Fig. 7. Maternal XLPA₁ is required in vivo for modulating actin assembly in early Xenopus development. (A) Injection of 10 ng of an antisense phosphorothioate oligodeoxynucleotide (LPA₁-10MP) into oocytes caused a reduction in XLPA₁ mRNA to 16% of control levels after fertilization. At the beginning of gastrulation (stage 10), this reduction was one-third of control levels. (B) Bases from embryos depleted of maternal XLPA₁ healed more slowly than controls. Scale bar: 280 µm. (C) Animal caps from depleted embryos (middle) showed decreased levels of F-actin in the animal cap and in the purse-string after wounding. These caps were larger than controls (left) due to slower wound-healing. The effects of the oligo were rescued by injecting X. tropicalis XLPA₁ mRNA back into fertilized eggs that had been depleted of XLPA₁ (right). This demonstrates that the effects are specific to depletion of XLPA₁. Scale bars: 50 µm. (D) High-magnification image of the cortical actin network in control (left) and XLPA₁-depleted caps (right) after 10 minutes of healing. The density of actin filaments is greatly reduced in the depleted caps compared with controls. Scale bars: 10 µm. (E) Depletion of the maternal stores of XLPA₁ does not lead to long-term developmental defects. Embryos were able to gastrulate (left) and develop to tail-bud stages (right). Control embryos are red and XLPA₁ depleted are brown. Scale bars: 350 µm (left) and 750 µm (right).