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Determination of Reproductive Competence by Confirming Pubertal Onset and Performing a Fertility Assay in Mice and Rats
Published on: October 13, 2018
Female infertility in mice lacking connexin 37
A M Simon1, D A Goodenough, E Li
1Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Connexin 37 is crucial for ovarian follicle development and ovulation. Mice lacking connexin 37 show arrested oocyte development and impaired ovulation, highlighting the importance of cell-cell communication.
Area of Science:
- Reproductive Biology
- Cellular Signaling
- Developmental Biology
Background:
- Ovarian follicle development involves complex cell-cell communication.
- Gap junctions, formed by connexins, facilitate intercellular signaling.
- The specific role of connexins in oogenesis and ovulation is not fully understood.
Purpose of the Study:
- To investigate the role of connexin 37 in ovarian follicle development and ovulation.
- To determine the impact of connexin 37 deficiency on oocyte maturation and follicular growth.
Main Methods:
- Utilized connexin 37-deficient mice models.
- Examined ovarian follicle morphology and oocyte development.
- Assessed ovulation rates and corpus luteum formation.
Main Results:
- Connexin 37 is present in gap junctions between oocytes and granulosa cells.
- Connexin 37-deficient mice lack mature Graafian follicles and fail to ovulate.
- Oocyte development arrests before meiotic competence is achieved in deficient mice.
- Inappropriate corpora lutea develop in connexin 37-deficient ovaries.
Conclusions:
- Cell-cell signaling via gap junctions, specifically involving connexin 37, is critical for oogenesis.
- Connexin 37 is essential for the coordinated cellular interactions required for follicular development and ovulation.
- Disruption of connexin 37 function leads to severe reproductive defects.
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