First Author | Ashley PL | Year | 1987 |
Journal | J Biol Chem | Volume | 262 |
Issue | 31 | Pages | 15299-301 |
PubMed ID | 3117797 | Mgi Jnum | J:8888 |
Mgi Id | MGI:57353 | Doi | 10.1016/s0021-9258(18)48174-4 |
Citation | Ashley PL, et al. (1987) Chromosomal assignment of the murine Gi alpha and Gs alpha genes. Implications for the obese mouse. J Biol Chem 262(31):15299-301 |
abstractText | The G protein family of transmembrane signaling molecules includes Gs and Gi, the stimulatory and inhibitory regulators of adenylate cyclase. These and other characterized G proteins are comprised of beta, gamma, and alpha chains, the latter being the most variable among the proteins and thus serving to distinguish them. Previous results (Begin-Heick, N. (1985) J. Biol. Chem. 260, 6187-6193) suggested that the autosomal recessive mouse mutation obese (ob), which results in an abnormal response of adipose tissue to lipolytic hormones, is due to a defect in the gene coding for the alpha chain of Gi. In order to test this hypothesis we used a cloned cDNA probe representing murine Gi alpha mRNA in conjunction with a panel of Chinese hamster-mouse somatic cell hybrids segregating mouse chromosomes to map the Gi alpha gene in the mouse. In addition, we used a cDNA probe representing the murine Gs alpha gene to a specific mouse chromosome. Our results indicate that the Gi alpha locus maps to mouse chromosome 9, while Gs alpha is localized to region 2E1-2H3 of mouse chromosome 2. Localization of the Gi alpha gene to chromosome 9 excludes this gene as a site of the ob mutation, since the ob locus maps to chromosome 6. Furthermore, our findings indicate that certain members of the murine G protein alpha gene family have dispersed to different chromosomes since diverging from a common ancestral gene. |