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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

S Phase

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Disease relevance of S Phase


High impact information on S Phase

  • The ESCO2 protein product is a member of a conserved protein family that is required for the establishment of sister chromatid cohesion during S phase and has putative acetyltransferase activity [6].
  • These findings indicate that RPA activates telomerase by loading Est1p onto telomeres during S phase [7].
  • We show that during S phase, soluble MCM helicase, an essential initiation factor, is inactivated when it associates with exportin-1/Crm1 [8].
  • Proliferating cells depleted of Yph1p arrest in G(1) or G(2), with no cells in S phase, or significantly delay S phase progression after release from a hydroxyurea arrest [9].
  • Transient nuclear localization of Dnmt1o in 8-cell embryos suggests that this variant of Dnmt1 provides maintenance methyltransferase activity specifically at imprinted loci during the fourth embryonic S phase [10].

Chemical compound and disease context of S Phase


Biological context of S Phase

  • When gas1 is overexpressed from a constitutive promoter in quiescent cells, the serum-induced transition from the G0 to the S phase of the cell cycle is inhibited without affecting the normal early serum response [16].
  • Thymidine-catabolizing enzymes are active in the cells during G1, G2 and mitosis, but activity falls to very low levels just prior to the onset of S and remains low throughout the S period [17].
  • In cdc8 and cdc21, mutants defective in continued replication during the S phase of the cell cycle, mitochondrial DNA replication ceases at the nonpermissive temperature [18].
  • Protein expression studies showed that the Nap1l2 protein binds to condensing chromatin during S phase and in apoptotic cells, but remained cytoplasmic during G1 phase [19].
  • Pulse labeling of DNA and analysis of the products on alkaline sucrose gradients showed that synthesis of primary replication units (which will also be referred to as "Okazaki" fragments) occurred throughout the S period [20].

Anatomical context of S Phase

  • Acrylamide gel electrophoresis of the proteins from HeLa cells labeled with 3H-arginine during S phase showed that the core histones were labeled preferentially, constituting 30% of the total cellular tritium and 50% of the label in a crude nuclear fraction [21].
  • The distribution of stem cells and transit-amplifying cells is not random: patches of integrin-bright and integrin-dull cells have a specific location with respect to the epidermal-dermal junction that varies between body sites and that correlates with the distribution of S phase cells [22].
  • This catalytically active sedimentable fraction from S phase CHEF/18 cells or actively replicating calf thymus cells contains nascent and template DNA, and numerous enzymes required for DNA biosynthesis including ribonucleoside diphosphate reductase, thymidylate synthetase, dihydrofolate reductase, DNA methylase, topoisomerase and DNA polymerase [23].
  • In rat fibroblast, Cdk4 is tyrosine-phosphorylated during G1 progression, and its dephosphorylation is required for S phase [24].
  • Our results show that p27Kip1 governs Cdk activity during the transition from quiescence to S phase in T lymphocytes and that p21 function may be restricted to cycling cells [25].

Associations of S Phase with chemical compounds


Gene context of S Phase

  • Unlike sad1 mutants defective for multiple cell cycle checkpoints, pol2 mutants are defective only for the S phase checkpoint and the activation of DUN1 kinase necessary for the transcriptional response to damage [31].
  • The data are consistent with the hypothesis that Cln proteins activate the Cdc28 protein kinase, shown to be essential for the G1 to S phase transition in S. cerevisiae [32].
  • These proteins are thought to promote the proteolytic inactivation of the S-phase Cdk inhibitor Sic1p [33].
  • p19Skp1 and p45Skp2 are essential elements of the cyclin A-CDK2 S phase kinase [34].
  • CDC16 and CDC27 may contribute to replication control by targeted proteolysis of an S phase initiator [35].

Analytical, diagnostic and therapeutic context of S Phase

  • Here we show, by taking a conditional gene targeting approach, that the combined loss of these three E2F factors severely affects E2F target expression and completely abolishes the ability of mouse embryonic fibroblasts to enter S phase, progress through mitosis and proliferate [36].
  • Rats were subjected to 5/6 nephrectomy and then infused intraperitoneally with 5-bromodeoxyuridine (BrdU) to label S-phase cells [37].
  • Here we investigated the transcriptional regulation of the cyclin A gene, a key positive regulator of S phase that is induced after angioplasty [38].
  • A strong correlation was observed between PCNA labeling index and both [3H]thymidine labeling index (R = 0.993, P = 0.007) and percent of cells in S phase as determined by flow cytometry (R = 0.982, P = 0.018) and between the location of the maximal staining for PCNA and [3H]thymidine (R = 0.997, P less than 0.05) [39].
  • Immunofluorescence studies show the existence of two populations of cyclin during the S phase, one that is nucleoplasmic as in quiescent cells and is easily extracted by detergent, and another that is associated to specific nuclear structures [40].


