Ferroptosis is a newly discovered form of cell death accompanied by iron accumulation and lipid peroxidation. Both biotic and abiotic stresses can induce ferroptosis in plant cells. In the case of plant interactions with pathogenic Phytophthora oomycetes, the roles of ferroptosis are still largely unknown. Here, we performed transcriptome analysis on soybean plants treated with the biocontrol agent Pythium oligandrum, a soilborne and non‐pathogenic oomycete capable of inducing plant resistance against Phytophthora sojae infection. Expression of homologous soybean genes involved in ferroptosis and resistance was reprogrammed upon P. oligandrum treatment. Typical hallmarks for characterizing ferroptosis were detected in soybean hypocotyl cells, including decreased glutathione (GSH) level, accumulation of ferric ions, and lipid peroxidation by reactive oxygen species (ROS). Meanwhile, ferroptosis‐like cell death was triggered by P. oligandrum to suppress P. sojae infection in soybean. Protection provided by P. oligandrum could be attenuated by the ferroptosis inhibitor ferrostatin‐1 (Fer‐1), suggesting the critical role of ferroptosis in soybean resistance against P. sojae. Taken together, these results demonstrate that ferroptosis is a P. oligandrum‐inducible defence mechanism against oomycete infection in soybean.
Flowering is critical for sexual reproduction and fruit production. Several pear (Pyrus sp.) varieties produce few flower buds, but the underlying mechanisms are unknown. The circadian clock regulator EARLY FLOWERING3 (ELF3) serves as a scaffold protein in the evening complex that controls flowering. Here, we report that the absence of a 58-bp sequence in the 2nd intron of PbELF3 is genetically associated with the production of fewer flower buds in pear. From rapid amplification of cDNA ends sequencing results, we identified a short, previously unknown transcript from the PbELF3 locus, which we termed PbELF3β, whose transcript level was significantly lower in pear cultivars that lacked the 58-bp region. The heterologous expression of PbELF3β in Arabidopsis (Arabidopsis thaliana) accelerated flowering, whereas the heterologous expression of the full-length transcript PbELF3α caused late flowering. Notably, ELF3β was functionally conserved in other plants. Deletion of the 2nd intron reduced AtELF3β expression and caused delayed flowering time in Arabidopsis. AtELF3β physically interacted with AtELF3α, disrupting the formation of the evening complex and consequently releasing its repression of flower induction genes such as GIGANTEA (GI). AtELF3β had no effect in the absence of AtELF3α, supporting the idea that AtELF3β promotes flower induction by blocking AtELF3α function. Our findings show that alternative promoter usage at the ELF3 locus allows plants to fine-tune flower induction.
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