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Exposure to smoke is required for the germination of seeds from dormant genotypes of Nicotiana attenuata, a post-fire annual of the Great Basin Desert. Germination can be elicited by GA(1,3,4,7) treatments and inhibited by the GA biosynthesis inhibitor, paclobutrazol (PAC), abscisic acid (ABA) and terpenes leached from unburned litter of the plant’s natural habitat. We analysed the endogenous GA and ABA dynamics during the 22 h after imbibition, when smoke-treated dormant seeds commit to germination. Extractable GA(1+3) pools decreased in all seeds, but the decrease was more dramatic within 2 h of smoke exposure, which was followed by an increase between hours 2 and 4. Extractable ABA pools increased shortly after imbibition and remained stable in control, water-treated seeds, but decreased sharply in smoke-treated seeds. PAC completely inhibited smoke-induced germination when seeds were treated for 12 h after smoke exposure, consistent with the requirement of de novo GA synthesis for germination. Smoke treatment in the dark did not result in germination, whereas GA(3) treatment did, a result consistent with phytochrome-mediated GA biosynthesis. Smoke exposure dramatically increased the sensitivity of seeds to exogenous GA(3) treatments in both the light and dark, and light exposure increased this sensitivity an additional tenfold. Taken together, these results suggest that while germination requires endogenous GA synthesis, the effects of smoke treatment increase GA sensitivity, which is correlated with a decrease in endogenous ABA pools.