Meiosis in mammalian oocytes pauses in prophase until luteinizing hormone(LH) releases this arrest. One suggestion is that LH does this by closing the gap junctions between the somatic cells that surround the oocyte, thus blocking the transmission of a meiosis-inhibitory signal to oocytes. Now,Norris and co-workers show that LH-induced MAP kinase-dependent gap junction phosphorylation and closure is one of two paths to meiotic resumption in mouse ovarian follicles (see p. 3229). By monitoring the diffusion of fluorescent tracers in intact follicles, the researchers show for the first time that LH decreases the permeability of connexin 43-containing gap junctions between the somatic cells before nuclear envelope breakdown (NEBD; the start of the prophase-metaphase transition) occurs in oocytes. MAP kinase-dependent phosphorylation of connexin 43 causes this decreased permeability, they report. However,surprisingly, inhibition of MAP kinase activation does not prevent NEBD. Thus,they suggest, another pathway functions in parallel to MAP kinase-dependent gap junction closure to trigger meiosis resumption in response to LH.