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A clonal marker induced by mutation in mouse intestinal epithelium
D J Winton1, M A Blount, B A Ponder
1Section of Human Cancer Genetics, Institute of Cancer Research, Haddow Laboratories, Sutton, Surrey, UK.
Nature
|June 2, 1988
Summary
Researchers developed a novel cellular marker in mice by inducing a mutation at the Dlb-1 locus. This marker enables tracking of individual somatic cells and their clonal descendants in the intestinal epithelium, aiding lineage studies.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Investigating cell lineages and clonal organization in developing and renewing tissues requires cellular markers for individual somatic cells and their clonal descendants.
- Such markers are established in Drosophila but largely absent in mammalian tissues, except for specific cases like mutant melanocytes.
Purpose of the Study:
- To develop a mutation-induced cellular marker in mice for studying clonal organization and cell lineages.
- To demonstrate the utility of this marker in tracking clonal descendants during development and in adult tissues.
Main Methods:
- Induced a mutation at the Dlb-1 locus in mice heterozygous for the mutation.
- Utilized the mutation to create a marker based on altered expression of binding sites for Dolichos biflorus agglutinin (DBA) lectin in the intestinal epithelium.
- Applied the marker to study clonal organization in adult intestinal epithelium and trace developing clones.
Main Results:
- Successfully developed a mutation-induced marker in the intestinal epithelium of heterozygous mice.
- Demonstrated that the Dlb-1 locus marker can effectively track clonal organization in adult intestinal epithelium.
- Showed the marker's capability to identify descendant clones that arise during embryonic development.
Conclusions:
- A novel, mutation-induced cellular marker has been established for mammalian intestinal epithelium.
- This marker provides a valuable tool for investigating clonal dynamics during development and in adult tissues.
- The principle can be extended to other heterozygous markers, including those from transgenic animals.