Genome imprinting phenomena on mouse chromosome 7
- 1 October 1990
- journal article
- research article
- Published by Hindawi Limited in Genetics Research
- Vol. 56 (2-3), 237-244
- https://doi.org/10.1017/s0016672300035333
Abstract
Summary: 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 wasc/cand the other wild type yielded albino progeny at birth although about 17% would be expected, but albino foetuses were recovered when the mother wasc/cand 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 wasc/cand mother wild type, which suggested earlier lethality. Equivalent crosses withuw(chromosome 15) as proximal marker gave normal underwhite progeny when the mother wasuw/uwbut 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.This publication has 22 references indexed in Scilit:
- Genomic imprinting: normal complementation of murine chromosome 16Genetics Research, 1989
- Report of the nomenclature committee and the 1989 catalog of mapped genes (Part 1 of 3)Cytogenetic and Genome Research, 1989
- The Wiedemann‐Beckwith syndrome: Pedigree studies on five families with evidence for autosomal dominant inheritance with variable expressivityAmerican Journal of Medical Genetics, 1986
- A male-sterile insertion in the mouseCytogenetic and Genome Research, 1983
- Factors affecting the observed number of young resulting from adjacent-2 disjunction in mice carrying a translocationGenetics Research, 1977
- Congenital myotonic dystrophy in Britain. II. Genetic basis.Archives of Disease in Childhood, 1975
- Position effect variegation in the mouseGenetics Research, 1974
- AUTOSOMAL-DOMINANT SEX-DEPENDENT TRANSMISSION OF THE WIEDEMANN-BECKWITH SYNDROMEThe Lancet, 1974
- Meiotic disjunction in mouse translocations and the determination of centromere positionGenetics Research, 1971
- Definition of functional units in a small chromosomal segment of the mouse and its use in interpreting the nature of radiation-induced mutationsMutation Research, 1971