Cloning of the Flotillin Genes SaFlot1 and SaFlot2 Coding Sequences from the Euhalophyte Suaeda altissima (L.) PALL. and Effects of the Immune Response Elicitor FLG22 and NaCl on Their Expression

Flotillins, membrane-associated proteins, belonging to a SPFH protein superfamily are essential constituents of the membrane microdomains and involved in many vital processes. In a number of studies, the flotillin-associated endocytosis has been shown to play an important role in plant response to biotic and abiotic stresses by regulating abundance of key to resistance proteins in plasma membrane (PM) and activating signaling cascades. Here, we report the identification of two flotillin genes, SaFlot1 and SaFlot2, in the euhalophyte Suaeda altissima, a species exhibiting high tolerance to NaCl and bacterial infections, the cloning of their full-length coding sequences, and the effects of an abiotic (NaCl) and a biotic (immune response elicitor, bacterial peptide fls22) stress-factors on their expression. Treatment of S. altissima plants with flg22 stimulated transcription, while NaCl lowered transcript levels of both SaFlot1 and SaFlot2. We hypothesis that observed changes in the levels of SaFlot1 and SaFlot2 transcripts reflect cell needs under stress conditions to modulate certain PM protein internalization accomplished by the flotillin-dependent (microdomain-associated) endocytic pathway. The A. thaliana plasma membrane receptor FLS2, a protein playing a signaling role at bacterial infections, forms the flg22-FLS2 complex that undergoes internalization into the cytoplasm. The flg22-induced stimulation of SaFlot1 and SaFlot2 expression may be associated with need to activate flg22-AtFLS2 homolog signaling by the flotillin-dependent endocytosis. NaCl-induced decrease in SaFlot1 and SaFlot2 transcription may be due to the cell need under salt stress conditions to keep in the plasma membrane the important for response to NaCl proteins, such as H⁺-ATPase, inward K⁺ channel AKT1 and some others, reducing flotillin-dependent endocytic activity.