H. Nechushtan et al., MICROPHTHALMIA (MI) IN MURINE MAST-CELLS - REGULATION OF ITS STIMULI-MEDIATED EXPRESSION ON THE TRANSLATIONAL LEVEL, Blood, 89(8), 1997, pp. 2999-3008
Mice harboring a mutation in the microphthalmia (mi) gene display a va
riety of abnormalities, including microphthalmia, depletion of skin me
lanocytes, 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, cha
racterization 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 physiolo
gic stimuli. Using a specific rabbit polyclonal anti-mi antibody, we f
ound that interleukin-3, interleukin-C or aggregation of the mast cell
high-affinity receptor for IgE (Fc epsilon RI) induced the synthesis
of mi protein in these cells. None of these stimuli significantly affe
cted 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 b
ound to upstream stimulating factor 2 was detected only in activated m
ast cells. We conclude that the regulation of mi expression is on the
translational level. Thus, stimulation of mast cells by a variety of s
timuli elicits a signaling pathway that regulates mi expression. (C) 1
997 by The American Society of Hematology.