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IN BRIEF
Lipids in Leaves: Fatty Acid b-Oxidation Affects Lipid Homeostasis
DNA, RNA, and proteins get a lot of attention,
but without lipids, a cell is just a soup. Cellular
membranes have a remarkable variety of
lipids, and different organelles have different lipid compositions that must be maintained despite changes caused by vesicular
trafficking among organelles (reviewed in
Holthuis and Menon, 2014). Lipids move via
vesicular trafficking, direct membrane contact between organelles, and via so-called
pipelines operated by lipid transfer proteins.
Changes in lipid composition can alter the
surface charge, thickness, and fluidity of a
membrane—characteristics that affect, for
example, secretion via the Golgi and endoplasmic reticulum. Lipid homeostasis involves a balance between accumulation of
membrane lipids and storage lipids such
as triacylglycerol. Remobilization of stored
triacylglycerol occurs via b-oxidation in the
peroxisome, which provides both fatty acid
components for membrane lipids and energy for seedling development.
Although lipid metabolism in seeds has
received substantial attention, the importance
of lipid synthesis and turnover in leaves
remains unclear. To examine this, Fan et al.
(2014) used trigalactosyl diacylglycerol1-1
(tgd1) mutants, in which a defect in thylakoid
lipid synthesis diverts fatty acids, causing
accumulation of triacylglycerol in leaves. They
found that overexpression of PHOSPHOLIPID:
DIACYLGLYCEROL ACYLTRANSFERASE1
(PDAT1) causes increased fatty acid synthesis and turnover, and this requires the lipase
SUGAR-DEPENDENT1 (SDP1), as PDAT1overexpressing sdp1 plants produce high
levels of triacylglycerol. Also, tgd1 sdp1
double mutants showed triacylglycerol accumulation in leaves, an effect not seen in
double mutants with other lipases (see figure).
This turnover appears to occur via b-oxidation
in peroxisomes, as double mutants of tgd1
with peroxisomal transporter1 (pxa1) also
accumulated triacylglycerol (see figure). However, markers for the b-oxidation pathway did
Mutants affecting triacylglycerol accumulation in
tgd1 mutants. Neutral lipids, including triacylglycerol (TAG) visualized by thin-layer chromatography and sulfuric acid charring, in leaves from
different mutant backgrounds: tgd1, sdp1, pxa1,
comparative gene identifier58-like (cgi58L), and
adipose triglyceride lipase-like (atg1L). (Reprinted
from Fan et al. [2014], Figure 2A.)
not increase in the tgd1 mutants, indicating
that this pathway has sufficient capacity to
handle the increased turnover. Also, overexpression of SDP1, but not other lipases,
was associated with decreased triacylglycerol accumulation in tgd1 mutants. Mutants
lacking the phosphatidic acid phosphohydrolases PAH1 and PAH2 also showed decreased triacylglycerol accumulation in the
tgd1 background, indicating that these lipids
provide key precursors for triacylglycerol
synthesis. Thus, the authors identified a key
role for lipid turnover and the b-oxidation
pathway in accumulation of triacylglycerol in
leaves.
Researchers working on biofuels have
taken an interest in lipids in leaves, as
lipids make energy-dense, easily extractable
biofuels that require no saccharification or
fermentation and oil-rich leaves would provide a superb biomass feedstock. However,
leaves as source tissues have proven recalcitrant to oil accumulation (Chapman et al.,
2013), as their metabolism favors starch
accumulation. The increase in triacylglycerol
in the double mutants examined here, up to
9% of leaf dry weight in tgd1 pxa1 and tgd1
sdp1 plants, indicates that strategies to
increase lipid accumulation should target
turnover. However, in addition to increased
lipid droplets and changes in membrane
lipid composition, these double mutants also
show somewhat slower growth and impaired
pollen germination (in tgd1 pxa1), indicating
that perturbation of lipid homeostasis with
the entire plant might also have unintended
agronomic effects. Thus, this emerging research informs efforts to produce oil for
biofuels by highlighting the importance of
peroxisomal b-oxidation in triacylglycerol
accumulation in leaves and provides cautionary information on potential problems
with such approaches.
Jennifer Mach
Science Editor
[email protected]
ORCID ID: 0000-0002-1141-6306
REFERENCES
Chapman, K.D., Dyer, J.M., and Mullen, R.T.
(2013). Commentary: why don’t plant leaves
get fat? Plant Sci. 207: 128–134.
Fan, J., Yan, C., Roston, R., Shanklin, J., and Xu,
C. (2014). Arabidopsis lipins, PDAT1 acyltransferase, and SDP1 triacylglycerol lipase synergistically direct fatty acids toward b-oxidation,
thereby maintaining membrane lipid homeostasis. Plant Cell 26: 10.1105/tpc.114.130377.
Holthuis, J.C., and Menon, A.K. (2014). Lipid
landscapes and pipelines in membrane homeostasis. Nature 510: 48–57.
www.plantcell.org/cgi/doi/10.1105/tpc.114.133447
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Lipids in Leaves: Fatty Acid β-Oxidation Affects Lipid Homeostasis
Jennifer Mach
Plant Cell; originally published online October 28, 2014;
DOI 10.1105/tpc.114.133447
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