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Summary   Arabidopsis thaliana  AKR2A plays an important role in plant responses to cold stress. However, its exact function in plant resistance to cold stress remains unclear. In the present study, we found that the contents of very long‐chain fatty acids (VLCFAs) in  akr2a  mutants were decreased, and the expression level of KCS1 was also reduced. Overexpression of  KCS1  in the  akr2a  mutants could enhance VLCFAs contents and chilling tolerance. Yeast‐2‐hybrid and bimolecular fluorescence complementation (BIFC) results showed that the transmembrane motif of KCS1 interacts with the PEST motif of AKR2A both  in vitro  and  in vivo . Overexpression of  KCS1  in  akr2a  mutants rescued  akr2a  mutant phenotypes, including chilling sensitivity and a decrease of VLCFAs contents. Moreover, the transgenic plants co‐overexpressing  AKR2A  and  KCS1  exhibited a greater chilling tolerance than the plants overexpressing  AKR2A  or  KCS1  alone, as well as the wild‐type.  AKR2A  knockdown and  kcs1  knockout mutants showed the worst performance under chilling conditions. These results indicate that AKR2A is involved in chilling tolerance via an interaction with KCS1 to affect VLCFA biosynthesis in  Arabidopsis .

AKR2A interacts with KCS1 to improve VLCFAs contents and chilling tolerance of Arabidopsis thaliana