The probable answer to this question is no. Much of the current eviden
ce summarised elsewhere in this issue points to nuclear Ca2+ changes c
hanging in response to cytosolic Ca2+ with little evidence for an inde
pendently controlled nuclear Ca2+ homeostasis. There are InsP(3) recep
tors in the nuclear membrane, and it is possible that during nuclear m
embrane assembly the InsP(3) acting on these (Sullivan and Wilson, thi
s issue) is formed by an inositide cycle located on the assembling nuc
lear skeleton. But our current experimental data suggest that when the
nucleus is intact, InsP(3) generated by this cycle would have to exit
through the nuclear pores to act on any known InsP(3) receptors. Thus
the nuclear inositide cycle appears more likely to serve to generate
diacylglycerol to activate protein kinase C, and/or to generate inosit
ol phosphates such as InsP(2), which may have distinct intranuclear fu
nctions.