Elevated ambient temperature has wide effects on plant growth and development. ELF3, a proposed thermosensor, negatively regulates protein activity of the growth-promoting factor PIF4, and such an inhibitory effect is subjected to attenuation at warm temperature. However, how ELF3 stability is regulated at warm temperature remains enigmatic. Here, we report the identification of XBAT31 as the E3 ligase that mediates ELF3 degradation in response to warm temperature in Arabidopsis. XBAT31 interacts with ELF3, ubiquitinates ELF3, and promotes ELF3 degradation via the 26S proteasome. Mutation of XBAT31 results in enhanced accumulation of ELF3 and reduced hypocotyl elongation at warm temperature. In contrast, overexpression of XBAT31 accelerates ELF3 degradation and promotes hypocotyl growth. Furthermore, XBAT31 interacts with the B-box protein BBX18, and the XBAT31-mediated ELF3 degradation is dependent on BBX18. Thus, our findings reveal that XBAT31-mediated destruction of ELF3 represents an additional regulatory layer of complexity in temperature signaling during plant thermomorphogenesis.

Although the alteration of DNA methylation due to abiotic stresses, such as exposure to the toxic metal cadmium (Cd), has been often observed in plants, little is known about whether such epigenetic changes are linked to the ability of plants to adapt to stress. Herein, we report a close linkage between DNA methylation and the adaptational responses in Arabidopsis plants under Cd stress. Exposure to Cd significantly inhibited the expression of three DNA demethylase genes ROS1/DML2/DML3 (RDD) and elevated DNA methylation at the genome‐wide level in Col‐0 roots. Furthermore, the profile of DNA methylation in Cd‐exposed Col‐0 roots was similar to that in the roots of rdd triple mutants, which lack RDD, indicating that Cd‐induced DNA methylation is associated with the inhibition of RDD. Interestingly, the elevation in DNA methylation in rdd conferred a higher tolerance against Cd stress and improved cellular Fe nutrition in the root tissues. In addition, lowering the Fe supply abolished improved Cd tolerance due to the lack of RDD in rdd. Together, these data suggest that the inhibition of RDD‐mediated DNA demethylation in the roots by Cd would in turn enhance plant tolerance to Cd stress by improving Fe nutrition through a feedback mechanism.

No abstract

No abstract