| Summary: | <p>Embryos morphogenesis relies on the interactions between different tissues and their constituent cells. These interactions are controlled by different signalling and adhesion molecules, such as the Fibronectin Leucine-rich Repeat transmembrane (Flrt) family of proteins. The closely related <em>Flrt2</em> and <em>Flrt3</em> share 45% amino acid sequence identity, and show several sites of co-expression in the developing mouse embryo. Experiments in this laboratory have shown that mice deficient in either one of <em>Flrt2</em> or <em>Flrt3</em> are embryonic lethal due to cardiac insufficiency, and structural defect in the AVE and a fusion failure of the lateral body walls of the embryo respectively. The highly conserved structural features shared between <em>Flrt2</em> and <em>Flrt3</em> suggest possible shared functional roles between the two closely related genes. The aims of this study were first to generate a <em>Flrt2</em> and <em>Flrt3</em> double mutant embryos, and examine the hypothesis that the two genes function cooperatively at sites of their co-expression. The second goal was to generate a <em>Flrt2</em> <em>LacZ</em> reporter and a conditional alleles, using the EUCOMM/KOMP resource, to further analyse <em>Flrt2</em> expression patterns and function.</p> <p><em>Flrt2</em> and <em>Flrt3</em> double mutant embryos were embryonic lethal at embryonic day (E) 10. The genetic experiment designed in this study suggests that <em>Flrt3</em> seems to function in cooperation with <em>Flrt2</em>, to maintain tissue integrity in the developing mouse embryo as loss of both exhibits a more severe phenotype than the single mutants, and has a more severe impact on the embryonic development.</p> <p>The Flrt2 LacZ reporter and conditional alleles generated in this study were shown to be useful tools in dissecting Flrt2 expression patterns, and can be used in further experiments to study the expression of Flrt2 in particular sites that have not been studied or extensively mentioned in the literature, or in site-specific deletion of Flrt2 in tissues where Flrt2 is expressed but the function has not been elucidated.</p>
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