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PubMed1983

Analysis of the hematopoietic effects of new dominant spotting (W) mutations of the mouse. II. Effects on mast cell development.

In addition to their anemia, sterility and lack of coat pigment (1,2), W/Wv mice are mast cell deficient (3,4). Our analysis of three recently described W alleles (5) confirms reports (3,6) that (a) W mutations alter skin mast cell number in parallel with their influence on red cell number (but not with pigmentation), (b) that mast cells arise from hematopoietic tissue (7) and (c) that injections of normal bone marrow cells, which cure the anemias of W/Wv recipients, also alleviate the deficiency of skin mast cells in these mice. Transplants of bone marrow cells from mice homozygous for two new anemia-causing W alleles, W39 and W41, fail to cure the anemias of W/Wv recipients (companion paper) or increase the number of mast cells in their skin. Marrow cell implants from non-anemic W44/W44 mice cure the anemia, but do not change the number of mast cells in the skin of W/Wv recipients. The fact that the bone marrows of all three new homozygotes have fewer than normal numbers of CFUs hematopoietic stem cells (see companion paper) and have reduced mast cell-regenerating capacities, supports Kitamura's contention (8) that mast cell precursors may be closely related to or identical with the CFUs.

Alleles↗

PubMed1981

Analysis of pleiotropism at the dominant white-spotting (W) locus of the house mouse: a description of ten new W alleles.

Characterization of the pleiotropic effects of ten new putative W locus mutations, nine co-isogenic and one highly congenic with the C57BL/6J strain, reveals a wide variety of influences upon pigmentation, blood formation and gametogenesis. None of the putative alleles, each of which is closely linked to Ph, a gene 0.1 cM from W, gave evidence of complementation with W39, a new allele previously shown to be allelic to Wv. All W/W39 genotypes resulted in black-eyed-white anemics with reduced gametogenic activity. Homozygotes for seven of these mutations are lethal during perinatal life; anemic embryos have been identified in litters produced by intercross matings involving each of these alleles.--Phenotypes of mice of several mutant genotypes provide exceptions to the frequent observation that a double dose of dominant W alleles (e.g., W/Wv or W/W) results in defects of corresponding severity in each of the three affected tissues. One viable homozygote has little or no defect in blood formation, and another appears to have normal fertility. The phenotypes of these homozygotes support the conclusion that the three tissue defects are not dependent on each other for their appearance and probably do not result from a single physiological disturbance during the development of the embryo.--Although homozygosity for members of this series results in a wide range of phenotypes, the absence of complementation of any allele with W39, the close proximity of each mutant to Ph, and the fact that all alleles produce detectable (though sometimes marginal) defects in the same tissues affected by W and Wv, support the hypothesis that each new mutant gene is a W allele.

Alleles↗