Summary Legumes establish symbioses with rhizobia by forming nitrogen‐fixing nodules. Nitrate is a major environmental factor that affects symbiotic functioning. However, the molecular mechanism of nitrate‐induced nodule senescence is poorly understood. Comparative transcriptomic analysis reveals an NAC‐type transcription factor in Lotus japonicus, LjNAC094, that acts as a positive regulator in nitrate‐induced nodule senescence. Stable overexpression and mutant lines of NAC094 were constructed and used for phenotypic characterization. DNA‐affinity purification sequencing was performed to identify NAC094 targeting genes and results were confirmed by electrophoretic mobility shift and transactivation assays. Overexpression of NAC094 induces premature nodule senescence. Knocking out NAC094 partially relieves nitrate‐induced degradation of leghemoglobins and abolishes nodule expression of senescence‐associated genes (SAGs) that contain a conserved binding motif for NAC094. Nitrate‐triggered metabolic changes in wild‐type nodules are largely affected in nac094 mutant nodules. Induction of NAC094 and its targeting SAGs was almost blocked in the nitrate‐insensitive nlp1, nlp4, and nlp1 nlp4 mutants. We conclude that NAC094 functions downstream of NLP1 and NLP4 by regulating nitrate‐induced expression of SAGs. Our study fills in a key gap between nitrate and the execution of nodule senescence, and provides a potential strategy to improve nitrogen fixation and stress tolerance of legumes.

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Petroleum hydrocarbons can serve as a carbon source for marine phytoplankton; so, marine high-acid crude oil pollution events are likely to result in algal outbreaks or harmful algal blooms (HABs) in surface waters. Naphthenic acids (NAs) are the primary acidic component of crude oil, and red tide is of great concern due to its high diffusivity and strong destructive properties. It is important to study the mechanism of the toxic effect of NAs on the typical red tide algae, Heterosigma akashiwo, for the balance and stability of marine algae. The mechanism of NAs’ damage effect was investigated in terms of the antioxidant enzyme activity, cell number, the chlorophyll positive fluorescence parameters, and the cell morphology of microalgae. Experiments confirmed the hormesis of low-concentration (0.5, 2, and 4 mg/L) NAs on Heterosigma akashiwo, and the indicators of high-concentration (8 and 16 mg/L) NA exposures showed inhibition. In this study, the toxic effect of NAs on the target organism showed a clear concentration–dose relationship. The 16 mg/L NAs stress caused severe damage to the morphology and structure of the target biological cells in a short time (96 h), and the population growth decreased. The target organisms showed a staged oxidative stress response to NAs. The behavior in the low-concentration treatment groups showed toxicant excitatory effects on the photosynthetic efficiency and antioxidant enzyme activity of the target organisms. This study provides theoretical and practical data for the development of an important toxicological model of the toxicant’s excitement effects and antioxidant defense mechanisms. In addition, it provides prospective research data for the prediction and avoidance of ecological risk from NA pollution in marine environments.