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. 2013 Feb 19;110(10):E918–E927. doi: 10.1073/pnas.1300769110

Fig. 2.

Fig. 2.

wrm-1 suppresses the EMS spindle orientation defect of wnt; src double mutants. (A) Model depicting the rotation of EMS mitotic spindle to a-p orientation (black double-headed arrow) from the default l-r orientation (red double-headed arrow) in response to P2/EMS signal. In P2/EMS signaling mutants, EMS mitotic spindle fails to rotate, and induction of E cell fate does not occur. (B) Schematic representation of the EMS mitotic spindle orientation categories (A, B, and C) analyzed in C. A/P denotes a-p axis. L/R denotes l-r axis. Details on the scoring method are in Materials and Methods. (C) Stacked bar graphs show the percentage of EMS cells exhibiting each mitotic spindle orientation category depicted in B in various genetic backgrounds shown. RNAi treatments or presence of mutant alleles are specified by +. For mom-2, + in red indicates the existence of mom-2(ne834ts) allele, and mom-2(RNAi) treatment is shown with black +. In double RNAi knockdown experiments, src-1 knockdown was always confirmed first by checking the phenotype of src-1(RNAi) dead embryos before the animals were subjected to wrm-1 or mom-2 (RNAi). N, number of embryos scored.