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Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in <i>Arabidopsis thaliana</i>. The <i>lsd1</i> mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the <i>lsd1</i> with the <i>sid2</i> mutant, caring mutation in <i>ISOCHORISMATE SYNTHASE 1</i><i>(ICS1</i>) gene and having deregulated SA synthesis, and with plants expressing the bacterial <i>nahG</i> gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the <i>lsd1</i> mutant exhibited clear cell death phenotype, which was reversed in <i>lsd1/sid2</i> and <i>lsd1</i>/<i>NahG</i> plants. The expression of <i>PR</i>-genes and the H₂O₂ content in UV-treated <i>lsd1</i> were significantly higher when compared with the wild type. In contrast, <i>lsd1/sid2</i> and <i>lsd1</i>/<i>NahG</i> plants demonstrated comparability with the wild-type level of <i>PR</i>-genes expression and H₂O₂. Our results demonstrate that SA accumulation is crucial for triggering cell death in <i>lsd1</i>, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.