Seo, S. Y. | bioRxiv Science

bioRxiv2021

Translocation of chloroplast NPR1 to the nucleus in retrograde signaling for adaptive response to salt stress in tobacco

Chloroplasts play a pivotal role in biotic and abiotic stress responses, accompanying changes in the cell reduction/oxidation (redox) state. Chloroplasts are an endosymbiotic organelle that sends retrograde signals to the nucleus to integrate with environmental changes. This study showed that salt stress causes the rapid accumulation of the nonexpressor of pathogenesis-related genes 1 (NPR1) protein, a redox-sensitive transcription coactivator that elicits many tolerance responses in chloroplasts and the nucleus. The transiently accumulated chloroplast NPR1 protein was translocated to the nucleus in a redox-dependent manner under salinity stress. In addition, immunoblotting and fluorescence image analysis showed that chloroplast-targeted NPR1-GFP fused with cTP (chloroplast transit peptide from RbcS) was localized in the nucleus during the responses to salt stress. Chloroplast functionality was essential for retrograde translocation, in which the stomules and cytoplasmic vesicles participated. Treatments with H2O2 and an ethylene precursor enhanced this retrograde translocation. Compared to each wild-type plant, retrograde signaling-related gene expression was severely impaired in the npr1-1 mutant in Arabidopsis, but enhanced transiently in the NPR1-Ox transgenic tobacco line. Therefore, NPR1 might be a retrograde signaling hub that improves a plants adaptability to changing environments.

plant biology↗

bioRxiv2020

Phytosphingosine induces systemic acquired resistance through activation of sphingosine kinase

Phytosphingosine (PHS) is a naturally occurring bioactive sphingolipid molecule. Intermediates such as sphingolipid long-chain bases (LCBs) in sphingolipid biosynthesis have been shown to have important roles as signaling molecules. In this study, exogenous addition of PHS caused rapid induction of transcripts responsible for transient synthesis of LCBs, reactive oxygen species, and ethylene. These events were followed by the induction of sphingolipid kinase (SphK), which metabolized PHS to phytosphingosine-1-phosphate in an biphasic manner. PHS alleviated not only pathogen-induced cell damage but also reduced the growth of virulent pathogens in the entire upper part of the PHS-treated plant stem during the necrotic stage after inoculation, suggesting the development of systemic acquired resistance (SAR) and plant immunity. Moreover, PHS treatment up-regulated the transcription and activity of SphK, accompanied by prominent increases in the transcription levels of serine palmitoyltransferase (LCB1 and LCB2) for de novo synthesis of sphingolipids, as well as ROS-detoxifying enzymes and PR proteins at 48 h after virulent pathogen infection. The impairment of ROS production at this time is more beneficial for the activation of SphK and inhibition of pathogenicity during the necrotic stage of hemibiotrophic infection, indicating that necrotic cell death at the late stage is regulated by ROS-independent SphK. Phosphorylated LCBs significantly reduced pathogen-induced cell damage. These observations suggest that selective channeling of sphingolipids into phosphorylated forms in a time-dependent manner has a pro-survival effect by promoting SAR in plant immunity. 4. One Sentence SummarySelective gene expression in sphingolipid biosynthesis and channeling into their phosphorylated forms are significant determinants of their roles as pro-survival signaling molecules.

plant biology↗