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Gene Review

Mos  -  Moloney sarcoma oncogene

Mus musculus

Synonyms: Oocyte maturation factor mos, Proto-oncogene c-Mos, Proto-oncogene serine/threonine-protein kinase mos, c-mos
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Disease relevance of Mos


High impact information on Mos

  • Differential DNA repair in transcriptionally active and inactive proto-oncogenes: c-abl and c-mos [6].
  • Within 24 hr, 85% of the dimers were removed from the 20 kb intragenic BamHl restriction fragment of the expressed c-abl gene, while only 22% of the dimers were removed from the 15 kb EcoRl fragment that spans the transcriptionally inactive c-mos locus [6].
  • DNA repair was examined in the c-abl and c-mos proto-oncogenes in UV-irradiated mouse 3T3 fibroblasts using an optimized assay for measuring pyrimidine dimers in single-copy nucleotide sequences [6].
  • In Xenopus the c-mos proto-oncogene product (Mos) is essential for the initiation of oocyte maturation, for the progression from meiosis I to meiosis II and for the second meiotic metaphase arrest, acting as an essential component of the cytostatic factor CSF [7].
  • The results indicate that in mice Mos plays a role in the second meiotic metaphase arrest, but does not seem to be essential for the initiation of oocyte maturation, spermatogenesis or somatic cell cycle [7].

Chemical compound and disease context of Mos


Biological context of Mos


Anatomical context of Mos

  • Overexpression of Mos, Ras, Src, and Fos inhibits mouse mammary epithelial cell differentiation [14].
  • Because c-kit and c-mos are expressed differentially in male and female day 13-15 germ cells, they may play roles in initiating or mediating progress along the sex-specific pathways of development that PGCs embark upon at this time [15].
  • Mos overexpression in Swiss 3T3 cells induces meiotic-like alterations of the mitotic spindle [16].
  • Mos is required for MAP kinase activation and is involved in microtubule organization during meiotic maturation in the mouse [17].
  • Furthermore, comparison of Mos, Abl and actin RNA expression in mouse and rat testes revealed species-specific variations in the regulation of gene expression [18].

Associations of Mos with chemical compounds

  • This stabilization of c-Fos required Mos-induced phosphorylation of its C-terminal region on Ser362 and Ser374, and double replacements of these serines with acidic (Asp) residues markedly increased the stability and transforming efficiency of c-Fos even in the absence of Mos [10].
  • We investigated the function of the Mos/MAPK pathway during goldfish oocyte maturation induced by 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP), a natural maturation-inducing hormone in fishes [19].
  • The c-mos proto-oncogene encodes a 37-39K cytoplasmic serine/threonine kinase implicated in the meiotic maturation events during murine spermatogenesis and oogenesis [20].
  • Microinjection of chimeric mRNAs in which the coding and 3'-untranslated regions (3'UTR) were exchanged between c-mos and hypoxanthine phosphoribosyltransferase mRNAs revealed that the 3'UTR plays a role in the rapid degradation that occurs after fertilization [21].
  • Here, we report that inhibition of Mos synthesis by morpholino antisense oligonucleotides does not prevent the progesterone-induced initiation of Xenopus oocyte meiotic maturation, as previously thought [22].

Physical interactions of Mos

  • This study investigated the participation of MAPK in the resumption of meiosis [germinal vesicle breakdown (GVB)] in oocytes and cumulus expansion using oocyte-cumulus cell complexes (OCC) from Mos-null mice (Mos(tm1Ev)/Mos(tm1Ev), hereafter Mos(-/-)) [23].
  • MyoD binds to Mos and inhibits the Mos/MAP kinase pathway [24].
  • In the absence of ATP from cell extracts, protein kinase activity of Mos was lost within 6 h on ice even though the Mos protein was not degraded and remained bound to Hsp70 [25].

Enzymatic interactions of Mos


Regulatory relationships of Mos


Other interactions of Mos

  • We show that c-Fos (the c-fos protooncogene product), which is an intrinsically unstable nuclear protein, is metabolically highly stabilized, and greatly enhances the transforming efficiency of NIH 3T3 cells, by Mos [10].
  • These results indicate that c-Fos undergoes stabilization, and mediates at least partly the oncogenic signalling, by the Mos/MEK/ERK pathway [10].
  • Strikingly, Ras, Src, and Mos expression switch Net activity to positive [32].
  • MAPK activity was not detected in Mos(-/-) oocytes whether they matured in vivo or in vitro, with or without gonadotropin stimulation [23].
  • The Mos/mitogen-activated protein kinase (MAPK) pathway regulates the size and degradation of the first polar body in maturing mouse oocytes [33].

