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Gene Review

lgl  -  legless

Mus musculus

 
 
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Disease relevance of lgl

 

High impact information on lgl

  • Hindlimbs were uniformly truncated at the distal end of the femur, resulting in a "legless" appearance [3].
  • Consistent with this, complementation tests confirm allelism of lgl and iv and suggest that the transgene insertion may have disrupted more than one gene [4].
  • Phylogenetically conserved sequences flanking the transgene insertions were identified and used to isolate candidate lgl and iv cDNAs [4].
  • In this report we describe the developmental expression and function of Sp8, a member of the Sp family of zinc finger transcription factors, and provide evidence that the legless transgene insertional mutant is a hypomorphic allele of the Sp8 gene [5].
  • The resulting left-right phenotype, randomization of laterality, is identical to that of iv and lgl mutants [6].
 

Biological context of lgl

 

Anatomical context of lgl

  • In lgl, the expression of these genes is initiated but not maintained and the disto-ventral marginal ectoderm does not thicken [8].
  • The limb mesenchyme of lgl and non-mutant embryos initially expresses lmx-1b and fgf-10 uniformly [8].
  • Correlation of forelimb malformation asymmetries with visceral organ situs in the transgenic mouse insertional mutation, legless [9].
  • The control of asymmetry in visceral development appears to be random in the legless mutant; that is, 50% develop normally (situs solitus) and 50% develop with inverted viscera (situs inversus) [9].
 

Associations of lgl with chemical compounds

 

Other interactions of lgl

  • In legless, a mouse mutant exhibiting both limb and left/right patterning defects, Gja1 transcripts could not be detected in this region [11].

References

  1. Mutation of an axonemal dynein affects left-right asymmetry in inversus viscerum mice. Supp, D.M., Witte, D.P., Potter, S.S., Brueckner, M. Nature (1997) [Pubmed]
  2. Enhanced expression of limb malformations and axial skeleton alterations in legless mutants by transplacental exposure to retinoic acid. Scott, W.J., Collins, M.D., Ernst, A.N., Supp, D.M., Potter, S.S. Dev. Biol. (1994) [Pubmed]
  3. Legless, a novel mutation found in PHT1-1 transgenic mice. McNeish, J.D., Scott, W.J., Potter, S.S. Science (1988) [Pubmed]
  4. legless insertional mutation: morphological, molecular, and genetic characterization. Singh, G., Supp, D.M., Schreiner, C., McNeish, J., Merker, H.J., Copeland, N.G., Jenkins, N.A., Potter, S.S., Scott, W. Genes Dev. (1991) [Pubmed]
  5. Sp8 is crucial for limb outgrowth and neuropore closure. Bell, S.M., Schreiner, C.M., Waclaw, R.R., Campbell, K., Potter, S.S., Scott, W.J. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  6. Targeted deletion of the ATP binding domain of left-right dynein confirms its role in specifying development of left-right asymmetries. Supp, D.M., Brueckner, M., Kuehn, M.R., Witte, D.P., Lowe, L.A., McGrath, J., Corrales, J., Potter, S.S. Development (1999) [Pubmed]
  7. The Jagged2 gene maps to chromosome 12 and is a candidate for the lgl and sm mutations. Lan, Y., Jiang, R., Shawber, C., Weinmaster, G., Gridley, T. Mamm. Genome (1997) [Pubmed]
  8. The loss of ventral ectoderm identity correlates with the inability to form an AER in the legless hindlimb bud. Bell, S.M., Schreiner, C.M., Scott, W.J. Mech. Dev. (1998) [Pubmed]
  9. Correlation of forelimb malformation asymmetries with visceral organ situs in the transgenic mouse insertional mutation, legless. Schreiner, C.M., Scott, W.J., Supp, D.M., Potter, S.S. Dev. Biol. (1993) [Pubmed]
  10. Exacerbation of limb malformations in legless (lgl) homozygotes by retinoic acid (RA). Scott, W.J., Collins, M.D., Ernst, A.N., Supp, D.M., Potter, S.S. Prog. Clin. Biol. Res. (1993) [Pubmed]
  11. Developmental regulation and asymmetric expression of the gene encoding Cx43 gap junctions in the mouse limb bud. Meyer, R.A., Cohen, M.F., Recalde, S., Zakany, J., Bell, S.M., Scott, W.J., Lo, C.W. Dev. Genet. (1997) [Pubmed]
 
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