  1. A viral mechanism for remodeling chromatin structure in G0 cells. Ghosh, M.K., Harter, M.L. Mol. Cell (2003) [Pubmed]
  2. Transient inhibition of initiation of S-phase associated with dimethyl sulfoxide induction of murine erythroleukemia cells to erythroid differentiation. Terada, M., Fried, J., Nudel, U., Rifkind, R.A., Marks, P.A. Proc. Natl. Acad. Sci. U.S.A. (1977) [Pubmed]
  3. The Rb-related p107 protein can suppress E2F function independently of binding to cyclin A/cdk2. Smith, E.J., Nevins, J.R. Mol. Cell. Biol. (1995) [Pubmed]
  4. Apoptosis in megaloblastic anemia occurs during DNA synthesis by a p53-independent, nucleoside-reversible mechanism. Koury, M.J., Price, J.O., Hicks, G.G. Blood (2000) [Pubmed]
  5. Proliferation-dependent cytotoxicity of methotrexate in murine L5178Y leukemia. Fernandes, D.J., Sur, P., Kute, T.E., Capizzi, R.L. Cancer Res. (1988) [Pubmed]
  6. Roberts syndrome is caused by mutations in ESCO2, a human homolog of yeast ECO1 that is essential for the establishment of sister chromatid cohesion. Vega, H., Waisfisz, Q., Gordillo, M., Sakai, N., Yanagihara, I., Yamada, M., van Gosliga, D., Kayserili, H., Xu, C., Ozono, K., Jabs, E.W., Inui, K., Joenje, H. Nat. Genet. (2005) [Pubmed]
  7. RPA regulates telomerase action by providing Est1p access to chromosome ends. Schramke, V., Luciano, P., Brevet, V., Guillot, S., Corda, Y., Longhese, M.P., Gilson, E., Géli, V. Nat. Genet. (2004) [Pubmed]
  8. A role for Ran-GTP and Crm1 in blocking re-replication. Yamaguchi, R., Newport, J. Cell (2003) [Pubmed]
  9. Yph1p, an ORC-interacting protein: potential links between cell proliferation control, DNA replication, and ribosome biogenesis. Du, Y.C., Stillman, B. Cell (2002) [Pubmed]
  10. Genomic imprinting disrupted by a maternal effect mutation in the Dnmt1 gene. Howell, C.Y., Bestor, T.H., Ding, F., Latham, K.E., Mertineit, C., Trasler, J.M., Chaillet, J.R. Cell (2001) [Pubmed]
  11. Rate of replication of the murine immunoglobulin heavy-chain locus: evidence that the region is part of a single replicon. Brown, E.H., Iqbal, M.A., Stuart, S., Hatton, K.S., Valinsky, J., Schildkraut, C.L. Mol. Cell. Biol. (1987) [Pubmed]
  12. Combined cytotoxic effect of low-dose 5-fluorouracil and hydroxyurea on 9L cells in vitro. Kobayashi, S., Hoshino, T. Cancer Res. (1983) [Pubmed]
  13. Guanine nucleotide depletion and toxicity in mouse T lymphoma (S-49) cells. Cohen, M.B., Maybaum, J., Sadee, W. J. Biol. Chem. (1981) [Pubmed]
  14. Aberrant cell cycle progression contributes to the early-stage accelerated carcinogenesis in transgenic epidermis expressing the dominant negative TGFbetaRII. Go, C., He, W., Zhong, L., Li, P., Huang, J., Brinkley, B.R., Wang, X.J. Oncogene (2000) [Pubmed]
  15. Role of Gas1 down-regulation in mitogenic stimulation of quiescent NIH3T3 cells by v-Src. Grossi, M., La Rocca, S.A., Pierluigi, G., Vannucchi, S., Ruaro, E.M., Schneider, C., Tatò, F. Oncogene (1998) [Pubmed]
  16. The growth arrest-specific gene, gas1, is involved in growth suppression. Del Sal, G., Ruaro, M.E., Philipson, L., Schneider, C. Cell (1992) [Pubmed]
  17. Catabolism of thymidine during the lymphocyte cell cycle. Usher, D.C., Reiter, H. Cell (1977) [Pubmed]
  18. Mitochondrial DNA synthesis in cell cycle mutants of Saccharomyces cerevisiae. Newlon, C.S., Fangman, W.L. Cell (1975) [Pubmed]
  19. Control of neurulation by the nucleosome assembly protein-1-like 2. Rogner, U.C., Spyropoulos, D.D., Le Novère, N., Changeux, J.P., Avner, P. Nat. Genet. (2000) [Pubmed]
  20. Size distribution and maturation of newly replicated DNA through the S and G2 phases of Physarum polycephalum. Funderud, S., Andreassen, R., Haugli, F. Cell (1978) [Pubmed]
  21. Arginine-rich histones do not exchange between human and mouse chromosomes in hybrid cells. Manser, T., Thacher, T., Rechsteiner, M. Cell (1980) [Pubmed]
