raskind, B.J. Reid, A p53-dependent mouse spindle checkpoint, Science 267 (1995) 1353-1356.
15. [15] K. Fukasawa, T. Choi, R. Kuriyama, S. Rulong, G.F. Vande Woude, Abnormal centrosome amplification in the absence of p53, Science 271 (1996) 1744-1747.
16. [16] P. Whyte, K.J. Buchkovich, J.M. Horowitz, S.H. Friend, M. Raybuck, R.A. Weinberg, E. Harlow, Association between an oncogene and an antioncogene: the adenovirus E1A proteins bind to the retinoblastoma gene product, Nature (London) 334 (1988) 124-129.
17. [17] J.R. Nevins, E2F: a link between the Rb tumor suppressor protein and viral oncoproteins, Science 258 (1992) 424-429.
18. [18] J.A. DeCaprio, J.W. Ludlow, J. Figge, J.-Y. Shew, C.-M. Huang, W.-H. Lee, E. Marsilio, E. Paucha, D.M. Livingston, SV40 large tumor antigen forms a specific complex with the product of the retinoblastoma susceptibility gene, Cell 54 (1988) 275-283.
19. [19] N. Dyson, R. Bernards, S.H. Friend, L.R. Gooding, J.A. Hassell, E.O. Major, J.M. Pipas, T. Vandyke, E. Harlow, Large T antigens of many polyomaviruses are able to form complexes with the retinoblastoma protein, J. Virol. 64 (1990) 1353-1356.
20. [20] D.C. Pallas, H. Fu, L.C. Haehnel, W. Weller, R.J. Collier, T.M. Roberts, Association of polyomavirus middle tumor antigen with 14-3-3 proteins, Science 265 (1994) 535-537.
21. [21] J.W. Ludlow, G.R. Skuse, Viral oncoprotein binding to pRB, p107, p130, and p300, Virus Res. 35 (1995) 113-121.
22. [22] W.C. Morgan, D.R. Kaplan, D.C. Pallas, T.M. Roberts, Recombinant retroviruses that transduce middle T antigen cDNAs derived from polyomavirus mutants: separation of focus formation and soft-agar growth in transformation assays and correlations with kinase activities in vitro, J. Virol. 62 (1988) 3407-3414.
23. [23] P.S. Jat, C.L. Cepko, R.D. Mulligan, P.A. Sharp, Recombinant retroviruses encoding simian virus 40 large T antigen and polyomavirus large and middle T antigens, Mol. Cell. Biol. 6 (1986) 1204-1217.
24. [24] H.E. Ruley, Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture, Nature (London) 304 (1983) 602-606.
25. [25] P. Whyte, H.E. Ruley, E. Harlow, Two regions of the adenovirus early region 1A proteins are required for transformation, J. Virol. 62 (1988) 257-265.
26. [26] P.C. Nowell, The clonal evolution of tumor cell populations, Science 194 (1976) 23-28.
27. [27] P.C. Nowell, Mechanisms of tumor progression, Cancer Res. 46 (1986) 2203-2207.
28. [28] T.D. Tlsty, A. White, J. Sanchez, Suppression of gene amplification in human cell hybrids, Science 255 (1992) 1425-1427.
29. [29] D.I. Schaefer, E.M. Livanos, A.E. White, T.D. Tlsty, Multiple mechanisms of N-(phosphonoacetyl)-L-aspartate drug resistance in SV40-infected precrisis human fibroblasts, Cancer Res. 53 (1993) 4946-4951.
30. [30] K. Buchkovich, L.A. Duffy, E. Harlow, The retinoblastoma protein is phosphorylated during specific phases of the cell cycle, Cell 58 (1989) 1097-1105.
31. [31] J.A. DeCaprio, J.W. Ludlow, D. Lynch, Y. Furukawa, J. Griffin, H. Piwnica-Worms, C.-M. Huang, D.M. Livingston, The product of the retinoblastoma susceptibility gene has properties of a cell cycle regulatory element, Cell 58 (1989) 1085-1095.
32. [32] A.R. Clarke, E.R. Maandag, M. van Roon, N.M. van der Lugt, M. van der Valk, M.L. Hooper, A. Berns, H. te Riele, Requirement for a functional Rb-1 gene in murine development, Nature (London) 359 (1992) 328-330.
33. [33] D. Cobrinik, P. Whyte, D.S. Peeper, T. Jacks, R.A. Weinberg, Cell cycle-specific association of E2F with the p130 E1A-binding protein, Genes Dev. 7 (1993) 2392-2404.
34. [34] G.J. Hannon, D. Demetrick, D. Beach, Isolation of the Rb-related p130 through its interaction with CDK2 and cyclins, Genes Dev. 7 (1993) 2378-2391.
35. [35] G. Vairo, D.M. Livingston, D. Ginsberg, Functional interaction between E2F-4 and p130: evidence for distinct mechanisms underlying growth suppression by different retinoblastoma protein family members, Genes Dev. 9 (1995) 869-881.
36. [36] R. Eckner, M.E. Ewen, D. Newsome, M. Gerdes, J.A. DeCaprio, J.B. Lawrence, D.M. Livingston, Molecular cloning and functional analysis of the adenovirus E1A-associated 300-kD protein (p300) reveals a protein with properties of a transcriptional adaptor, Genes Dev. 8 (1994) 869-884.
