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Gene Review

Gdf1  -  growth differentiation factor 1

Mus musculus

Synonyms: AI385651, Embryonic growth/differentiation factor 1, GDF-1, Gdf-1
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Disease relevance of Gdf1

  • Gdf1-/- mice exhibited a spectrum of defects related to left-right axis formation, including visceral situs inversus, right pulmonary isomerism and a range of cardiac anomalies [1].

High impact information on Gdf1

  • Growth/differentiation factor-1 (Gdf-1, encoded by Gdf1) is a TGF-beta family member of unknown function that was originally isolated from an early mouse embryo cDNA library and is expressed specifically in the nervous systemin late-stage embryos and adult mice [1].
  • Our findings suggest that Gdf1 acts early in the pathway of gene activation that leads to the establishment of left-right asymmetry [1].
  • We report that Vg1 and GDF1 signaling in zebrafish also depends on EGF-CFC proteins, but not on Nodal signals [2].
  • To understand further the mechanism of regulation of ceramide synthesis, we now characterize a mammalian homolog of LAG1, upstream of growth and differentiation factor-1 (uog1). cDNA clones of uog1 were obtained from expression sequence-tagged clones and sub-cloned into a mammalian expression vector [3].
  • UOG1 was localized to the endoplasmic reticulum, demonstrating that the fatty acid selectivity and the fumonisin B(1) resistance are not due to a subcellular localization different from that found previously for ceramide synthase activity [3].

Biological context of Gdf1

  • Growth differentiation factor (GDF15) is a distant member of the transforming growth factor-beta superfamily, a diverse group of structurally related proteins that exert multiple effects on cell fate such as on cell growth and differentiation but little is known about GDF15 in these processes [4].
  • Transient transfection of human embryonic kidney 293T cells with uog1 followed by metabolic labeling with [4,5-(3)H]sphinganine or L-3-[(3)H]serine demonstrated that uog1 conferred fumonisin B(1) resistance with respect to the ability of the cells to continue to produce ceramide [3].

Anatomical context of Gdf1

  • Gdf1 is expressed uniformly throughout the embryonic region at 5.5-6.5 days postcoitum and later in the node, midbrain, spinal cord, paraxial mesoderm, lateral plate mesoderm, and limb bud [5].
  • Gdf1-/-;Nodal+/- mutants displayed several abnormalities that were not present in either Gdf1-/- or Nodal+/- single mutants, including absence of notochord and prechordal plate, and malformation of the foregut; organizing centers implicated in the development of the anterior head and branchial arches, respectively [6].
  • Unlike that in the lateral plate mesoderm, Nodal expression in the node was independent of GDF-1, indicating that both factors act in parallel to control the development of mesendodermal precursors [6].
  • These results indicate that GDF-1 and Nodal converge on ALK4 in the anterior primitive streak to control the formation of organizing centers that are necessary for normal forebrain and branchial arch development [6].
  • The absence of these defects in single mutants indicated a synergistic interaction between Nodal and GDF-1 in the node, from which the axial mesendoderm that gives rise to the notochord, prechordal plate, and foregut endoderm originates, and where the two factors are co-expressed [6].

Associations of Gdf1 with chemical compounds


Other interactions of Gdf1

  • Mesendoderm induction and reversal of left-right pattern by mouse Gdf1, a Vg1-related gene [5].
  • In contrast, a chimeric protein containing the prodomain of Xenopus BMP2 fused to the GDF1 mature domain is efficiently processed and signals via Smad2 to induce mesendoderm and axial duplication [5].
  • In contrast to the BMPs, OP-1 upregulated significantly the six GDF members examined (GDF-1, -3, -5, -6, -8, and -9) by three- to four-fold [8].
  • GDF-1 and -3 mRNA expression increased throughout the chondrogenic process, and GDF-5, -6, -8, and -9 mRNA expressions were not changed [8].
  • From postnatal day 21, GDF-1 expression is strong in the hippocampus, cortex, and thalamic nuclei, while GDF-10 expression becomes restricted to the granule cell layer in the dentate gyrus [9].


  1. Regulation of left-right patterning in mice by growth/differentiation factor-1. Rankin, C.T., Bunton, T., Lawler, A.M., Lee, S.J. Nat. Genet. (2000) [Pubmed]
  2. EGF-CFC proteins are essential coreceptors for the TGF-beta signals Vg1 and GDF1. Cheng, S.K., Olale, F., Bennett, J.T., Brivanlou, A.H., Schier, A.F. Genes Dev. (2003) [Pubmed]
  3. Upstream of growth and differentiation factor 1 (uog1), a mammalian homolog of the yeast longevity assurance gene 1 (LAG1), regulates N-stearoyl-sphinganine (C18-(dihydro)ceramide) synthesis in a fumonisin B1-independent manner in mammalian cells. Venkataraman, K., Riebeling, C., Bodennec, J., Riezman, H., Allegood, J.C., Sullards, M.C., Merrill, A.H., Futerman, A.H. J. Biol. Chem. (2002) [Pubmed]
  4. Dynamics of expression of growth differentiation factor 15 in normal and PIN development in the mouse. Noorali, S., Kurita, T., Woolcock, B., de Algara, T.R., Lo, M., Paralkar, V., Hoodless, P., Vielkind, J. Differentiation (2007) [Pubmed]
  5. Mesendoderm induction and reversal of left-right pattern by mouse Gdf1, a Vg1-related gene. Wall, N.A., Craig, E.J., Labosky, P.A., Kessler, D.S. Dev. Biol. (2000) [Pubmed]
  6. Synergistic interaction between Gdf1 and Nodal during anterior axis development. Andersson, O., Reissmann, E., Jörnvall, H., Ibáñez, C.F. Dev. Biol. (2006) [Pubmed]
  7. In vivo treatment with GDF-9 stimulates primordial and primary follicle progression and theca cell marker CYP17 in ovaries of immature rats. Vitt, U.A., McGee, E.A., Hayashi, M., Hsueh, A.J. Endocrinology (2000) [Pubmed]
  8. Differential effects of osteogenic protein-1 (BMP-7) on gene expression of BMP and GDF family members during differentiation of the mouse MC615 chondrocyte cells. Yeh, L.C., Mallein-Gerin, F., Lee, J.C. J. Cell. Physiol. (2002) [Pubmed]
  9. Localized expression of BMP and GDF mRNA in the rodent brain. Söderström, S., Ebendal, T. J. Neurosci. Res. (1999) [Pubmed]
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