Analytical, diagnostic and therapeutic context of Mos


  1. Characterization of activated and normal mouse Mos gene in murine 3T3 cells. Paules, R.S., Resnick, J., Kasenally, A.B., Ernst, M.K., Donovan, P., Vande Woude, G.F. Oncogene (1992) [Pubmed]
  2. Parthenogenetic development of Mos-deficient mouse oocytes. Hirao, Y., Eppig, J.J. Mol. Reprod. Dev. (1997) [Pubmed]
  3. Activation of a cellular oncogene by DNA rearrangement: possible involvement of an IS-like element. Rechavi, G., Givol, D., Canaani, E. Nature (1982) [Pubmed]
  4. Activation of the c-mos oncogene in a mouse plasmacytoma by insertion of an endogenous intracisternal A-particle genome. Canaani, E., Dreazen, O., Klar, A., Rechavi, G., Ram, D., Cohen, J.B., Givol, D. Proc. Natl. Acad. Sci. U.S.A. (1983) [Pubmed]
  5. Functional analysis of sperm from c-mos(-/-) mice. Gross, V.S., Cooper, G.M. Mol. Reprod. Dev. (2002) [Pubmed]
  6. Differential DNA repair in transcriptionally active and inactive proto-oncogenes: c-abl and c-mos. Madhani, H.D., Bohr, V.A., Hanawalt, P.C. Cell (1986) [Pubmed]
  7. Parthenogenetic activation of oocytes in c-mos-deficient mice. Hashimoto, N., Watanabe, N., Furuta, Y., Tamemoto, H., Sagata, N., Yokoyama, M., Okazaki, K., Nagayoshi, M., Takeda, N., Ikawa, Y. Nature (1994) [Pubmed]
  8. Progressive hind limb paralysis in mice carrying a v-Mos transgene. Propst, F., Cork, L.C., Kovatch, R.M., Kasenally, A.B., Wallace, R., Rosenberg, M.P. J. Neuropathol. Exp. Neurol. (1992) [Pubmed]
  9. Suppression of c-mos expression in teratocarcinoma cells with a new type of inducer of differentiation, 3,5-di-tert-butylchalcone 4'-carboxylic acid. Ogiso, Y., Kitagawa, K., Nishino, H., Iwashima, A., Shudo, K. Exp. Cell Res. (1987) [Pubmed]
  10. The Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cells. Okazaki, K., Sagata, N. EMBO J. (1995) [Pubmed]
  11. Chromosomal organization and transcriptional regulation of human GEM and localization of the human and mouse GEM loci encoding an inducible Ras-like protein. Santoro, T., Maguire, J., McBride, O.W., Avraham, K.B., Copeland, N.G., Jenkins, N.A., Kelly, K. Genomics (1995) [Pubmed]
  12. Linkage analysis of the murine mos proto-oncogene on chromosome 4. Dandoy, F., De Maeyer-Guignard, J., De Maeyer, E. Genomics (1989) [Pubmed]
  13. Synthesis and function of Mos: the control switch of vertebrate oocyte meiosis. Gebauer, F., Richter, J.D. Bioessays (1997) [Pubmed]
  14. Overexpression of Mos, Ras, Src, and Fos inhibits mouse mammary epithelial cell differentiation. Jehn, B., Costello, E., Marti, A., Keon, N., Deane, R., Li, F., Friis, R.R., Burri, P.H., Martin, F., Jaggi, R. Mol. Cell. Biol. (1992) [Pubmed]
  15. Changes in protooncogene expression correlated with general and sex-specific differentiation in murine primordial germ cells. Coucouvanis, E.C., Jones, P.P. Mech. Dev. (1993) [Pubmed]
  16. Mos overexpression in Swiss 3T3 cells induces meiotic-like alterations of the mitotic spindle. Fukasawa, K., Vande Woude, G.F. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  17. Mos is required for MAP kinase activation and is involved in microtubule organization during meiotic maturation in the mouse. Verlhac, M.H., Kubiak, J.Z., Weber, M., Géraud, G., Colledge, W.H., Evans, M.J., Maro, B. Development (1996) [Pubmed]
  18. Genetic analysis and developmental regulation of testis-specific RNA expression of Mos, Abl, actin and Hox-1.4. Propst, F., Rosenberg, M.P., Oskarsson, M.K., Russell, L.B., Nguyen-Huu, M.C., Nadeau, J., Jenkins, N.A., Copeland, N.G., Vande Woude, G.F. Oncogene (1988) [Pubmed]
