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Gene Review

Nf1  -  Neurofibromin 1

Drosophila melanogaster

Synonyms: CG8318, Dmel\CG8318, NF-1, NF1, Nf-1, ...
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Disease relevance of Nf1


Psychiatry related information on Nf1


High impact information on Nf1

  • A new study suggests that manipulating the expression of a Drosophila melanogaster neurofibromatosis-1 ortholog affects organismal lifespan through protein kinase A-mediated regulation of mitochondrial respiration and reactive oxygen species production [7].
  • The tumour-suppressor gene Neurofibromatosis 1 (Nf1) encodes a Ras-specific GTPase activating protein (Ras-GAP) [5].
  • Mitogen-activated protein kinase (MAPK) activity is increased in Nf1 mutants, and the circadian phenotype is rescued by loss-of-function mutations in the Ras/MAPK pathway [6].
  • The human neurofibromatosis type 1 (NF1) tumor suppressor protein functions as a Ras-specific guanosine triphosphatase-activating protein, but the identity of Ras- mediated pathways modulated by NF1 remains unknown [8].
  • Loss of NF1 resulted in a reduction in size of larvae, pupae, and adults [9].

Biological context of Nf1

  • However, most Drosophila NF1 mutant phenotypes, including an overall growth deficiency, are not readily modified by manipulating Ras signaling strength, but are rescued by increasing signaling through the cAMP-dependent protein kinase A pathway [10].
  • The neurofibromatosis type 1 (NF1) tumor suppressor protein is thought to restrict cell proliferation by functioning as a Ras-specific guanosine triphosphatase-activating protein [9].
  • Functional analysis of the neurofibromatosis type 2 protein by means of disease-causing point mutations [11].
  • This finding implies a function for merlin in regulating cell-matrix attachment, and changes in cell adhesion caused by mutant protein expression may be an initial step in the pathogenesis of NF2 [11].
  • Our data demonstrate both stage and parent-of-origin specific changes in methylation patterns within the neurofibromatosis type 1 coding region-involving cytosines located at both CpG and non-CpG dinucleotides [12].

Anatomical context of Nf1


Associations of Nf1 with chemical compounds

  • In other Drosophila systems, push and NF1 are required for signaling pathways mediated by Amn or the pituitary adenylate cyclase activator peptide [1].
  • As is the case for NF2 tumors, Drosophila cells lacking Merlin function overproliferate relative to their neighbors [3].

Other interactions of Nf1


Analytical, diagnostic and therapeutic context of Nf1

  • Neurofibromatosis type 1: II. Answers from animal models [16].
  • Northern blot analysis has shown that the human neurofibromatosis type 2 (NF2) cDNA hybridizes to multiple RNA species [4].
  • To examine whether these hybridizing RNA species represent NF2 transcripts, we cloned the complete NF2 cDNA by a combination of techniques: 5' and 3' rapid amplification of cDNA ends, RT-PCR, and searching and sequencing the NF2-related cDNA clones from the IMAGE consortium [4].


  1. Control of Drosophila perineurial glial growth by interacting neurotransmitter-mediated signaling pathways. Yager, J., Richards, S., Hekmat-Scafe, D.S., Hurd, D.D., Sundaresan, V., Caprette, D.R., Saxton, W.M., Carlson, J.R., Stern, M. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  2. Phosphatidylinositol 3-kinase and Akt nonautonomously promote perineurial glial growth in Drosophila peripheral nerves. Lavery, W., Hall, V., Yager, J.C., Rottgers, A., Wells, M.C., Stern, M. J. Neurosci. (2007) [Pubmed]
  3. Structural analysis of Drosophila merlin reveals functional domains important for growth control and subcellular localization. LaJeunesse, D.R., McCartney, B.M., Fehon, R.G. J. Cell Biol. (1998) [Pubmed]
  4. Multiple transcription initiation sites, alternative splicing, and differential polyadenylation contribute to the complexity of human neurofibromatosis 2 transcripts. Chang, L.S., Akhmametyeva, E.M., Wu, Y., Zhu, L., Welling, D.B. Genomics (2002) [Pubmed]
  5. A neurofibromatosis-1-regulated pathway is required for learning in Drosophila. Guo, H.F., Tong, J., Hannan, F., Luo, L., Zhong, Y. Nature (2000) [Pubmed]
  6. A circadian output in Drosophila mediated by neurofibromatosis-1 and Ras/MAPK. Williams, J.A., Su, H.S., Bernards, A., Field, J., Sehgal, A. Science (2001) [Pubmed]
  7. Drosophila melanogaster neurofibromatosis-1: ROS, not Ras? Walker, J.A., Bernards, A. Nat. Genet. (2007) [Pubmed]
  8. Requirement of Drosophila NF1 for activation of adenylyl cyclase by PACAP38-like neuropeptides. Guo, H.F., The, I., Hannan, F., Bernards, A., Zhong, Y. Science (1997) [Pubmed]
  9. Rescue of a Drosophila NF1 mutant phenotype by protein kinase A. The, I., Hannigan, G.E., Cowley, G.S., Reginald, S., Zhong, Y., Gusella, J.F., Hariharan, I.K., Bernards, A. Science (1997) [Pubmed]
  10. Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons. Walker, J.A., Tchoudakova, A.V., McKenney, P.T., Brill, S., Wu, D., Cowley, G.S., Hariharan, I.K., Bernards, A. Genes Dev. (2006) [Pubmed]
  11. Functional analysis of the neurofibromatosis type 2 protein by means of disease-causing point mutations. Stokowski, R.P., Cox, D.R. Am. J. Hum. Genet. (2000) [Pubmed]
  12. Allele-specific non-CpG methylation of the Nf1 gene during early mouse development. Haines, T.R., Rodenhiser, D.I., Ainsworth, P.J. Dev. Biol. (2001) [Pubmed]
  13. PDF receptor signaling in Drosophila contributes to both circadian and geotactic behaviors. Mertens, I., Vandingenen, A., Johnson, E.C., Shafer, O.T., Li, W., Trigg, J.S., De Loof, A., Schoofs, L., Taghert, P.H. Neuron (2005) [Pubmed]
  14. Evolution and origin of merlin, the product of the Neurofibromatosis type 2 (NF2) tumor-suppressor gene. Golovnina, K., Blinov, A., Akhmametyeva, E.M., Omelyanchuk, L.V., Chang, L.S. BMC Evol. Biol. (2005) [Pubmed]
  15. The lethal prune/Killer-of-prune interaction of Drosophila causes a syndrome resembling human neurofibromatosis (NF1). Hackstein, J.H. Eur. J. Cell Biol. (1992) [Pubmed]
  16. Neurofibromatosis type 1: II. Answers from animal models. Lakkis, M.M., Tennekoon, G.I. J. Neurosci. Res. (2001) [Pubmed]
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