alexa Possible Role of Sphingolipids in Developmental Programmed Cell Death of Petunia Petals
ISSN: 2329-6577

Biological Systems: Open Access
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Research Article

Possible Role of Sphingolipids in Developmental Programmed Cell Death of Petunia Petals

Domenico Prisa*, Gianluca Burchi
Research Unit for the Nursery and the Management of Environmental and Ornamental Green, Pescia (PT), Italy
Corresponding Author : Prisa D
Research Unit for the Nursery and the Management of Environmental and Ornamental Green
Pescia (PT), 51017, Italy
Tel: 0039 3391062935
Email: [email protected]
Received: October 13, 2015 Accepted: November 25, 2015 Published: December 03, 2015
Citation: Prisa D, Burchi G (2015) Possible Role of Sphingolipids in Developmental Programmed Cell Death of Petunia Petals. Biol syst Open Access 4:146. doi:10.4172/2329-6577.1000146
Copyright: © 2015 Prisa D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

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-acetylcysteine 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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