Unraveling the roles of sphingolipids in plant innate immunity

Iwate Biotechnology Research Center, Kitakami, Iwate, Japan
Plant signaling & behavior 06/2009; 4(6):536-8. DOI: 10.4161/psb.4.6.8583
Source: PubMed


It has long been known that fungal pathogens like Fusarium and Alternaria spp. produce toxins (mycotoxin) to kill plant cells. These mycotoxins have been shown to perturb the plant sphingolipid biosynthesis pathway, resulting in the necrotic cell death of plant cells. A recent study by Shi et al.1 revealed that an increase in the amount of cellular sphingoid bases triggers plant programmed cell death (PCD) through accumulation of reactive oxygen species (ROS). These studies point to the importance of sphingolipids in the regulation of plant cell in disease development as well as in defense responses. In the latest report,2 we showed that serine palmitoyltransferase (SPT), the key enzyme of sphingolipid biosynthesis, regulates not only plant cell death but also defense response against a non-host pathogen, soliciting further studies to elucidate the roles of sphingolipids in plant innate immunity.

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Available from: Ryohei Terauchi
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    • "Moreover, several studies revealed that ceramides (Cers) and longchain bases (LCBs) are also potent inducers of PCD in plants. For example, exogenously applied Cers and LCBs (d18:0, d18:1, or t18:0) induced PCD either in cell suspension cultures (Liang et al., 2003; Lachaud et al., 2010, 2011; Alden et al., 2011) or in whole seedlings (Shi et al., 2007; Takahashi et al., 2009; Saucedo-García et al., 2011). AAL-and FB1-induced PCD seemed to be due to the accumulation of free sphingoid bases (dihydrosphingosine [d18:0] and phytosphingosine [t18:0]; Abbas et al., 1994; Brandwagt et al., 2000; Shi et al., 2007). "
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