We detected pERK in both the cytoplasm and nucleus at 24 h p.i. but by 48 h p.i., the majority of pERK was concentrated in the nucleus (Figure 2), leading us to originally hypothesize that substrate activation might be skewed towards nuclear targets at later times p.i. Instead, we found phosphorylation of bothnuclear and cytoplasmic substrates following infection, suggesting persistent ERK activation in both cellular compartments. This evidence concerns the gene MAPK1 and infection.