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Summary  In   A rabidopsis thaliana , acyl‐CoA‐binding proteins ( ACBP s) are encoded by a family of six genes (  ACBP 1  to   ACBP 6 ), and are essential for diverse cellular activities. Recent investigations suggest that the membrane‐anchored  ACBP s are involved in oxygen sensing by sequestration of group  VII  ethylene‐responsive factors under normoxia. Here, we demonstrate the involvement of  A rabidopsis  ACBP 3 in hypoxic tolerance.   ACBP 3  transcription was remarkably induced following submergence under both dark ( DS ) and light ( LS ) conditions.   ACBP 3 ‐overexpressors (  ACBP 3‐ OE s ) showed hypersensitivity to  DS ,  LS  and ethanolic stresses, with reduced transcription of hypoxia‐responsive genes as well as accumulation of hydrogen peroxide in the rosettes. In contrast, suppression of   ACBP 3  in   ACBP 3‐ KO s  enhanced plant tolerance to  DS ,  LS  and ethanol treatments. By analyses of double combinations of   OE ‐1  with  npr1‐5 ,  coi1‐2 ,  ein3‐1  as well as  ctr1‐1  mutants, we observed that the attenuated hypoxic tolerance in   ACBP 3‐ OE s  was dependent on  NPR 1‐ and  CTR 1‐mediated signaling pathways. Lipid profiling revealed that both the total amounts and very‐long‐chain species of phosphatidylserine (C42:2‐ and C42:3‐ PS ) and glucosylinositolphosphorylceramides (C22:0‐, C22:1‐, C24:0‐, C24:1‐, and C26:1‐ GIPC ) were significantly lower in   ACBP 3‐ OE s  but increased in   ACBP 3‐ KO s  upon  LS  exposure. By microscale thermophoresis analysis, the recombinant  ACBP 3 protein bound  VLC  acyl‐CoA esters with high affinities  in vitro . Further, a knockout mutant of  MYB 30, a master regulator of very‐long‐chain fatty acid ( VLCFA ) biosynthesis, exhibited enhanced sensitivities to  LS  and ethanolic stresses, phenotypes that were ameliorated by   ACBP 3‐ RNA i . Taken together, these findings suggest that  A rabidopsis  ACBP 3 participates in plant response to hypoxia by modulating  VLCFA  metabolism.

Arabidopsis acyl‐ C o A ‐binding protein ACBP 3 participates in plant response to hypoxia by modulating very‐long‐chain fatty acid metabolism