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Gene Review

ct  -  curly tail

Mus musculus

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Disease relevance of ct

  • Neural tube defects can be prevented in cultured ct/ct embryos by experimentally correcting either the proliferative imbalance or the ventral curvature [1].
  • BACKGROUND: The curly tail (ct) mutant mouse is one of the best-studied mouse models of spina bifida [2].
  • RESULTS: We report the absence of gross chromosomal abnormalities and the precise mapping of the ct gene to a 3-Mb region at 135 Mb (66 cM) from the centromere, closely linked to the polymorphic microsatellite marker D4Mit148 [2].
 

High impact information on ct

 

Chemical compound and disease context of ct

  • These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway [5].
 

Biological context of ct

 

Anatomical context of ct

  • Five percent of embryos homozygous for the ct gene and 89% of embryos homozygous for the Pax3Sp-d gene develop spina bifida in the lumbosacral region of the neuraxis [8].
  • In ct/ct embryos the average PNP length showed a slight increase between the stage of 23 to 28 somites, indicating a temporary deceleration of closure rate, and the range of PNP sizes increased markedly [9].
  • Quantitation of BrdU uptake revealed that at early stages of neurulation, cell proliferation was specifically reduced in the paraxial mesoderm of all ct/ct embryos compared with wild type controls, but at later stages (more cranial levels) it was increased [10].
  • Chick embryos cultured on a curved substratum show a transient enlargement of the posterior neuropore (PN), mimicking the temporary delay of PN closure as seen in the curly tail (ct) mouse mutant (van Straaten et al. [1993] Development 117:1163-1172) [11].
  • All of the Ts16 (ct/Rb;Rb) fetuses, studied between days 14-19 gestation had tail malformations, 86% of which were tail flexion defects (TFD) apparently very similar to the curly tail phenotype [12].
 

Associations of ct with chemical compounds

  • On control and folate-/choline-deficient diets, ct mice exhibited higher plasma homocysteine levels than control C57Bl/6 mice [13].
  • With higher inositol concentrations, the majority of ct/ct embryos completed head closure normally, and their development was generally similar to that obtained in whole serum [14].
  • Vitamin A increases the penetrance of the ct gene at doses that hardly cause any NTD in A mice [15].
 

Other interactions of ct

  • In addition, our expression data do not provide strong evidence that Grhl-3 is indeed the ct gene [2].
  • The two mutant strains examined, curly tail (ct) and splotch-delayed (Pax3Sp-d), develop an open neural tube for unrelated reasons, and thus provided for a complementary analysis [8].
  • No effect of mct1 was seen in a higher penetrance cross with the BXD-8/Ty strain, confirming that ct is the major gene in the model [16].
  • We have confirmed that ct maps to this region, close to the locus D4Mit69 [17].
  • Finally, we examined Pax7 as a candidate gene for the ct mutation and found no evidence of protein sequence differences in ct compared with wild-type mice [17].
 

Analytical, diagnostic and therapeutic context of ct

  • The curly-tail (ct) mouse, an animal model for NTD, has been suggested to display features that closely resemble the human defect [13].

References

  1. Genetic models of mammalian neural tube defects. Copp, A.J. Ciba Found. Symp. (1994) [Pubmed]
  2. Toward positional cloning of the curly tail gene. Brouns, M.R., Peeters, M.C., Geurts, J.M., Merckx, D.M., Engelen, J.J., Hekking, J.W., Terwindt-Rouwenhorst, E.A., Oosterbaan, M.E., Geraedts, J.P., van Straaten, H.W. Birth defects research. Part A, Clinical and molecular teratology. (2005) [Pubmed]
  3. Multifactorial inheritance of neural tube defects: localization of the major gene and recognition of modifiers in ct mutant mice. Neumann, P.E., Frankel, W.N., Letts, V.A., Coffin, J.M., Copp, A.J., Bernfield, M. Nat. Genet. (1994) [Pubmed]
  4. Inositol- and folate-resistant neural tube defects in mice lacking the epithelial-specific factor Grhl-3. Ting, S.B., Wilanowski, T., Auden, A., Hall, M., Voss, A.K., Thomas, T., Parekh, V., Cunningham, J.M., Jane, S.M. Nat. Med. (2003) [Pubmed]
  5. Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma. Chen, W.H., Morriss-Kay, G.M., Copp, A.J. Development (1995) [Pubmed]
  6. Interaction between splotch (Sp) and curly tail (ct) mouse mutants in the embryonic development of neural tube defects. Estibeiro, J.P., Brook, F.A., Copp, A.J. Development (1993) [Pubmed]
  7. Curvature of the caudal region is responsible for failure of neural tube closure in the curly tail (ct) mouse embryo. Brook, F.A., Shum, A.S., Van Straaten, H.W., Copp, A.J. Development (1991) [Pubmed]
  8. Patterns of neuronal differentiation in neural tube mutant mice: curly tail and Pax3 splotch-delayed. Keller-Peck, C.R., Mullen, R.J. J. Comp. Neurol. (1996) [Pubmed]
  9. Deceleration and acceleration in the rate of posterior neuropore closure during neurulation in the curly tail (ct) mouse embryo. van Straaten, H.W., Hekking, J.W., Copp, A.J., Bernfield, M. Anat. Embryol. (1992) [Pubmed]
  10. Effects of the curly tail genotype on neuroepithelial integrity and cell proliferation during late stages of primary neurulation. Hall, M., Gofflot, F., Iseki, S., Morriss-Kay, G.M. J. Anat. (2001) [Pubmed]
  11. Raphe of the posterior neural tube in the chick embryo: its closure and reopening as studied in living embryos with a high definition light microscope. van Straaten, H.W., Jaskoll, T., Rousseau, A.M., Terwindt-Rouwenhorst, E.A., Greenberg, G., Shankar, K., Melnick, M. Dev. Dyn. (1993) [Pubmed]
  12. The induction of tail malformations in trisomy 16 mouse fetuses heterozygous for the curly tail recessive gene. Crolla, J.A., Lakeman, S.K., Seller, M.J. Genet. Res. (1990) [Pubmed]
  13. The curly-tail (ct) mouse, an animal model of neural tube defects, displays altered homocysteine metabolism without folate responsiveness or a defect in Mthfr. Tran, P., Hiou-Tim, F., Frosst, P., Lussier-Cacan, S., Bagley, P., Selhub, J., Bottiglieri, T., Rozen, R. Mol. Genet. Metab. (2002) [Pubmed]
  14. Inositol deficiency increases the susceptibility to neural tube defects of genetically predisposed (curly tail) mouse embryos in vitro. Cockroft, D.L., Brook, F.A., Copp, A.J. Teratology (1992) [Pubmed]
  15. Differential response of heterozygous curly-tail mouse embryos to vitamin A teratogenesis depending on maternal genotype. Seller, M.J., Perkins, K.J., Adinolfi, M. Teratology (1983) [Pubmed]
  16. A curly-tail modifier locus, mct1, on mouse chromosome 17. Letts, V.A., Schork, N.J., Copp, A.J., Bernfield, M., Frankel, W.N. Genomics (1995) [Pubmed]
  17. Haplotype analysis of intra-specific backcross curly-tail mice confirms the localization of ct to chromosome 4. Beier, D.R., Dushkin, H., Telle, T. Mamm. Genome (1995) [Pubmed]
 
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