Adventitious rooting is a quantitative genetic trait regulated by both environmental and endogenous factors. To better understand the physiological and molecular basis of adventitious rooting, we took advantage of two classes of Arabidopsis thaliana mutants altered in adventitious root formation: the superroot mutants, which spontaneously make adventitious roots, and the argonaute1 (ago1) mutants, which unlike superroot are barely able to form adventitious roots. The defect in adventitious rooting observed in ago1 correlated with light hypersensitivity and the deregulation of auxin homeostasis specifically in the apical part of the seedlings. In particular, a clear reduction in endogenous levels of free indoleacetic acid (IAA) and IAA conjugates was shown. This was correlated with a downregulation of the expression of several auxininducible GH3 genes in the hypocotyl of the ago1-3 mutant. We also found that the Auxin Response Factor17 (ARF17) gene, a potential repressor of auxin-inducible genes, was overexpressed in ago1-3 hypocotyls. The characterization of an ARF17-overexpressing line showed that it produced fewer adventitious roots than the wild type and retained a lower expression of GH3 genes. Thus, we suggest that ARF17 negatively regulates adventitious root formation in ago1 mutants by repressing GH3 genes and therefore perturbing auxin homeostasis in a light-dependent manner. These results suggest that ARF17 could be a major regulator of adventitious rooting in Arabidopsis.

The FK506-binding proteins (FKBPs) are peptidyl prolyl cis/trans isomerases and the information gathered in the last 10 years reveals their involvement in diverse biological systems affecting the function and structure of target proteins. Members of the FKBP family were shown to be growth-regulated and participate in signal transduction. In this review we have chosen to focus on a few examples of the mammalian and plant systems in which members of the FKBP family have been demonstrated to affect the function of proteins or development. The technologies that enable production of knockout mice, Arabidopsis mutants and overexpression in transgenic organisms have revealed the contribution of FKBP to development in higher eukaryotes. It appears that members of the FKBP family have conserved some of their basic functions in the animal and plant kingdom, whereas other functions became unique. Studies that will take advantage of the full genome sequence available for Arabidopsis and the human genome, DNA chip technologies and the use of transgenic complementation system will contribute to the elucidation of the molecular mechanism and biological function of FKBPs.

A mutant screen was developed to isolate Arabidopsis thaliana mutants affected in the regulation of the nitrate assimilation pathway. A fusion between the tobacco Nii1 gene (that encodes a foliar nitrite reductase involved in nitrate assimilation) and the Gus reporter gene was introduced into A. thaliana, and shown to be properly regulated by nitrate. Moreover, β‐glucuronidase (GUS) activity in the transgenic plants was essentially detected in the cotyledons and leaves, showing that the organ‐specific expression of the tobacco Nii1 gene was retained in Arabidopsis. M2 plantlets derived from mutagenized seeds homozygous for the Nii‐Gus fusion were screened by histochemical staining of whole plates for GUS activity after growth on nitrate or glutamine. About 250 progenies were screened, leading to the isolation of plants showing an enhanced or reduced staining compared to the control non‐mutagenized plants. Several mutants were analyzed for the transmission of the phenotype to the M3 generation, as well as for levels of GUS or nitrite reductase activities or mRNA levels. A major problem encountered during the screening was the high background of false positives that reproducibly showed altered GUS histochemical staining compared to control plants and did not, however, display any changes in GUS activity levels. One interesting family of mutants was isolated that overexpressed GUS activity and Nii mRNA in the absence of nitrate. These mutants turned out to be cnx mutants impaired in the molybdenum cofactor biosynthesis that is necessary for nitrate reductase activity. These results may indicate that active nitrate reductase is necessary for a correct regulation of nitrate assimilation genes by nitrate.

A mutant screen was developed to isolate Arabidopsis thaliana tagenized plants. Several mutants were analyzed for the transmutants affected in the regulation of the nitrate assimilation mission of the phenotype to the M3 generation, as well as for pathway. A fusion between the tobacco Nii1 gene (that en-levels of GUS or nitrite reductase activities or mRNA levels. codes a foliar nitrite reductase involved in nitrate assimilation) A major problem encountered during the screening was the and the Gus reporter gene was introduced into A. thaliana, high background of false positives that reproducibly showed altered GUS histochemical staining compared to control and shown to be properly regulated by nitrate. Moreover, -glucuronidase (GUS) activity in the transgenic plants was plants and did not, however, display any changes in GUS essentially detected in the cotyledons and leaves, showing that activity levels. One interesting family of mutants was isolated that overexpressed GUS activity and Nii mRNA in the ab-the organ-specific expression of the tobacco Nii1 gene was retained in Arabidopsis. M2 plantlets derived from mutage-sence of nitrate. These mutants turned out to be cnx mutants nized seeds homozygous for the Nii-Gus fusion were screened impaired in the molybdenum cofactor biosynthesis that is necessary for nitrate reductase activity. These results may by histochemical staining of whole plates for GUS activity after growth on nitrate or glutamine. About 250 progenies indicate that active nitrate reductase is necessary for a correct regulation of nitrate assimilation genes by nitrate. were screened, leading to the isolation of plants showing an enhanced or reduced staining compared to the control non-mu-