Human Marfan and Marfan-like Syndrome associated mutations lead to altered trafficking of the Type II TGFβ receptor in Caenorhabditis elegans - Fig 2

A. Schematic overview of the transgenic construct to determine the functionality of the type II TGFβ receptors bearing MFS-like mutations. The SL2 splice leader makes it possible for the one-to-one expression of the DAF-4 and NLS-tdTomato-NLS cassette. This allows quantification of the levels of transcription from the hypodermal specific promoter elt-3. B., C. Hypodermal specific transgenic expression of type II TGFβ receptors bearing either the LTA → A substitutions or the MFS-like mutations are capable of increasing body length in wild-type animals (B), or partially rescuing the body size of daf-4(e1364) mutant animals (C). K338R is a substitution mutation that generates a kinase-dead receptor. Graph shows the mean body lengths values +/- S.E.M. Statistical comparisons were performed using a One-way ANOVA with Dunnett’s correction for multiple comparisons against wild-type or daf-4(e1364) strains. These data suggest that MFS-like mutations do not abrogate receptor function. A minimum of 30 animals were measured for each genotype.