Epidermal expression of a sterol biosynthesis gene regulates root growth by a non-cell-autonomous mechanism in Arabidopsis.

The epidermis is hypothesized to play a signalling role during plant development. One class of mutants showing defects in signal transduction and radial patterning are those in sterol biosynthesis. The expectation is that living cells require sterols, but it is not clear that all cell types express sterol biosynthesis genes. The HYDRA1 (HYD1) gene of Arabidopsis encodes sterol Δ8-Δ7 isomerase, and although hyd1 seedlings are defective in radial patterning across several tissues, we show that the HYD1 gene is expressed most strongly in the root epidermis. Transgenic activation of HYD1 transcription in the epidermis of hyd1 null mutants reveals a major role in root patterning and growth. HYD1 expression in the vascular tissues and root meristem, though not endodermis or pericycle, also leads to some phenotypic rescue. Phenotypic rescue is associated with rescued patterning of the PIN1 and PIN2 auxin efflux carriers. The importance of the epidermis in controlling root growth and development is proposed to be, in part, due to its role as a site for sterol biosynthesis, and auxin is a candidate for the non-cell-autonomous signal.

A stress-specific calcium signature regulating an ozone-responsive gene expression network in Arabidopsis.

Changes in gene expression form a key component of the molecular mechanisms by which plants adapt and respond to environmental stresses. There is compelling evidence for the role of stimulus-specific Ca(2+) signatures in plant stress responses. However, our understanding of how they orchestrate the differential expression of stress-induced genes remains fragmentary. We have undertaken a global study of changes in the Arabidopsis transcriptome induced by the pollutant ozone in order to establish a robust transcriptional response against which to test the ability of Ca(2+) signatures to encode stimulus-specific transcriptional information. We show that the expression of a set of co-regulated ozone-induced genes is Ca(2+)-dependent and that abolition of the ozone-induced Ca(2+) signature inhibits the induction of these genes by ozone. No induction of this set of ozone-regulated genes was observed in response to H(2)O(2), one of the reactive oxygen species (ROS) generated by ozone, or cold stress, which also generates ROS, both of which stimulate changes in [Ca(2+)](cyt). These data establish unequivocally that the Ca(2+)-dependent changes in gene expression observed in response to ozone are not simply a consequence of an ROS-induced increase in [Ca(2+) ](cyt) per se. The magnitude and temporal dynamics of the ozone, H(2)O(2) , and cold Ca(2+) signatures all differ markedly. This finding is consistent with the hypothesis that stimulus-specific transcriptional information can be encoded in the spatiotemporal dynamics of complex Ca(2+) signals in plants.