Animal development is a generally continuous process that is robust to delays arising from internal or external perturbations. Now, Chen-Hui Chen and colleagues use a forward genetic screen to identify a temperature-sensitive mutation, called pan, able to suspend development in zebrafish. When grown at restrictive temperature, 4-week-old juvenile pan mutants exhibit significantly slowed growth, which can be restored even after 8 weeks of treatment without a noticeable effect on adult fitness. The authors determine that pan mutants have a 25 amino acid C-terminal deletion in the putative RNA helicase ddx52. Deletion mutants of ddx52 exhibit developmental defects and are not able to complement the pan mutation. Interestingly, depletion of the Drosophiladdx52 ortholog, CG5589, prevents the larva-to-adult transition, arguing for a conserved role of this helicase in growth regulation. The authors further show that mutation of zebrafish ddx52 significantly decreases the levels of 47S pre-rRNA, leading to a reduction in transcription. Interestingly, inhibiting global transcription in zebrafish or mice with the transcriptional inhibitor actinomycin D leads to a juvenile growth delay similar to that observed in ddx52 mutants. Taken together, these results suggest that transcriptional stalling, as induced by ddx52 mutation or by actinomycin D treatment, could be a conserved mechanism leading to a reversible growth delay in a variety of vertebrates.