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Genome imprinting phenomena on mouse chromosome 7
1Medical Research Council, Radiobiology Unit, Chilton, Didcot, Oxon.
Genetical Research
|October 1, 1990
Summary
Genetic imprinting on mouse chromosome 7 affects development. Maternal duplication/paternal deficiency for chromosome 7 regions causes developmental issues, unlike paternal duplication/maternal deficiency, suggesting imprinted gene regions.
Area of Science:
- Genetics
- Developmental Biology
- Mammalian Genetics
Background:
- Genetic imprinting, where gene expression depends on parental origin, is crucial for mammalian development.
- Mouse chromosome 7 is homologous to human chromosomal regions associated with developmental disorders.
Purpose of the Study:
- To investigate genetic complementation and imprinting effects on mouse chromosome 7 using reciprocal translocations and genetic markers.
- To identify regions on chromosome 7 exhibiting parent-of-origin-specific lethality or developmental abnormalities.
Main Methods:
- Intercrossing heterozygotes for the reciprocal translocation T(7;15)9H.
- Utilizing albino (c) and underwhite (uw) genetic markers on mouse chromosome 7 and 15.
- Analyzing fetal and neonatal development in offspring from reciprocal crosses with different parental genotypes.
Main Results:
- Maternal duplication/paternal deficiency for distal chromosome 7 resulted in retarded albino fetuses with small placentae.
- Paternal duplication/maternal deficiency for distal chromosome 7 led to earlier lethality, with no albino fetuses observed.
- Similar imprinting effects were observed for the proximal marker (uw) on chromosome 7, indicating distinct imprinted regions.
Conclusions:
- Mouse chromosome 7 harbors at least two regions with defective genetic complementation, likely due to imprinting.
- These imprinted regions are located distal to the T(7;18)50H breakpoint (7E2-F2) and between the centromere and 7B3.
- Homologous regions on human chromosomes may harbor loci for Beckwith-Weidemann syndrome, dystrophia myotonia, and rhabdomyosarcoma, suggesting conserved imprinting mechanisms.
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