Abstract
The widely used non-steroidal anti-inflammatory drugs (NSAIDs) are derivatives of the phytohormone salicylic acid (SA). SA is well known to regulate plant immunity and development, whereas there have been few reports focusing on the effects of NSAIDs in plants. Our studies here reveal that NSAIDs exhibit largely overlapping physiological activities to SA in the model plant Arabidopsis. NSAID treatments lead to shorter and agravitropic primary roots and inhibited lateral root organogenesis. Notably, in addition to the SA-like action, which in roots involves binding to the protein phosphatase 2A (PP2A), NSAIDs also exhibit PP2A-independent effects. Cell biological and biochemical analyses reveal that many NSAIDs bind directly to and inhibit the chaperone activity of TWISTED DWARF1, thereby regulating actin cytoskeleton dynamics and subsequent endosomal trafficking. Our findings uncover an unexpected bioactivity of human pharmaceuticals in plants and provide insights into the molecular mechanism underlying the cellular action of this class of anti-inflammatory compounds.
Highlights
The active compounds from willow (Salix alba L.) barks, salicylic acid (SA) or salicylates, have been used to treat pain and fever since prehistoric times (Lichterman, 2004; Yin et al, 1998)
Triple Inhibitory Effects of non-steroidal anti-inflammatory drugs (NSAIDs) on Arabidopsis Root Morphology Given the fact that both SA and synthetic NSAIDs function in a common way (Duggan et al, 2011; Yin et al, 1998), we were wondering whether these synthetic NSAIDs could retain some SA bioactivity in plants
We grew Arabidopsis seedlings on plates with different concentrations of NSAIDs and found that most of them exhibited a pronounced effect in the 10- to 100-mM range
Summary
The active compounds from willow (Salix alba L.) barks, salicylic acid (SA) or salicylates, have been used to treat pain and fever since prehistoric times (Lichterman, 2004; Yin et al, 1998). SA can function through various SA binding proteins (Choi et al, 2015, 2016; Klessig et al, 2016), and SA participates in regulating plant growth and development (Kazan and Manners, 2009; Wang et al, 2007) This developmental role of SA is realized via crosstalk with the transport mechanism for the phytohormone auxin (Du et al, 2013; Pasternak et al, 2019; Rong et al, 2016; Wang et al, 2017). SA regulates root development through both the clathrin-mediated endocytosis pathway (Du et al, 2013; Wang et al, 2016) and protein phosphatase 2A (PP2A)-mediated (de)phosphorylation of PINFORMED (PIN) auxin transporters (Tan et al, 2020a), together regulating the plasma membrane (PM) targeting and polar distribution of PINs (Grones and Friml, 2015). Little is known about the effects of NSAIDs in plants—whether they preserve the function of SA or even have any activity at all
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