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- W8205054 abstract "The mouse Steel locus is involved in a crucial step of the early development of three important stem cell types: skin melanocytes, erythropoietic stem cells, and primordial germ cells. Homozygotes of the more severe alleles are typically white with black eyes, sterile, and suffer from a severe macrocytic anemia which often results in the death of affected animals in utero, or shortly after birth (Sarvella and Russell, 1956). The effects of SI mutations can first be detected during the period when the three stem cell populations begin to migrate from their distinct sites of origin to colonize specific target tissues, within which their proliferation and further differentiation will be completed. In SI homozygotes, the migrating cells apparently do not reach their targets in sufficient numbers to allow continued normal development (Bennett, 1956). The stem cells themselves are not defective, and can develop normally when placed into the proper wild type environment (McCulloch et al, 1965; Mayer, 1973); instead it is the tissues with which the stem cells interact as they proliferate and differentiate, during migration and beyond, that are responsible for expression of the mutant phenotype. Although no simple plan for the isolation of SI coding sequences can be currently envisioned, the extensive genetic analysis of the locus makes it a good candidate for the application of recently developed “reverse genetic” approaches. Toward the goal of the isolation and analysis of DNA sequences at SI, we have initiated such a molecular approach, beginning with the mapping of the locus relative to closely linked markers, and the directed movement from the markers toward the gene using chromosome jumping (Poustka and Lehrach, 1986) and related techniques." @default.
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- W8205054 date "1988-01-01" @default.
- W8205054 modified "2023-09-27" @default.
- W8205054 title "Approaching the Mouse Steel Locus from Closely Linked Molecular Markers" @default.
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- W8205054 doi "https://doi.org/10.1007/978-3-642-50059-6_8" @default.
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