International Mammalian Genome Society

logo18th International Mouse Genome Conference

17-22 October 2004, Seattle, USA


Tabeta K, Du X, Sovath S, Mudd S, Beutler B

The Scripps Research Institute, La Jolla, United States

Using ENU, we have produced a novel recessive mutation on the C57BL/6 background, associated with an inducible defect of hind limb movement. The mutation was named seal because homozygotes appeared to “waddle” like seals on land.  For a time, transmissibility of seal appeared sporadic.  However, it was eventually realized that homozygous animals show normal locomotion and cage activities if undisturbed, but demonstrate hind limb paralysis after being picked up for examination by grasping the loose skin over the nape of the neck.  Once triggered in this manner, paralysis persists for about 8 days before the hind legs regain function.  However, most of the mice still show a partial residual “seal-like” deficit. About 50% of seal homozygotes also have swollen heels and foot pads.  This lesion is normally unilateral.  Moreover, seal homozygotes seem to be very sensitive to environmental changes, and appear anxious, as exemplified by vigorous tail trembling and self-confinement to corners when a cage is opened. The seal phenotype is fully penetrant on the C57BL/6 and C3H/HeN x C57BL/6 hybrid backgrounds.  The mutation has been mapped to mouse chromosome 11 using a panel of microsatellite markers and at present, has been confined to a 0.7 Mbp critical region on 1300 meioses. Further characterization of phenotype and responsible gene will be presented.

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