Controlling cell proliferation in differentiating tissues: Genetic analysis of negative regulators of G1→S-phase progression

Current Opinion in Cell Biology

Volumn 9, Issue 6, 1997, Pages 773-781

  Zavitz, Kenton H ^a   Zipursky, S Lawrence ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN DEPENDENT KINASE; CYCLIN DEPENDENT KINASE INHIBITOR; CYCLINE; REGULATOR PROTEIN;

CELL CYCLE; CELL CYCLE G1 PHASE; CELL CYCLE G2 PHASE; CELL CYCLE S PHASE; CELL DIFFERENTIATION; CELL PROLIFERATION; DROSOPHILA; EMBRYO DEVELOPMENT; ORGAN SIZE; PRIORITY JOURNAL; PROTEIN DEGRADATION; REVIEW;

EID: 0030692745     PISSN: 09550674     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0955-0674(97)80077-4     Document Type: Article

References (45)

1. 1 cyclin-dependent kinases. Genes Dev 1995, 9:1149-1163.
2. Morgan DO: Principles of CDK regulation. Nature 1995, 374:131-134.
3. INK4A as a tumor suppressor.
4. 1 phase and complete one additional cell cycle. These studies establish that a higher eukaryotic cyclin dependent kinase inhibitor can be essential for proliferate control during development.
5. ••].
6. Knoblich JA, Sauer K, Jones L, Richardson H, Saint R, Lehner CF: Cyclin E controls S phase progression and its down-regulation during Drosophila embryogenesis is required for the arrest of cell proliferation. Cell 1994, 77:107-120.
7. KIP1 are normal at birth, but grow to be larger than wild-type mice. Tissues that normally express the highest levels of p27 (thymus, spleen and testes) were most affected. Enlargement reflects an increase in cell number. Although the development of most tissues appeared normal, defects were seen in several tissues including the pituitary, ovarian follicles, and retina Thus, the absence of a cyclin dependent kinase inhibitor can have a profound effect on tissue size and may affect the correct development of specific tissues.
8. ••].
9. ••].
10. Polyak K, Kato JY, Solomon MJ, Sherr CJ, Massague J, Roberts JM, Koff A: p27Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-beta and contact inhibition to cell cycle arrest. Genes Dev 1994, 8:9-22.
11. Nourse J, Firpo E, Flanagan WM, Coats S, Polyak K, Lee MH, Massague J, Crabtree GR, Roberts JM: Interleukin-2-mediated elimination of the p27Kip1 cyclin-dependent kinase inhibitor prevented by rapamycin. Nature 1994, 372:570-573.
12. Coats S, Flanagan WM, Nourse J, Roberts JM: Requirement of p27Kip1 for restriction point control of the fibroblast cell cycle. Science 1996, 272:877-880.
13. Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, Baldini A, Harper JW, Elledge SJ: p57KIP2, a structurally distinct member of the p21CIP1 Cdk inhibitor family, is a candidate tumor suppressor gene. Genes Dev 1995, 9:650-662.
14. Lee MH, Reynisdottir I, Massague J: Cloning of p57KIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev 1995, 9:639-349.
15. KIP2 in this disease.
16. ••].
17. Erlebacher A, Filvaroff EH, Gilelman SE, Derynck R: Toward a molecular understanding of skeletal development. Cell 1995, 80:371-378.
18. Weinberg RA: The retinoblastoma protein and cell cycle control. Cell 1995, 81:323-330.
19. Bartek J, Bartkova J, Lukas J: The retinoblastoma protein pathway and the restriction point. Curr Opin Cell Biol 1996, 8:805814.
20. Zhu L, van den Heuvel S, Helin K, Fattaey A, Ewen M, Livingston D, Dyson N, Harlow E: Inhibition of cell proliferation by. p107, a relative of the retinoblastoma protein. Genes Dev 1993, 7:1111-1125.
21. Claudio PP, Howard CM, Baldi A, De Luca A, Fu Y, Condorelli G, Sun Y, Colbum N, Calabretta B, Giordano A: p130/pRb2 has growth suppressive properties similar to yet distinctive from those of retinoblastoma family members pRb and p107. Cancer Res 1994, 54:5556-5560.
22. Jacks T, Fazeli A, Schmitt EM, Bronson RT, Goodell MA, Weinberg RA: Effects of an Rb mutation in the mouse. Nature 1992, 359:295-300.
23. Lee EY, Chang CY, Hu N, Wang YC, Lai CC, Herrup K, Lee WH, Bradley A: Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis. Nature 1992, 359:288-294.
