An annotated catalogue of the mutant genes of the house mouse / H. Grüneberg.

  • Grüneberg, H. (Hans)
Date:
1956
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: An annotated catalogue of the mutant genes of the house mouse / H. Grüneberg. Source: Wellcome Collection.

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    12 MUTANT GENES OF THE HOUSE MOUSE In all three mutants, a normal baby fur is formed; this is shed during the third and fourth week so that the animals are then almost completely naked. The shedding starts on the head and, in 'hairless', proceeds in a sharply defined wave in a posterior direction; in 'rhino', the hair loss is usually more difíuse, and 'bald' (Garber, 1952a) is intermediate in this respect. Later hair generations are shed almost as soon as they are formed; they become increasingly feeble so that the animals are practically naked throughout their lives. In older animals the skin becsmes progressively thickened by the formation of cysts from hair roots and sebaceous glands; this process is comparatively slight in 'hairless', more marked in 'bald', and very extreme in 'rhino' where it leads to the formation of enormous skin folds. In all three mutants the claws become long and spiralized; whether this is due to overgrowth or to reduced wear and tear is not certain. 38. Hypotrichosis hypokeratotica* {Naked, N; VI) Heterozygotes for this semi-dominant gene (N/+) grow a baby fur which is, however, not so sleek as that of normal mice. During the second and third week the hairs break off above the skin level, except at the nose, feet, tail, and genital region, the process starting on the head and spreading in a posterior direction. Later hair generations, which become increasingly irregular, share the same fate, but Л''/+ mice usually show more or less irregular patches of hair belong¬ ing to different hair generations simultaneously, and thus usually do not look as bare as 'hairless' mice (No. 37). The claws are not affected. iV/iV homozygotes never grow a complete coat and lack the sensory hairs. The claws are under¬ developed and abnormal in structure. The anomaUes of iV/+ and N/N are due to a dyskeratosis or hypokeratosis. 39. Hypotrichosis juvenilis* (hj) A recessive condition in which anomalies are confined to the baby fur while the adult coat is completely normal. This gene is now extinct. 40. Pituitary dwarfism* {dw) This much-studied recessive condition is basically due to reduction or absence of eosinophil cells in the anterior lobe of the pituitary. Virtually all the other endocrine organs are secondarily involved to a greater or less extent. 'Pituitary dwarfs' react to parabiosis with a normal mouse, to implantation of normal pituitaries and to the administration of various endocrine preparations. 41. Obese {ob) This recessive condition (Ingalls, Dickie and Snell, 1950) has given rise to an extensive American literature, some of which has been summarized (Mayer, 1953; Mayer, Russell, Bates and Dickie, 1953). 'Obese' animals become inordinately fat, with weights of two or three times the normal. Both sexes are sterile. Obesity is associated with hyperglycaemia, glycosuria, increased resistance to insulin, and hyperplasia of the islands of Langerhans. The blood cholesterol is high. The basal metaboHc rate is very low. The basic biochemical lesion of the obese animals seems to be a slowing down of the rate of oxidation of acetate to carbon dioxide and water. Whether this metabolic block is primarily enzymatic or hormonal is not yet clear. 42. Absence of the corpus callosum* {ac) Mice with this recessive anomaly lack the corpus callosum completely or in part, but have a tract of fibres (longitudinal callosal bundle) in the brain which does not occur in normal mice. Clinically, the animals are completely normal. The condition is now extinct.