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SUMMARY: The Arabidopsis thaliana aldehyde oxidase 3 (AAO3) catalyzes the oxidation of abscisic aldehyde (ABal) to abscisic acid (ABA). Besides ABal, plants generate other aldehydes that can be toxic above a certain threshold. AAO3 knockout mutants (aao3) exhibited earlier senescence but equivalent relative water content compared with wild‐type (WT) during normal growth or upon application of UV‐C irradiation. Aldehyde profiling in leaves of 24‐day‐old plants revealed higher accumulation of acrolein, crotonaldehyde, 3Z‐hexenal, hexanal and acetaldehyde in aao3 mutants compared with WT leaves. Similarly, higher levels of acrolein, benzaldehyde, crotonaldehyde, propionaldehyde, trans‐2‐hexenal and acetaldehyde were accumulated in aao3 mutants upon UV‐C irradiation. Aldehydes application to plants hastened profuse senescence symptoms and higher accumulation of aldehydes, such as acrolein, benzaldehyde and 4‐hydroxy‐2‐nonenal, in aao3 mutant leaves as compared with WT. The senescence symptoms included greater decrease in chlorophyll content and increase in transcript expression of the early senescence marker genes, Senescence‐Related‐Gene1, Stay‐Green‐Protein2 as well as NAC‐LIKE, ACTIVATED‐BY AP3/P1. Notably, although aao3 had lower ABA content than WT, members of the ABA‐responding genes SnRKs were expressed at similar levels in aao3 and WT. Moreover, the other ABA‐deficient mutants [aba2 and 9‐cis‐poxycarotenoid dioxygenase3‐2 (nced3‐2), that has functional AAO3] exhibited similar aldehydes accumulation and chlorophyll content like WT under normal growth conditions or UV‐C irradiation. These results indicate that the absence of AAO3 oxidation activity and not the lower ABA and its associated function is responsible for the earlier senescence symptoms in aao3 mutant. Significance Statement: The current study demonstrates that AAO3, known to catalyze the last step of ABA biosynthesis by oxidizing ABal, is essential in preventing leaf damage by oxidizing toxic levels of aldehydes in rosette leaves. We provided credible evidences that premature senescence in this study was not because of low ABA content and its consequential function in aao3, but rather due to higher aldehyde accumulation, which is caused by AAO3 deficiency. [ABSTRACT FROM AUTHOR]