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. 2000 Aug;11(8):2743–2756. doi: 10.1091/mbc.11.8.2743

Figure 4.

Figure 4

Redundancy of unc-101 and apm-1 during embryogenesis. Lethal phenotypes caused by RNAi of unc-101, apm-1, ς1, β1, or γ. (A) F1 progeny from a wild-type animal injected with unc-101 double-strand RNA. About half of the animals arrested at various stages of development, and this specific figure shows an animal arrested at the L1 stage. (B) F1 progeny from a wild-type animal injected with apm-1 double-strand RNA. All the animals arrested as L1 larvae, and the anterior intestine was bloated, suggesting that, although pharyngeal pumping was not affected, the bacterial stream was blocked due to some malfunction or structural defect in the intestine. L1 animals arrested by apm-1 RNAi have a slightly different posture when they arrest. This is because they can move and feed on bacteria for a short period of time before suddenly stopping. On the other hand, arrested L1 animals of unc-101 mutants hardly move, if at all, and arrest in a straight posture. (C) F1 progeny from an unc-101(sy108) animal injected with apm-1 double-strand RNA. All the animals arrested as embryos, as shown in this figure. (D) F1 progeny from an N2 animal injected with ς1 double-strand RNA. (E) F1 animal from a wild-type animal injected with β1 double-strand RNA. (F) F1 animal from a wild-type animal injected with γ double-strand RNA. As can be easily noticed in (C-F), the phenotypes caused by double RNAi of both apm-1 and unc-101 are identical to those caused by single RNAi of ς1, β1, or γ chain gene. The scale bar is 10 μm.