Disease relevance of Slit3

• Congenital diaphragmatic hernia, kidney agenesis and cardiac defects associated with Slit3-deficiency in mice [1].

High impact information on Slit3

• In Slit3 null mice, the central tendon region of the diaphragm fails to separate from liver tissue because of abnormalities in morphogenesis [2].
• In vitro assays show that Slit1-Slit3 chemorepel VNO axons, suggesting that basal axons are guided to the posterior AOB due to chemorepulsive activity of Slits in the anterior AOB [3].
• Robo-2 is expressed in mesenchymal cells immediately adjacent to large airways, whereas Slit-3 expression predominates in mesenchyme remote from airway epithelium [4].
• The hearts of Slit3-deficient mice have an enlarged right ventricle [1].
• We created a Slit3-deficient mouse model from an OmniBank ES cell line with a Slit3 allele trapped by insertional mutagenesis to analyze the in vivo functions of this protein [1].

Anatomical context of Slit3

• Slit-3 and Robo-2 expression is restricted to specific, complementary subsets of mesenchyme [4].
• Immunohistochemistry demonstrates Slit-2 and Slit-3 expression by the pulmonary mesenchyme and airway epithelium [5].

Regulatory relationships of Slit3

• Slit2 was expressed at the tips of the UT and both Slit2 and Slit3 were expressed at the far proximal end of the comma shaped and S-shaped bodies [6].

Other interactions of Slit3

• We now demonstrate that Slit-2 and Slit-3 are developmentally regulated in embryonic murine lung [5].

Analytical, diagnostic and therapeutic context of Slit3

• Slit3-deficient mice represent a genetic animal model for physiological and pathological studies of congenital diaphragmatic hernia [1].

References