The morphology and development of ragged— a mutant affecting the skin and hair of the house mouse II. Genetics, Embryology and Gross Juvenile Morphology
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Ra + mice were normally viable. In the original stock allRaRa mice died before birth or at birth, showing generalized oedema. Later a selected substock provided some viableRaRa mice, although the mortality rate both before and after birth was still above normal.
- 2. (a)
Embryological studies in the unselected stock proved that about 40% ofRaRa mice died as embryos.
RaRa embryos exhibited varying grades of oedema; those embryos with high-grade oedema were probably selectively liable to die.
Ra+ embryos could be classified from 16 1/2 days’ gestation by the retardation of sinus hair growth.RaRa embryos were identified from 13 1/2 days onwards by the occurrence of oedema and retardation of the development of sinus hairs and their follicles.
Phenotypic continuity for the + +,Ra+ andRaRa genotypes was observed from their identification as embryos until after birth. NeonatalRa + mice had shorter than normal sinus hairs, and the pre-weanmg development of pelage hairs was slower than normal. All neonatalRaRa mice showed very retarded sinus hair growth; in viableRaRa mice there was no visible pelage hair growth, at least up to the age of 2 weeks.RaRa mice were significantly heavier than normal at birth, but the survivors were significantly lighter than normal at weaning.
There were no gross anomalies in the blood ofRa + orRaRa mice.
After discussion it was concluded that:
Hair-growth retardation was a fundamental aspect of the ragged syndrome.
Among the many possible causes of oedema inRaRa mice, the two most likely were: (i) partial heart failure, or (ii) endocrine abnormality.
The cause of death, when it occurred inRaRa mice, was probably heart failure and/or pulmonary oedema.
KeywordsHair Follicle Neonatal Mouse Generalize Oedema Ragged Gene Dead Embryo
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