ArticleMammalian genome : official journal of the International Mammalian Genome Society1992
The same genomic region is disrupted in two transgene-induced limb deformity alleles.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 25 citations in OpenAlex.
- Genetic cold cases: lessons from solving complex congenital limb disorders.Genes & development · 2023Review
- Efficient mapping of transgene integration sites and local structural changes in Cre transgenic mice using targeted locus amplification.Nucleic acids research · 2017Article
- Formin1 disruption confers oligodactylism and alters Bmp signaling.Human molecular genetics · 2009Article
- Mouse limb deformity mutations disrupt a global control region within the large regulatory landscape required for Gremlin expression.Genes & development · 2004Article
- The role of a single formin isoform in the limb and renal phenotypes of limb deformity.Molecular medicine (Cambridge, Mass.) · 1997Article
- Insertional mutagenesis in transgenic mice.Transgenic research · 1994Review
- Formins: phosphoprotein isoforms encoded by the mouse limb deformity locus.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Mutations of the mouse limb deformity locus, ld, map to Chromosome (Chr) 2 and result in defects in the morphogenesis and patterning of the limb and kidney. Complementation studies have defined the existence of five recessive ld alleles. Remarkably, two of these, ldTgHd and ldTgBri, are transgene-induced mutations. Recovery of the first transgene insertional allele, ldTgHd, facilitated the molecular cloning of a large (greater than 200 kb) candidate gene at the ld locus. This gene is broadly transcribed and encodes a set of novel protein isoforms, termed formins. Here we present characterization of the ldTgBri mutation that supports the molecular identification of the ld gene. We show that the ldTgBri fails to complement both the ldTgHd and the ldOR alleles and that it has undergone a genomic deletion that disrupts the cloned ld gene and its transcripts. Curiously, the ldTgBri deletion encompasses the same 11-kb interval in which the ldTgHd insertion occurred and in which a chromosomal rearrangement has been identified in a third allele, ldIn2. These findings suggest that this region of the ld gene is a preferential site for illegitimate recombination.
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