Heterozygotes for the reciprocal translocation T(7;15)9H were intercrossed, with albino (c) and underwhite (uw) as genetic markers, in order to study genetic complementation in mouse chromosome 7. Chromosome 15 is known to show normal complementation. Neither reciprocal cross in which one parent was c/c and the other wild type yielded albino progeny at birth although about 17% would be expected, but albino foetuses were recovered when the mother was c/c and father wild type. These products of maternal duplication/paternal deficiency for distal 7 were markedly retarded with small placentae. No albino foetuses were found when the father was c/c and mother wild type, which suggested earlier lethality. Equivalent crosses with uw (chromosome 15) as proximal marker gave normal underwhite progeny when the mother was uw/uw but small placentae, retardation and neonatal death of presumptive underwhites in the reciprocal cross. These abnormal newborn would have had a maternal duplication/paternal deficiency for proximal 7. These and other findings indicate that one region of defective complementation probably lies distal to the breakpoint of T(7;18)50H at 7E2-F2, while another is between the centromere and 7B3. Examination of man-mouse homologies suggests that the loci for three pathological human conditions (Beckwith-Weidemann syndrome, dystrophia myotonia and rhabdomyosarcoma) with differential parental transmission may be located in homologous regions to those affected by imprinting phenomena on mouse chromosome 7.

Animals↗

PubMedDate not supplied

Chromosome 18 of the house mouse.

Evidence is presented that places LG XV on chromosome 18 and shows that the centromere is at the Tw end of the chromosome. The linear order and distances of the three marker genes on Chr 18 are shown to be centromere--10--Tw--14--bc--11--sy. They occupy a total genetic length of 35 cM. The positions of the breakpoints of the two reciprocal translocations T(10;18) 18H and T(7;18) 5OH are discussed and shown to be closely linked to the sy locus.

Animals↗

PubMedDate not supplied

Brown and rust mutants of the Syrian hamster are p and b genes of mammalian coat colors.

The mutant genes of the Syrian hamster, which were originally designated as brown (b) and rust (r), are shown by morphological and phenotypic criteria, as well as by linkage studies in the case of brown, to be homologous with pink-eyed dilution (p) and brown (b), respectively, two well established loci in the genetics of mammalian pigmentation. It is proposed that the two mutants be appropriately redesignated.

Animals↗