A type of programmed cell death (PCD) in animals is due to lysosomal membrane permeabilisation or rupture.
One of the suggested reasons is sphingolipid accumulation in the membrane. In plants many examples of PCD, including petal senescence, are due to vacuolar permeabilisation and rupture. Using Petunia flowers, we tested the effect on PCD of sphingolipids and of sphinglolipid synthesis inhibitors. Feeding flowers with five main sphingolipids (sphinganine, phytosphingosine, dihydroceramide, ceramide and sphingosine) hastened PCD. Feeding phytosphingosine together with silver thiosulphate, an inhibitor of ethylene perception, completely prevented the PCD-promoting effect of phytosphingosine, suggesting that its acts through ethylene. Feeding together with the
reactive oxygen species scavenger N-acetyl
cysteine had no effect, while the scavenger ascorbic acid only had a slight alleviating effect. These data suggested that phytosphingosine did not act through reactive oxygen species.
Treatments with four inhibitors of sphingolipid synthesis (desipramide, fumonisin B1, myriocin, N,Ndimethylsphingosine) hastened PCD. The data indicate that changes in the endogenous sphingolipid levels resulted in early PCD. The effect of phytosphingosine was abrogated by blocking ethylene perception, suggesting that it acted upstream of ethylene, thus not by directly affecting vacuolar membrane composition.
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