First published online February 24, 2002; 10.1104/pp.010780
Plant Physiol, March 2002, Vol. 128, pp. 885-895
Digalactosyldiacylglycerol Synthesis in Chloroplasts of the
Arabidopsis dgd1 Mutant1
Dörte
Klaus,
Heiko
Härtel,2
Lynda M.
Fitzpatrick,
John E.
Froehlich,
Jamie
Hubert,2
Christoph
Benning, and
Peter
Dörmann*
Max-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Golm, Germany (D.K., P.D.); and Department of Biochemistry and
Molecular Biology (H.H., J.H., C.B.) and Plant Research Laboratory
(L.M.F., J.E.F.), Michigan State University, East Lansing, Michigan
48824
Galactolipid biosynthesis in plants is highly complex. It
involves multiple pathways giving rise to different molecular species. To assess the contribution of different routes of galactolipid synthesis and the role of molecular species for growth and
photosynthesis, we initiated a genetic approach of analyzing double
mutants of the digalactosyldiacylglycerol (DGDG) synthase mutant
dgd1 with the acyltransferase mutant,
act1, and the two desaturase mutants, fad2 and fad3. The double mutants showed
different degrees of growth retardation: act1,dgd1 was
most severely affected and growth of fad2,dgd1 was
slightly reduced, whereas fad3,dgd1 plants were very
similar to dgd1. In act1,dgd1, lipid and
chlorophyll content were reduced and photosynthetic capacity was
affected. Molecular analysis of galactolipid content, fatty acid
composition, and positional distribution suggested that the growth
deficiency is not caused by changes in galactolipid composition per se.
Chloroplasts of dgd1 were capable of synthesizing
monogalactosyldiacylglycerol, DGDG, and tri- and
tetragalactosyldiacylglycerol. Therefore, the reduced growth of
act1,dgd1 and fad2,dgd1 cannot be
explained by the absence of DGDG synthase activity from chloroplasts.
Molecular analysis of DGDG accumulating in the mutants during phosphate deprivation suggested that similarly to the residual DGDG of
dgd1, this additional lipid is synthesized in
association with chloroplast membranes through a pathway independent of
the mutations, act1, dgd1,
fad2, and fad3. Our data imply that the
severe growth defect of act1,dgd1 is caused by a reduced
metabolic flux of chloroplast lipid synthesis through the eukaryotic
and prokaryotic pathway as well as by the reduction of photosynthetic
capacity caused by the destabilization of photosynthetic complexes.
1
This work was supported in part by the U.S.
Department of Energy (grant no. DE-FG02-98ER20305 to C.B.) and by the
Alexander von Humboldt Foundation (Feodor-Lynen fellowship to
P.D.).
2
Present address: BASF Plant Science L.L.C., 26 Davis Dr., Research Triangle Park, NC 27709.
*
Corresponding author; e-mail Doermann{at}mpimp-golm.mpg.de; fax
49-331-567-8250.
© 2002 American Society of Plant Physiologists
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