First published online September 5, 2008
Development 135, 1905e (2008)
© The Company of Biologists Limited
LH frees oocytes from meiotic arrest
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.

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Related articles in Development:
- Luteinizing hormone causes MAP kinase-dependent phosphorylation and closure of connexin 43 gap junctions in mouse ovarian follicles: one of two paths to meiotic resumption
- Rachael P. Norris, Marina Freudzon, Lisa M. Mehlmann, Ann E. Cowan, Alexander M. Simon, David L. Paul, Paul D. Lampe, and Laurinda A. Jaffe
Development 2008 135: 3229-3238.
[Abstract]
[Full Text]