title: Gap junctional intercellular communication in the mouse ovarian follicle.
abstract: A targeted disruption of the gene encoding the gap junction protein connexin37 (Cx37; alpha 4) results in female infertility. Mutant follicles are not observed to develop beyond early antral stages, and there is a lack of both observable mature Graafian follicles and ovulation. The oocytes are unable to acquire meiotic competence. Following oocyte failure, the residual follicular cells do not undergo atresia but rather transdifferentiate into luteal cells, resulting in a mutant ovary populated with numerous, inappropriate corpora lutea. These results indicate that the Cx37-containing gap junctions formed between oocyte and follicular cells permit bidirectional signalling between the two cell types. These junctions are required for oocyte growth and development during preantral stages of the follicle, and for the inhibition of follicle cell luteinization. An additional role for these junctions may be to permit transfer of cytoplasmic signals required to hold oocytes in meiotic arrest. Since the mutant follicles never acquire meiotic competence, this latter role for gap junctional communication cannot be tested in this model.
authors: Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
authors: D A
authors: DA
authors: Goodenough
authors: A M
authors: AM
authors: Simon
authors: D L
authors: DL
authors: Paul
mesh_terms: D000818:Animals; D002450:Cell Communication / Q000502:physiology*; D017630:Connexins / Q000235:genetics; D005260:Female; D017629:Gap Junctions / Q000502:physiology*; D018390:Gene Targeting; D006107:Granulosa Cells / Q000502:physiology; D008540:Meiosis; D051379:Mice; D009865:Oocytes / Q000502:physiology; D010053:Ovary / Q000166:cytology / Q000502:physiology*; D015398:Signal Transduction; D000097006:Gap Junction alpha-4 Protein
chemical_list: D017630:Connexins; D000097006:Gap Junction alpha-4 Protein