Abstract
In Arabidopsis thaliana, a family of six genes (ACBP1 to ACBP6) encodes acyl-CoA binding proteins (ACBPs). Investigations on ACBP3 reported here show its upregulation upon dark treatment and in senescing rosettes. Transgenic Arabidopsis overexpressing ACBP3 (ACBP3-OEs) displayed accelerated leaf senescence, whereas an acbp3 T-DNA insertional mutant and ACBP3 RNA interference transgenic Arabidopsis lines were delayed in dark-induced leaf senescence. Acyl-CoA and lipid profiling revealed that the overexpression of ACBP3 led to an increase in acyl-CoA and phosphatidylethanolamine (PE) levels, whereas ACBP3 downregulation reduced PE content. Moreover, significant losses in phosphatidylcholine (PC) and phosphatidylinositol, and gains in phosphatidic acid (PA), lysophospholipids, and oxylipin-containing galactolipids (arabidopsides) were evident in 3-week-old dark-treated and 6-week-old premature senescing ACBP3-OEs. Such accumulation of PA and arabidopsides (A, B, D, E, and G) resulting from lipid peroxidation in ACBP3-OEs likely promoted leaf senescence. The N-terminal signal sequence/transmembrane domain in ACBP3 was shown to be essential in ACBP3-green fluorescent protein targeting and in promoting senescence. Observations that recombinant ACBP3 binds PC, PE, and unsaturated acyl-CoAs in vitro and that ACBP3 overexpression enhances degradation of the autophagy (ATG)-related protein ATG8 and disrupts autophagosome formation suggest a role for ACBP3 as a phospholipid binding protein involved in the regulation of leaf senescence by modulating membrane phospholipid metabolism and ATG8 stability in Arabidopsis. Accelerated senescence in ACBP3-OEs is dependent on salicylic acid but not jasmonic acid signaling.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
Acyl Coenzyme A / metabolism
-
Arabidopsis / cytology*
-
Arabidopsis / drug effects
-
Arabidopsis / genetics
-
Arabidopsis / growth & development*
-
Arabidopsis Proteins / genetics
-
Arabidopsis Proteins / metabolism*
-
Carrier Proteins / genetics
-
Carrier Proteins / metabolism*
-
Cellular Senescence* / drug effects
-
Cellular Senescence* / genetics
-
DNA, Bacterial / genetics
-
Darkness
-
Down-Regulation / drug effects
-
Esters / metabolism
-
Gene Expression Regulation, Plant / drug effects
-
Green Fluorescent Proteins / metabolism
-
Membrane Lipids / metabolism
-
Mutagenesis, Insertional / genetics
-
Oxidation-Reduction / drug effects
-
Phagosomes / drug effects
-
Phagosomes / metabolism
-
Phenotype
-
Phosphatidylcholines / metabolism
-
Phosphatidylethanolamines / metabolism
-
Plant Leaves / cytology*
-
Plant Leaves / drug effects
-
Plant Leaves / genetics
-
Plant Leaves / growth & development*
-
Plants, Genetically Modified
-
Protein Binding / drug effects
-
Protein Processing, Post-Translational / drug effects
-
RNA Interference / drug effects
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
Recombinant Fusion Proteins / metabolism
-
Salicylic Acid / pharmacology
Substances
-
ACBP3 protein, Arabidopsis
-
Acyl Coenzyme A
-
Arabidopsis Proteins
-
Carrier Proteins
-
DNA, Bacterial
-
Esters
-
Membrane Lipids
-
Phosphatidylcholines
-
Phosphatidylethanolamines
-
RNA, Messenger
-
Recombinant Fusion Proteins
-
T-DNA
-
Green Fluorescent Proteins
-
phosphatidylethanolamine
-
Salicylic Acid
Associated data
-
RefSeq/NM_111436
-
RefSeq/NM_112443
-
RefSeq/NM_117255
-
RefSeq/NM_118556
-
RefSeq/NM_119743
-
RefSeq/NM_119745
-
RefSeq/NM_121497
-
RefSeq/NM_123957
-
RefSeq/NM_124726
-
RefSeq/NM_129765
-
RefSeq/NM_180100