24. Morgenbesser SD, Williams BO, Jacks T, DePinho RA: p53-dependent apoptosis produced by Rb-deficiency in the developing mouse lens. Nature 1994, 371:72-74.
25. Clarke AR, Maandag ER, van Roon M, van der Lugt NM, van der Valk M, Hooper ML, Berns A, te Riele H: Requirement for a functional Rb-1 gene in murine development [see comments]. Nature 1992, 359:328-330.
26. ••]). However, homozygous p107 p130 double knock-out mice have dramatic defects in bone development and exhibit neonatal lethality. These findings demonstrate that these two pRb relatives functionally overlap in specific tissues and cannot be compensated for by pRb.
27. -/- embryos.
28. Hurlord R Jr, Cobrinik D, Lee MH, Dyson N: pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes. Genes Dev 1997, 11:1447-1463. The overlapping functions of pRb, p107, and p130 were analyzed at a molecular level. Mouse embryo fibroblasts (MEFs) lacking p107 or p130 displayed no changes in E2F-induced target gene expression. In contrast, deregulated expression of some E2F target genes was seen in MEFs lacking either pRb or both p107 and p130. Interestingly, the subsets of genes deregulated in these cells were different. Most intriguingly, lack of p107/p130 resulted in the upregulation of a previously uncharacterized E2F-binding activity, suggesting that homeostatic mechanisms might compensate for the absence of an individual regulatory molecule.
29. 1-phase cyclin.
30. 1-phase cyclin Cln2, and is required for Cln2 ubiquitination and instability in vivo. These interactions all require Cln2 phosphorylation. Cdc53 also binds to Cdc34 (a ubiqutin-conjugating enzyme, or E2), suggesting that Cdc53 is part of a ubiquitin-protein ligase (E3) complex that targets Clns and perhaps other proteins for rapid degradation.
31. SIC1. These mutant loci genetically interact and the encoded proteins physically associate in vivo. A complex including these proteins probably acts to target specific substrates for ubiquitination. The sequence of Cdc53 define it as a member of the cullin gene family.
32. Jackson PK: Cell cycle: cull and destroy. Curr Biol 1996, 6:1209-1212. A short review of the roles of the Cdc53/cullin family in cell cycle regulation via targeted ubiquitin-dependent proteolysis.
33. King RW, Deshaies RJ, Peters JM, Kirschner MW: How proteolysis drives the cell cycle. Science 1996, 274:1652-1659. A comprehensive review of how proteolysis regulates cyclin dependent kinase activity as well as chromosome and spindle dynamics.
34. 1 cyclin Cln2 induced by CDK-dependent phosphorylation. Science 1996, 271:1597-1601.
35. 1 cyclins in the next cycle. Cell 1994, 77:1037-1050.
36. Brandeis M, Hunt T: The proteolysis of mitotic cyclins in mammalian cells persists from the end of mitosis until the onset of S phase. EMBO J 1996, 15:5280-5269.
37. 1 phase in a developing tissue.
38. 1. Cell 1994, 77:1003-1014.
39. Ready DF, Hanson TE, Benzer S: Development of the Drosophila retina, a neurocrystalline lattice. Dev Biol 1976, 53:217-240.
40. Gönczy P, Thomas BJ, DiNardo S: roughex is a dose-dependent regulator of the second meiotic division during Drosophila spermatogenesis. Cell 1994, 77:1015-1025.
41. 1 in the developing Drosophila eye: rca1 regulates cyclin A. Genes Dev 1997, 11:94-105.
42. Edgar BA, O'Farrell PH: Genetic control of cell division patterns in the Drosophlia embryo. Cell 1989, 57:177-187.
43. Kumagai A, Dunphy WG: The cdc25 protein controls tyrosine dephosphorylation of the cdc2 protein in a cell-free system, Cell 1991, 64:903-914.
44. Heberlein U, Singh CM, Luk AY, Donohoe TJ: Growth and differentiation in the Drosophila eye coordinated by hedgehog. Nature 1995, 373:709-711.
45. 1 phase, thus preventing early S-phase entry. That the roughex gene functions in a partially redundant way during embryogenesis is demonstrated by ectopic cyclin A expression studies.