ABSTRACT Tandem CCCH zinc finger (TZF) proteins play diverse roles in plant growth and stress response. Although as many as 11 TZF proteins have been identified in Arabidopsis , little is known about the mechanism by which TZF proteins select and regulate the target mRNAs. Here, we report that Arabidopsis TZF1 is a bona-fide stress granule protein. Ectopic expression of TZF1 ( TZF1 OE ), but not an mRNA binding-defective mutant ( TZF1 H186Y OE ), enhances salt stress tolerance in Arabidopsis . RNA-seq analyses of NaCl-treated plants revealed that the down-regulated genes in TZF1 OE plants are enriched for functions in salt and oxidative stress responses. Because many of these down-regulated mRNAs contain AU- and/or U-rich elements (AREs and/or UREs) in their 3’-UTRs, we hypothesized that TZF1—ARE/URE interaction might contribute to the observed gene expression changes. Results from RNA immunoprecipitation-quantitative PCR analysis, gel-shift, and mRNA half-life assays indicate that TZF1 binds and triggers degradation of the autoinhibited Ca 2+ -ATPase 11 ( ACA11 ) mRNA, encoding a tonoplast-localized calcium pump that extrudes calcium and dampens the signal transduction pathways necessary for salt stress tolerance. Furthermore, this salt stress-tolerance phenotype was recapitulated in aca11 null mutants. Remarkably, a set of positive regulators for salt stress tolerance was upregulated in TZF1 OE plants. These include Na + /H + Exchanger ( NHX ) family members known to contribute to Na + homeostasis and salinity stress tolerance. Collectively, we present a model in which TZF1 targets ACA11 and ACA4 directly, and repressors of NHXs and other negative regulators indirectly for mRNA degradation to enhance plant salt stress tolerance.