  22. Stem cell patterning and fate in human epidermis. Jones, P.H., Harper, S., Watt, F.M. Cell (1995) [Pubmed]
  23. Rapid incorporation of label from ribonucleoside disphosphates into DNA by a cell-free high molecular weight fraction from animal cell nuclei. Noguchi, H., Prem veer Reddy, G., Pardee, A.B. Cell (1983) [Pubmed]
  24. Requirement for tyrosine phosphorylation of Cdk4 in G1 arrest induced by ultraviolet irradiation. Terada, Y., Tatsuka, M., Jinno, S., Okayama, H. Nature (1995) [Pubmed]
  25. Interleukin-2-mediated elimination of the p27Kip1 cyclin-dependent kinase inhibitor prevented by rapamycin. Nourse, J., Firpo, E., Flanagan, W.M., Coats, S., Polyak, K., Lee, M.H., Massague, J., Crabtree, G.R., Roberts, J.M. Nature (1994) [Pubmed]
  26. Reversion of the transformed phenotype of B16 mouse melanoma: involvement of an 83 kd cell surface glycoprotein in specific growth inhibition. Wieland, I., Müller, G., Braun, S., Birchmeier, W. Cell (1986) [Pubmed]
  27. Movement and segregation of kinetochores experimentally detached from mammalian chromosomes. Brinkley, B.R., Zinkowski, R.P., Mollon, W.L., Davis, F.M., Pisegna, M.A., Pershouse, M., Rao, P.N. Nature (1988) [Pubmed]
  28. Inhibitor evidence for allosteric interaction in the replitase multienzyme complex. veer Reddy, G.P., Pardee, A.B. Nature (1983) [Pubmed]
  29. Rise and fall of cyclic AMP required for onset of lymphocyte DNA synthesis. Wang, T., Sheppard, J.R., Foker, J.E. Science (1978) [Pubmed]
  30. Two genes differentially regulated in the cell cycle and by DNA-damaging agents encode alternative regulatory subunits of ribonucleotide reductase. Elledge, S.J., Davis, R.W. Genes Dev. (1990) [Pubmed]
  31. DNA polymerase epsilon links the DNA replication machinery to the S phase checkpoint. Navas, T.A., Zhou, Z., Elledge, S.J. Cell (1995) [Pubmed]
  32. An essential G1 function for cyclin-like proteins in yeast. Richardson, H.E., Wittenberg, C., Cross, F., Reed, S.I. Cell (1989) [Pubmed]
  33. A complex of Cdc4p, Skp1p, and Cdc53p/cullin catalyzes ubiquitination of the phosphorylated CDK inhibitor Sic1p. Feldman, R.M., Correll, C.C., Kaplan, K.B., Deshaies, R.J. Cell (1997) [Pubmed]
  34. p19Skp1 and p45Skp2 are essential elements of the cyclin A-CDK2 S phase kinase. Zhang, H., Kobayashi, R., Galaktionov, K., Beach, D. Cell (1995) [Pubmed]
  35. The yeast CDC16 and CDC27 genes restrict DNA replication to once per cell cycle. Heichman, K.A., Roberts, J.M. Cell (1996) [Pubmed]
  36. The E2F1-3 transcription factors are essential for cellular proliferation. Wu, L., Timmers, C., Maiti, B., Saavedra, H.I., Sang, L., Chong, G.T., Nuckolls, F., Giangrande, P., Wright, F.A., Field, S.J., Greenberg, M.E., Orkin, S., Nevins, J.R., Robinson, M.L., Leone, G. Nature (2001) [Pubmed]
  37. The calcimimetic compound NPS R-568 suppresses parathyroid cell proliferation in rats with renal insufficiency. Control of parathyroid cell growth via a calcium receptor. Wada, M., Furuya, Y., Sakiyama, J., Kobayashi, N., Miyata, S., Ishii, H., Nagano, N. J. Clin. Invest. (1997) [Pubmed]
  38. Role of c-fos and E2F in the induction of cyclin A transcription and vascular smooth muscle cell proliferation. Sylvester, A.M., Chen, D., Krasinski, K., Andrés, V. J. Clin. Invest. (1998) [Pubmed]
  39. Proliferating cell nuclear antigen expression in normal, preneoplastic, and neoplastic colonic epithelium of the rat. Yamada, K., Yoshitake, K., Sato, M., Ahnen, D.J. Gastroenterology (1992) [Pubmed]
  40. Existence of two populations of cyclin/proliferating cell nuclear antigen during the cell cycle: association with DNA replication sites. Bravo, R., Macdonald-Bravo, H. J. Cell Biol. (1987) [Pubmed]
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