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F-53B damages cell viability leading to impaired root development in Arabidopsis
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F-53B, a widely used replacement for legacy PFAS compounds, is shown to impair cell viability and disrupt root development in plant models. The findings raise concerns about the safety of this fluorinated chemical as a substitute, given its similar bioactive effects. This work contributes to growing evidence that PFAS replacements may not represent meaningful risk reductions.
ABSTRACT The emerging contaminant chlorinated polyfluoroalkyl ether sulfonate (Cl-PFAES/F-53B) has been detected in many plant species, however, the impact of F-53B on the development in plants and the underpinning mechanisms remain largely unelucidated. In this study, we demonstrate by molecular biology, cytogenetics, and fluorescence microscopy mythologies that F-53B impairs cell viability leading to disrupted root development in Arabidopsis ( Arabidopsis thaliana ). We show that F-53B suppresses root length and the inhibitory effect is pronunanced at increasing concentrations. F-53B disrupts cell wall and microtubule-mediated cell plate formation and configuration in meristem cells, revealing its toxicity to cell division and cytoskeleton organization. F-53B induces cell death predominantly at the meristematic zone, however, gene exression and genetic studies indicate that F-53B does not trigger DNA double-strand breaks, implying a divergent effect on DNA stability across species. Moreover, we show that F-53B damages nuclei stability and viability, and induces Autophagy-Related 8 protein foci formation implying that it triggers autophagy-mediated cell responses. Taken together, this study provides cellular and molecular insights into the toxicity of F-53B to plant cells, which highlights its damage to agriculture and ecology security that deserve imperative environmental management actions. Environmental Implication F-53B has been detected in many plant species, which raises increasing concerns on its toxicity to plants and thus agriculture and ecology safety. However, the toxicity of F-53B to development in plants and the underpinning mechanisms remain largely unelucidated. Here, we demonstrate that F-53B damages nuclei stability and viability leading to cell death and impaired root development in the model plant species Arabidopsis thaliana . Our study provides cytogenetic and molecular insights into the F-53B toxicity to plant cells, which highlights imperative environmental management actions and can be referenced for developing F-53B control and management policies. GRAPHICAL ABSTRACT One-sentence summary F-53B triggers DNA double-strand break-free cell unviability leading to impaired meristematic cell division and root development in plants. HIGHLIGHTS F-53B impairs root development in Arabidopsis. F-53B prohibits mitotic cell division at root tips. F-53B damages cell viability predominantly at the meristematic zone in seedlings. F-53B does not induce DNA double-strand breaks in Arabidopsis seedlings. F-53B damages nuclei viability and stability in seedlings.
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