AtTLP2, a Tubby-like protein, plays intricate roles in abiotic stress signalling

Key message The Arabidopsis Tubby-like protein (TLP) encoding gene, AtTLP2, plays intricate roles during ABA-dependent abiotic stress signalling, particularly salt and dehydration stress responses. TLPs (Tubby-like proteins) are a small group of eukaryotic proteins characterized by the presence of a Tubby domain. The plant TLPs have been widely shown to play important roles during abiotic stress signaling. In this study, we investigated the role of an Arabidopsis TLP, AtTLP2, in mediating abiotic stress responses. Both attlp2 null mutant and overexpression (OE) lines, in Arabidopsis, were studied which indicated the role of the gene also in development. The attlp2 mutant showed an overall dwarfism, while its overexpression caused enhanced growth. AtTLP2 localized to the plasma membrane (PM) and showed nuclear translocation in response to dehydration stress. The protein interacted with ASK1 and ASK2, but failed to show transactivation activity in yeast. AtTLP2 was transcriptionally induced by stress, caused by salt, dehydration and ABA. The attlp2 mutant was insensitive to ABA, but hypersensitive to oxidative stress at all stages of growth. ABA insensitivity conferred tolerance to salt and osmotic stresses at the germination and early seedling growth stages, but caused hypersensitivity to salt and drought stresses at advanced stages of growth. The OE lines were more sensitive to ABA, causing increased sensitivity to most stresses at the seed germination stage, but conferring tolerance to salt and osmotic stresses at more advanced stages of development. The stomata of the attlp2 mutant were less responsive to ABA and H2O2, while that of the OE lines exhibited greater sensitivity. Several ABA-regulated stress responsive marker genes were found to be downregulated in the mutant, but upregulated in the OE lines. The study establishes that AtTLP2 plays intricate roles in abiotic stress signaling, and the response may be largely ABA dependent.