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. Author manuscript; available in PMC: 2018 Dec 15.
Published in final edited form as: J Immunol. 2017 Nov 10;199(12):4036–4045. doi: 10.4049/jimmunol.1700460

FIGURE 6. Patient mutation in ARPC1B fails to rescue developmental anomalies resulting from Arpc1b knockdown.

FIGURE 6

A, Overexpression of human WT but not mutant ARPC1B mRNA (150pg) partially rescued the thrombocyte development in 3.5dpf Tg(CD41:EGFP) embryos (lateral view, red rectangles) treated with arpc1b-i3e4 MO (Arpc1b). The numbers refer to the fractions of embryos exhibiting the depicted phenotypes. B, Quantitation of EGFP+ cell numbers in the CHT region as depicted in the red boxes of Fig. 6A as the mean of five embryos of each phenotype. T bar indicates the standard deviation. C, Overexpression ARPC1B in arpc1b morphant embryos using heat-shock inducible plasmids (150pg) encoding WT or mutant human ARPC1B. Developing T cells were identified by performing WISH analysis at 5dpf for using a probe for lck (blue circles, lateral view). The numbers refer to the fractions of embryos exhibiting the depicted phenotypes.