References and Notes

pinocytosis and podosome disassembly re-mains to be determined. We did not observe major effects on the activation state of Rac or Cdc42 (fig. S6), so it seems likely that addi-tional regulators of actin dynamics are target-ed by the MAP kinases. Inhibition of both ERK and p38 kinases was required to fully block TLR-triggered effects on actin, which suggests that key downstream substrates can be activated by either pathway or that distinct ERK and p38 substrates deliver the effects observed. Because podosomes are continual-ly turning over their actin content, consump-tion of the available actin pool and/or asso-ciated cofactors after a primary stimulation of actin-dependent endocytosis might indirectly result in podosome disassembly. Alternative-ly, separate signals may drive enhanced ruf-fling/pinocytosis and podosome disassembly in DCs, which may nonetheless be interde-pendent through a finite actin pool