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Microphthalmia (mi) in murine mast cells: regulation of its stimuli-
mediated expression on the translational level
H Nechushtan, Z Zhang and E Razin
Department of Biochemistry, Hebrew University-Hadassah Medical School,
Jerusalem, Israel.
Mice harboring a mutation in the microphthalmia (mi) gene display a variety
of abnormalities, including microphthalmia, depletion of skin melanocytes,
deafness, a defect in osteoclasts, and a major decrease in mast cell number
and function. However, despite the possible critical role played by this
protein in mast cell development and function, characterization of its mRNA
and protein synthesis in these cells has not yet been performed. In this
study, we investigated the regulation of the synthesis of mi in murine mast
cells activated by various physiologic stimuli. Using a specific rabbit
polyclonal anti-mi antibody, we found that interleukin-3, interleukin-4, or
aggregation of the mast cell high-affinity receptor for IgE (Fc epsilonRI)
induced the synthesis of mi protein in these cells. None of these stimuli
significantly affected the level of mi mRNA in the mast cells at any of the
time points tested. Also, using this specific anti-mi antibody, an increase
in mi protein synthesis was shown during differentiation of mast cells from
their bone marrow cell precursors. Moreover, a complex containing mi bound
to upstream stimulating factor 2 was detected only in activated mast cells.
We conclude that the regulation of mi expression is on the translational
level. Thus, stimulation of mast cells by a variety of stimuli elicits a
signaling pathway that regulates mi expression.
Volume 89,
Issue 8,
pp. 2999-3008,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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