- CHILLING INJURY IN TOMATO FRUIT 235
degree of unsaturated fatty acids is thought to be correlated with the
incidence of CI (Lee et al. 2005). Higher levels of polyunsaturated fatty
acids of membrane lipids leads to increased low temperature toler-
ance in cyanobacterium (Wada and Murata 1990) and higher plants
like tobacco and squash (Murata et al. 1992), peach (Zhang and Tian
2009), or bell pepper (Liu et al. 2015). Hugly and Somerville (1992)
observed that chlorosis in the CI-hypersensitive phenotypes in mutant
plants ofArabidopsisat low temperature is correlated with a reduction
in polyunsaturated lipid content. Nishida and Murata (1996) demon-
strated that the concentration of unsaturated fatty acids can be modi-
fied by the action of different enzymes like acyl-lipid desaturases and
glycerol-3-phosphate acyltransferase (GPAT), thus subsequently manip-
ulating the chilling sensitivity of plants. Murata et al. (1992) used a
gene of the chloroplast-located enzyme GPAT (important for the degree
of unsaturation) fromArabidopsisand usedAgrobacterium-mediated
transformation to express it in tobacco. This transgenic tobacco had a
higher level of unsaturated fatty acid and showed increased chilling
tolerance, suggesting an important role for GPAT in cold resistance.
The hypothesis relating chilling sensitivity to a phase transition in
membrane lipids has many critical shortcomings (Raison and Orr 1990).
Detailed reviews about the shortcomings of this model can be found in
other studies (Parkin et al. 1989; Saltveit 2002). Other events proposed
as influencing the primary cause of CI include (1) the redistribution of
cellular calcium (Minorsky 1985); (2) a conformational change in some
key regulatory proteins (enzymes) (Graham et al. 1979); (3) a marked
decrease in the rate of cyclosis (protoplasmic streaming) and a change
in cell cytoskeletal structure (Woods et al. 1984); and (4) an accumu-
lation of reactive oxygen species (ROS) resulting in oxidative damage
leading to membrane breakdown and eventual visible signs of symp-
toms (Parkin and Kuo 1989).
Lipid composition of mitochondrial membranes is also affected dur-
ing low temperature stress that causes disorders in mitochondrial res-
piration resulting in loss of metabolic energy of affected cells (Sevillano
et al. 2009). Moline (1976) correlated low temperature injury with ultra-
structural modifications of fruit organelles, including swollen mito-
chondria and plastids. Lyons and Raison (1970) proposed a consis-
tent incidence of phase transition in the mitochondrial membrane as
the result of the physical effect of temperature. However, O’Neill and
Leopold (1982) suggested that no bulk phase transition was detectable
in mitochondrial membranes of chilling-sensitive soybean seed in the
temperature range where chilling occurs and argued that chilling injury
is not induced by phase transition. Raison and Orr (1986), however,