Interleukin-3 (IL-3) poor-responsive inbred mouse strains carry the
identical deletion of a branch point in the IL-3 receptor alpha subunit
gene
T Hara, M Ichihara, M Takagi and A Miyajima
Department of Cell Biology, DNAX Research Institute of Molecular and
Cellular Biology, Palo Alto, CA 94304, USA.
Interleukin-3 (IL-3) stimulates colony formation of multiple lineages of
hematopoietic cells. Bone marrow cells of A/J mice are nonresponsive to
IL-3, and this observation has recently been correlated with aberrant mRNA
splicing and impaired expression of the IL-3 receptor alpha subunit (IL-3R
alpha), a binding component of the high-affinity receptors. We examined the
IL-3R alpha gene in 27 inbred mouse strains and found the identical
mutation, a 5-bp deletion at the branch point of intron 7, in 10 of these
mouse strains. Bone marrow cells isolated from these 10 mouse strains did
not express IL-3R alpha on the cell surface and did not form colonies in
response to IL-3. Because the defective IL-3R alpha gene was found in
several distantly related mouse strains, it appears to be a recessive
allele rather than a sporadic mutation. In contrast, only 1 of 21
wild-derived mouse strains carried the 5-bp deletion in the IL-3R alpha
gene. This study suggests that IL- 3 function is not required for normal
hematopoiesis in mice, but the retention of the IL-3 and IL-3R system may
be of some selective advantage in wild populations.
Volume 85,
Issue 9,
pp. 2331-2336,
05/01/1995
Copyright © 1995 by The American Society of Hematology