37. [37] Z. Arany, D. Newsome, E. Oldread, D.M. Livingston, R. Eckner, A family of transcriptional adaptor proteins targeted by the E1A oncoprotein, Nature (London) 374 (1995) 81-84.
38. [38] J.R. Lundblad, R.P.S. Kwok, M.E. Laurance, M.L. Harter, R.H. Goodman, Adenoviral E1A-associated protein p300 as a functional homologue of the transcriptional co-activator CBP, Nature (London) 374 (1995) 85-88.
39. [39] X.-J. Yang, V.V. Ogryzko, J.-I. Nishikawa, B.H. Howard, Y. Nakatani, A p300/CBP-associated factor that competes with the adenoviral oncoprotein E1A, Nature (London) 382 (1996) 319-324.
40. [40] J.V. Geisberg, W.S. Lee, A.J. Berk, R.P. Ricciardi, The zinc finger region of the adenovirus E1A transactivating domain complexes with the TATA box binding protein, Proc. Natl. Acad. Sci. U.S.A. 91 (1994) 2488-2492.
41. [41] J.V. Geisberg, J.L. Chen, R.P. Ricciardi, Subregions of the adenovirus E1A transactivation domain target multiple components of the TFIID complex, Mol. Cell. Biol. 15 (1995) 6283-6290.
42. [42] E. Moran, M.B. Mathews, Multiple functional domains in the adenovirus E1A gene, Cell 48 (1987) 177-178.
43. [43] P. Whyte, N.M. Williamson, E. Harlow, Cellular targets for transformation by the adenovirus E1A proteins, Cell 56 (1989) 67-75.
44. [44] B. Krippl, B. Ferguson, N. Jones, M. Rosenberg, H. Westphal, Mapping of functional domains in adenovirus E1A proteins, Proc. Natl. Acad. Sci. U.S.A. 82 (1985) 7480-7484.
45. [45] R.E. Drews, M.T. Kolker, D.S. Sachar, C.P. Moran, L.E. Schnipper, Passage to non-selective media transiently alters growth of mycophenolic acid-resistant mammalian cells expressing the Escherichia coli xanthine-guanine phosphoribosyltransferase gene: implications for sequential selection strategies, Anal. Biochem. 235 (1996) 215-226.
46. [46] E. Harlow, D. Lane (Eds.), Antibodies: A Laboratory Manual, Cold Spring Harbor Laboratory Press, Plainview, NY, 1988.
47. [47] H.-G.H. Wang, E. Moran, P. Yaciuk, E1A promotes association between p300 and pRB in multimeric complexes required for normal biological activity, J. Virol. 69 (1995) 7917-7924.
48. [48] G. Hateboer, H.T. Timmers, A.K. Rustgi, M. Billaud, L.J. van't Veer, R. Bernards, TATA-binding protein and the retinoblastoma gene product bind to overlapping epitopes on c-Myc and adenovirus E1A protein, Proc. Natl. Acad. Sci. U.S.A. 90 (1993) 8489-8493.
49. [49] W. Krek, D.M. Livingston, S. Shirodkar, Binding to DNA and the retinoblastoma gene product promoted by complex formation of different E2F family members, Science 262 (1993) 1557-1560.
50. [50] R.A. Weinberg, The retinoblastoma protein and cell cycle control, Cell 81 (1995) 323-330.
51. [51] R.A. Weinberg, E2F and cell proliferation: a world turned upside down, Cell 85 (1996) 457-459.
52. [52] J. Zwicker, N. Liu, K. Engeland, F.C. Lucibello, R. Müller, Cell cycle regulation of E2F site occupation in vivo, Science 271 (1996) 1595-1597.
53. [53] J.A. Howe, J.S. Mymryk, C. Egan, P.E. Branton, S.T. Bayley, Retinoblastoma growth suppressor and a 300-kDa protein appear to regulate cellular DNA synthesis, Proc. Natl. Acad. Sci. U.S.A. 87 (1990) 5883-5887.
54. [54] A. Giordano, J.H. Lee, J.A. Scheppler, C. Herrmann, E. Harlow, U. Deuschle, D. Beach, B.R. Franza, Cell cycle regulation of histone H1 kinase activity associated with the adenoviral protein E1A, Science 253 (1991) 1271-1275.
55. [55] G.F. Morris, M.B. Mathews, The adenovirus E1A transforming protein activates the proliferating cell nuclear antigen promoter via an activating transcription factor site, J. Virol. 65 (1991) 6397-6406.
56. [56] M. Debbas, E. White, Wild-type p53 mediates apoptosis by E1A, which is inhibited by E1B, Genes Dev. 7 (1993) 546-554.
57. [57] S.W. Lowe, H.E. Ruley, Stabilization of the p53 tumor suppressor is induced by adenovirus 5 E1A and accompanies apoptosis, Genes Dev. 7 (1993) 535-545.
58. [58] J.G. Teodoro, G.C. Shore, P.E. Branton, Adenovirus E1A proteins induce apoptosis by both p53-dependent and p53-independent mechanisms, Oncogene 11 (1995) 467-474.