Linkage mapping of a mouse gene, iv, that controls left-right asymmetry of the heart and viscera.

AUTOR(ES)

Brueckner, M

RESUMO

Inherited single gene defects have been identified in both humans and mice that lead to loss of developmental control over the left-right asymmetry of the heart and viscera. In mice the recessively inherited mutation iv leads to such apparent loss of control over situs: 50% of iv/iv mice exhibit situs inversus and 50% exhibit normal situs. The affected gene product has not been identified in these animals. To study the normal function of iv, we have taken an approach directed to the gene itself. As a first step, we have mapped iv genetically, by examining its segregation in backcrosses with respect to markers defined by restriction fragment length polymorphisms. The iv locus lies 3 centimorgans (cM) from the immunoglobulin heavy-chain constant-region gene complex (Igh-C) on chromosome 12. A multilocus map of the region suggests the gene order centromere-Aat (alpha 1-antitrypsin gene complex)-(11 cM)-iv-(3 cM)-Igh-C-(1 cM)-Igh-V (immunoglobulin heavy-chain variable-region gene complex).

Documentos Relacionados

• Defects in the determination of left-right asymmetry.
• Nodal activity in the node governs left-right asymmetry
• Mapping and explaining the use of the left-right divide
• Fluid-dynamical basis of the embryonic development of left-right asymmetry in vertebrates
• Notch signaling regulates left–right asymmetry determination by inducing Nodal expression