Smad2 role in mesoderm formation, left-right patterning and craniofacial development

Article Abstract:

Smad2 function plays a key role in early development and in several patterning processes in mice, according to research in which gene targeting was used to generate two independent Smad2 mutant alleles in mice. Smad2 has been found to act in a dosage-sensitive manner during mouse development. Lack of Smad2 blocks the formation of the primitive streak and mesoderm. Smad4 links with Smad1 in response to bone morphogenetic protein and with Smad2 in response to activin in the induction of ventral and dorsal mesoderm respectively.

Abnormalities, Mammals, Mesoderm, Skull

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Female infertility in mice lacking connexin 37

Article Abstract:

The mechanisms of ovarian follicle development were analyzed by immunocytochemistry in the oocyte-granulosa cell gap junctions of frozen murine ovaries. Immunocytochemistry with murine oocyte gap junctions indicated the presence of connexin-37 which mediated junctional communication between oocytes and granulosa cells. Oocytes of connexin-37-deficient mice exhibited impaired ovulatory capabilities and oogenesis due to the absence of oocyte-granulosa junctional communication.

Physiological aspects, Cell interaction, Cell interactions, Junctional complexes (Epithelium), Mice as laboratory animals, House mouse, Oocytes, Oocyte donation, Oogenesis, Ovulation

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Connexin mutations in deafness

Article Abstract:

Genetic research shows that mutant connexin 26 gene expression produces proteins which prevent wild-type connexin 26 channel function activity. Experiments designed to assess genetic characteristics in Cx26 mutant M34T and W77R genes are described. Evidence suggests that M34T genetic mutation prevents hearing through the inhibition of wild-type Cx26 channels.

Gene mutations, Gene mutation, Genetic aspects, Hearing

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