Gap junctions were first characterized by electron microscopy as regionally specialized structures on plasma membranes of contacting adherent cells. These structures were shown to consist of cell-to-cell channels. Proteins, called connexins, purified from fractions of enriched gap junctions from different tissues differ. The connexins are designated by their molecular mass.
Johnson et al.(1999) determined that there is expression of gap junctional proteins connexin 43, 32, and 26 throughout follicular development and atresia in cows.
Expression regulated by
Comment
Ovarian localization
Oocyte, Granulosa, Theca
Comment
Johnson et al. (1999) discovered that Cx26 was present in the oocyte of primordial and primary/secondary follicles, and in the granulosa and/or thecal cell layers of healthy antral follicles. The percentage of healthy antral follicles that expressed Cx26 also increased during follicular development, but decreased during atresia. Grazul-Bilska et al.(1998) found that Cx26 was present in the ovarian surface epithelium, stroma, and blood vessels within the stroma and hilus, and in the CL. In healthy antral follicles, Cx26 was present only in the theca layer.
Follicle stages
Primary, Secondary, Antral
Comment
Phenotypes
Mutations
1 mutations
Species: human
Mutation name: None
type: None fertility: None Comment:Kelsell et al. (1997) found a T-to-C substitution in codon 34 (exon 1) of the GJB2 gene. The substitution resulted in a change in codon 34 from ATG (met) to ACG (thr). The M34T mutation segregated with the profound deafness phenotype but not with the skin disorder in the family studied.