Human GLTP and mutant forms of ACD11 suppress cell death in the Arabidopsis acd11 mutant

TY - JOUR

T1 - Human GLTP and mutant forms of ACD11 suppress cell death in the Arabidopsis acd11 mutant

AU - Petersen, Nikolaj H T

AU - McKinney, Lea V

AU - Pike, Helen

AU - Hofius, Daniel

AU - Zakaria, Asif

AU - Brodersen, Peter

AU - Petersen, Morten

AU - Brown, Rhoderick E

AU - Mundy, John

N1 - Keywords: Amino Acid Sequence; Apoptosis Regulatory Proteins; Arabidopsis Proteins; Base Sequence; Blotting, Western; Carrier Proteins; DNA Primers; Humans; Membrane Transport Proteins; Molecular Sequence Data; Mutation; Recombinant Proteins; Sequence Homology, Amino Acid

PY - 2008

Y1 - 2008

N2 - The Arabidopsis acd11 mutant exhibits runaway, programmed cell death due to the loss of a putative sphingosine transfer protein (ACD11) with homology to mammalian GLTP. We demonstrate that transgenic expression in Arabidopsis thaliana of human GLTP partially suppressed the phenotype of the acd11 null mutant, resulting in delayed programmed cell death development and plant survival. Surprisingly, a GLTP mutant form impaired in glycolipid transfer activity also complemented the acd11 mutants. To understand the relationship between functional complementarity and transfer activity, we generated site-specific mutants in ACD11 based on homologous GLTP residues required for glycolipid transfer. We show that these ACD11 mutant forms are impaired in their in vitro transfer activity of sphingolipids. However, transgenic expression of these mutant forms fully complemented acd11 mutant cell death, and transgenic plants showed normal induction of hypersensitive cell death upon infection with avirulent strains of Pseudomonas syringae. The significance of these findings with respect to the function(s) of ACD11 in sphingolipid transport and cell death regulation is discussed.

AB - The Arabidopsis acd11 mutant exhibits runaway, programmed cell death due to the loss of a putative sphingosine transfer protein (ACD11) with homology to mammalian GLTP. We demonstrate that transgenic expression in Arabidopsis thaliana of human GLTP partially suppressed the phenotype of the acd11 null mutant, resulting in delayed programmed cell death development and plant survival. Surprisingly, a GLTP mutant form impaired in glycolipid transfer activity also complemented the acd11 mutants. To understand the relationship between functional complementarity and transfer activity, we generated site-specific mutants in ACD11 based on homologous GLTP residues required for glycolipid transfer. We show that these ACD11 mutant forms are impaired in their in vitro transfer activity of sphingolipids. However, transgenic expression of these mutant forms fully complemented acd11 mutant cell death, and transgenic plants showed normal induction of hypersensitive cell death upon infection with avirulent strains of Pseudomonas syringae. The significance of these findings with respect to the function(s) of ACD11 in sphingolipid transport and cell death regulation is discussed.

U2 - 10.1111/j.1742-4658.2008.06584.x

DO - 10.1111/j.1742-4658.2008.06584.x

M3 - Journal article

C2 - 18657186

SN - 1742-464X

VL - 275

SP - 4378

EP - 4388

JO - FEBS Journal

JF - FEBS Journal

IS - 17

ER -