  19. The Mos/MAPK pathway is involved in metaphase II arrest as a cytostatic factor but is neither necessary nor sufficient for initiating oocyte maturation in goldfish. Kajiura-Kobayashi, H., Yoshida, N., Sagata, N., Yamashita, M., Nagahama, Y. Dev. Genes Evol. (2000) [Pubmed]
  20. Disruption of c-mos causes parthenogenetic development of unfertilized mouse eggs. Colledge, W.H., Carlton, M.B., Udy, G.B., Evans, M.J. Nature (1994) [Pubmed]
  21. Degradation of maternal mRNA in mouse embryos: selective degradation of specific mRNAs after fertilization. Alizadeh, Z., Kageyama, S., Aoki, F. Mol. Reprod. Dev. (2005) [Pubmed]
  22. Mos is not required for the initiation of meiotic maturation in Xenopus oocytes. Dupré, A., Jessus, C., Ozon, R., Haccard, O. EMBO J. (2002) [Pubmed]
  23. Mitogen-activated protein kinase activity in cumulus cells is essential for gonadotropin-induced oocyte meiotic resumption and cumulus expansion in the mouse. Su, Y.Q., Wigglesworth, K., Pendola, F.L., O'Brien, M.J., Eppig, J.J. Endocrinology (2002) [Pubmed]
  24. MyoD binds to Mos and inhibits the Mos/MAP kinase pathway. Solhonne, B., Lenormand, J.L., Pelpel, K., Leibovitch, M.P., Leibovitch, S.A. FEBS Lett. (1999) [Pubmed]
  25. Evidence of an interaction between Mos and Hsp70: a role of the Mos residue serine 3 in mediating Hsp70 association. Liu, H., Vuyyuru, V.B., Pham, C.D., Yang, Y., Singh, B. Oncogene (1999) [Pubmed]
  26. Mutation of MyoD-Ser237 abolishes its up-regulation by c-Mos. Pelpel, K., Leibovitch, M., Fernandez, A., Leibovitch, S.A. FEBS Lett. (2000) [Pubmed]
  27. Specific interference with gene function by double-stranded RNA in early mouse development. Wianny, F., Zernicka-Goetz, M. Nat. Cell Biol. (2000) [Pubmed]
  28. Characterization of MEK1 phosphorylation by the v-Mos protein. Pham, C.D., Arlinghaus, R.B., Zheng, C.F., Guan, K.L., Singh, B. Oncogene (1995) [Pubmed]
  29. Direct relationship between the expression of tumor suppressor H19 mRNA and c-mos proto-oncogene during myogenesis. Leibovitch, M.P., Solhonne, B., Guillier, M., Verrelle, P., Leibovitch, S.A., Verelle P [corrected to Verrelle, P. Oncogene (1995) [Pubmed]
  30. Mos activates myogenic differentiation by promoting heterodimerization of MyoD and E12 proteins. Lenormand, J.L., Benayoun, B., Guillier, M., Vandromme, M., Leibovitch, M.P., Leibovitch, S.A. Mol. Cell. Biol. (1997) [Pubmed]
  31. A binding site for germ cell nuclear factor within c-mos regulatory sequences. Zilz, A., Cooper, G.M. Mol. Reprod. Dev. (2004) [Pubmed]
  32. Net, a new ets transcription factor that is activated by Ras. Giovane, A., Pintzas, A., Maira, S.M., Sobieszczuk, P., Wasylyk, B. Genes Dev. (1994) [Pubmed]
  33. The Mos/mitogen-activated protein kinase (MAPK) pathway regulates the size and degradation of the first polar body in maturing mouse oocytes. Choi, T., Fukasawa, K., Zhou, R., Tessarollo, L., Borror, K., Resau, J., Vande Woude, G.F. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  34. Analysis of the mechanism(s) of metaphase I arrest in strain LT mouse oocytes: participation of MOS. Hirao, Y., Eppig, J.J. Development (1997) [Pubmed]
  35. The Mos proto-oncogene maps near the centromere on mouse chromosome 4. Propst, F., Vande Woude, G.F., Jenkins, N.A., Copeland, N.G., Lee, B.K., Hunt, P.A., Eicher, E.M. Genomics (1989) [Pubmed]
  36. Further characterization of the c-mos transcript and its cell cycle specific expression in NIH3T3 cells. Gao, C., Arlinghaus, R.B., Singh, B. Oncogene (1996) [Pubmed]
  37. Differential expression of the proto-oncogenes c-abl and c-mos in developing mouse germ cells. Iwaoki, Y., Matsuda, H., Mutter, G.L., Watrin, F., Wolgemuth, D.J. Exp. Cell Res. (1993) [Pubmed]
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