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Fig. 2 | BMC Developmental Biology

Fig. 2

From: Role of PRY-1/Axin in heterochronic miRNA-mediated seam cell development

Fig. 2

pry-1 mutants display seam cell defects in C. elegans and C. briggsae. Mutations in pry-1 lead to somatic defects. (a) Cuticle is weaker as demonstrated by the cuticle break assay. (b, c) pry-1 mutants having defective alae formation. (b) Control N2 animals have distinct rows of alae. pry-1(mu38) mutants have defect with frequent breaks (see arrow). (c) Quantification of alae defect in control N2 and pry-1(mu38) animals. (d-f) Heterochronic phenotypes in C. briggsae AF16 and Cbr-pry-1 mutants. (d) Alae defects are visible in Cbr-pry-1(sy5353). (e, f) Seam cells in control AF16 (e) and Cbr-pry-1(sy5353) (f) are visualized by adherens-junction-associated marker Cel-dlg-1p::GFP. Cbr-pry-1(sy5353) animals show defects in cell fusion (scale bar 0.1 mm). Boxed areas, marked by dotted lines, have been enlarged in the second row. Scale bars in b, d-f are 0.01 mm. (g) Both the pry-1(mu38) and pry-1(gk3682) animals show increased seam cell numbers compared to control N2 (scale bar 0.1 mm). (h) Each control animal has exactly 16 seam cells, whereas an average of 21 and 19 cells are found in pry-1(mu38) and pry-1(gk3682) mutants, respectively. (i) pry-1(mu38) animals show increased seam cell number by the end of the L2 stage. In panels a, h, and i, each data point represents the mean of at least two replicates (each batch with 30 or more worms) and error bar represents the STD. Student’s t-test was used to determine the statistical significance: *p < 0.05

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