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Abstract In addition to regulating the actin cytoskeleton, Cofilin also senses and responds to environmental stress. Cofilin can promote cell survival or death depending on context. Yet, many aspects of Cofilin’s role in survival need clarification. Here, we show that exposing earlyDrosophilaembryos to mild heat stress (32°C) induces a Cofilin-mediated Actin Stress Response and upregulation of heat- and ER-stress response genes. However, these responses do not alleviate the negative impacts of heat exposure. Instead, heat stressed embryos show downregulation of hundreds of developmental genes, including determinants of the embryonic body plan, and are less likely to hatch as larvae and adults. Remarkably, reducing Cofilin dosage blunts induction of all stress response pathways, mitigates downregulation of developmental genes, and completely rescues survival. Thus, Cofilin intersects with multiple stress response pathways, and modulates the transcriptomic response to heat stress. Strikingly, Cofilin knockdown emerges as a potent pro-survival manipulation for embryos. 

Significance Viral dormancy, in which the infected cell is not killed but rather becomes the long-term residence of the parasite, is a hallmark of viruses across kingdoms from bacteriophages to HIV. When and how viruses decide to opt for this lifestyle remains mysterious. Phage lambda, which serves as a paradigm for viral dormancy, is reported to count the number of coinfecting viruses and then uses this value to assess the abundance of potential hosts and decide whether to become dormant. Here, we use a single-cell measurement of viruses and messenger RNA together with mathematical modeling to illuminate how lambda performs this task.