The hexavalent form of chromium [Cr(VI)] causes a major reduction in yield and quality of crops worldwide. The root is the first plant organ that interacts with Cr(VI) toxicity, which inhibits primary root elongation, but the underlying mechanisms of this inhibition remain elusive. In this study, we investigate the possibility that Cr(VI) reduces primary root growth of Arabidopsis by modulating the cell cycle-related genes and that ethylene signalling contributes to this process. We show that Cr(VI)-mediated inhibition of primary root elongation was alleviated by the ethylene perception and biosynthesis antagonists silver and cobalt, respectively. Furthermore, the ethylene signalling defective mutants (ein2-1 and etr1-3) were insensitive, whereas the overproducer mutant (eto1-1) was hypersensitive to Cr(VI). We also report that high levels of Cr(VI) significantly induce the distribution and accumulation of auxin in the primary root tips, but this increase was significantly suppressed in seedlings exposed to silver or cobalt. In addition, genetic and physiological investigations show that AUXIN-RESISTANT1 (AUX1) participates in Cr(VI)-induced inhibition of primary root growth. Taken together, our results indicate that ethylene mediates Cr(VI)-induced inhibition of primary root elongation by increasing auxin accumulation and polar transport by stimulating the expression of AUX1.

The most recent outcomes about the transcription factors and transcription complexes mediated auxin signaling pathway by the histone acetylation and deacetylation. The phytohormone auxin, is required to regulate its accumulation spatiotemporally and responses to orchestrate various developmental levels in plants. Histone acetylation and deacetylation modulate auxin biosynthesis, its distribution and accumulation. In the absence of auxin, histone deacetylase represses the expression of auxin-responsive genes. Various transcription factors and transcription complexes facilitate the proper regulation of auxin signaling pathway genes. The primary and lateral root development, promotion of flowering and initiation of seed germination are all regulated by auxin-mediated histone acetylation and deacetylation. These findings conclude the auxin mode of action, which is mediated by histone acetylation and deacetylation, and associated phenotypic responses in plants, along with the underlying mechanism of these modifications.

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Bisphenol A (BPA) is an emerging environmental pollutant with potentially toxic effects on living organisms. The present study was undertaken to analyze the effects of BPA on the leaves of Arabidopsis thialina by determining the levels of photosynthetic pigments, reactive oxygen species (ROS), membrane lipid peroxidation, and ultrastructural malformation. The obtained results revealed that while a low dose of BPA (10µM) did not alter the test indices significantly, it did cause significant changes in all test indices at higher concentrations. Upon exposure to 40 µM BPA, chlorophyll a and chlorophyll b content showed a decrease of 33% and 30%, respectively. It significantly increased ROS contents and lipid peroxidation at 40 µM BPA exposure. Biochemical and gene expression analysis revealed that the antioxidant system was activated and mounted a defense against BPA-induced ROS. In the case of superoxide dismutase (SOD), 40 µM of BPA caused an increase of 151%. However, the malfunctioning of ascorbate peroxidase (APX) and catalase (CAT) at the highest dose of BPA (40 µM) resulted in incomplete activation of the antioxidant defensive system. BPA stress significantly altered the ultrastructure of cells as evidenced by the reduced number of starch grains, damaged chloroplast and mitochondria, and altered leaf epidermal surface, guard cells, and stomata. It is concluded that observed adverse effects in Arabidopsis leaves in response to BPA exposure could be attributed to BPA-induced oxidative stress.