<scp>CmCBF4</scp> crosstalk with <scp>H₂O₂</scp> signal involved in trehalose‐promoted cold tolerance of melon seedlings

SUMMARY Cold stress severely inhibits the normal growth of melon ( Cucumis melo var. makuwa Makino) seedlings. At low temperature, the moderate increase of apoplastic hydrogen peroxide (H 2 O 2 ) level and subsequent intracellular signal transduction are important to plant cold response. Our previous studies showed that trehalose (Tre) could activate H 2 O 2 signal and improve cold tolerance of melon seedlings. However, the specific mechanism is not completely clear. Here, we found that Tre‐promoted C‐repeat binding factor 4 (CmCBF4) could combine with the promoter of respiratory burst oxidase homologs D ( CmRBOHD ) to enhance the production of apoplastic H 2 O 2 . Further studies suggested that CmCBF4 could also activate the transcription of plasma membrane intrinsic protein 2;3 ( CmPIP2;3 ), which has H 2 O 2 transport capability in melon seedlings. In addition, abscisic acid‐responsive element (ABRE)‐binding factor 2 (CmABF2) and CmCBF4 could promote the transcription of each other to increase the expression of CmPIP2;3. Silencing CmCBF4 significantly reduced Tre‐promoted cold tolerance and apoplastic H 2 O 2 production and transport. In summary, this study reveals that CmCBF4 regulates Tre‐promoted cold tolerance in melon seedlings by promoting the production and transport of apoplastic H 2 O 2 signal.