Ethylene-Mediated Phospholipid Catabolic Pathway in
Glucose-Starved Carrot Suspension Cells1
Soo Hyun Lee,
Hyun Sook Chae,
Taek Kyun Lee,
Se Hee Kim,
Sung Ho
Shin,
Bong Huey Cho,
Sung Ho Cho,
Bin G. Kang, and
Woo Sung Lee*
Department of Biology, Sung Kyun Kwan University, Suwon 440-746,
Korea (S.H.L., T.K.L., S.H.K., W.S.L.); Department of Biology, Yonsei
University, Seoul 120-749, Korea (H.S.C., B.G.K.); Agency
for Defense Development, Yuseong 305-600, Korea (S.H.S.); Department
of Biology, Suwon University, Suwon 445-743,
Korea (B.H.C.); and Department of Biology, Inha University, Inchon
402-751, Korea (S.H.C.)
Glucose (Glc) starvation of
suspension-cultured carrot (Daucus carota
L.) cells resulted in sequential activation of phospholipid catabolic
enzymes. Among the assayed enzymes involved in the degradation, phospholipase D (PLD) and lipolytic acyl hydrolase were activated at
the early part of starvation, and these activities were followed by
-oxidation and the glyoxylate cycle enzymes in order. The activity
of PLD and lipolytic acyl hydrolase was further confirmed by in
vivo-labeling experiments. It was demonstrated that Glc added to a
medium containing starving cells inhibited the phospholipid catabolic
activities, indicating that phospholipid catabolism is negatively
regulated by Glc. There was a burst of ethylene production 6 h
after starvation. Ethylene added exogeneously to a Glc-sufficient
medium activated PLD, indicating that ethylene acts as an element in
the signal transduction pathway leading from Glc depletion to PLD
activation. Activation of lipid peroxidation, suggestive of cell death,
occurred immediately after the decrease of the phospholipid
degradation, suggesting that the observed phospholipid catabolic
pathway is part of the metabolic strategies by which cells effectively
survive under Glc starvation.
1
This work was supported by the Academic Research
Fund (GE 96-212) of the Ministry of Education, Republic of Korea,
awarded to W.S.L. This work was also partly supported by a grant from Korea Science and Engineering Foundation-Hormone Research Center (97-K-3-0401-03) awarded to B.G.K.
*
Corresponding author; e-mail wslee{at}yurim.skku.ac.kr; fax
82-331-290-7015.
Plant Physiol. (1998) 116: 223-229
Copyright Clearance Center: 0032-0889/98/116/0223/07
© 1998 American Society of Plant Physiologists
