The ETR1 receptor from Arabidopsis binds the gaseous hormone ethylene. A copper ion associated with the ethylene-binding domain is required for high-affinity ethylene-binding activity. A missense mutation in the domain that renders the plant insensitive to ethylene eliminates both ethylene binding and the interaction of copper with the receptor. A sequence from the genome of the cyanobacterium Synechocystis sp. strain 6803 that shows homology to the ethylene-binding domain of ETR1 encodes a functional ethylene-binding protein. On the basis of sequence conservation between the Arabidopsis and the cyanobacterial ethylene-binding domains and on in vitro mutagenesis of ETR1, a structural model for this copper-based ethylene sensor domain is presented.

The TRANSPARENT TESTA GLABRA1 ( TTG1 ) locus regulates several developmental and biochemical pathways in Arabidopsis, including the formation of hairs on leaves, stems, and roots, and the production of seed mucilage and anthocyanin pigments. The TTG1 locus has been isolated by positional cloning, and its identity was confirmed by complementation of a ttg1 mutant. The locus encodes a protein of 341 amino acid residues with four WD40 repeats. The protein is similar to AN11, a regulator of anthocyanin biosynthesis in petunia, and more distantly related to those of the ␤ subunits of heterotrimeric G proteins, which suggests a role for TTG1 in signal transduction to downstream transcription factors. The 1.5-kb TTG1 transcript is present in all major organs of Arabidopsis. Sequence analysis of six mutant alleles has identified base changes producing truncations or single amino acid changes in the TTG1 protein. INTRODUCTIONThe TRANSPARENT TESTA GLABRA1 ( TTG1 ) locus controls many apparently unrelated characters of Arabidopsis (catalogued by Koornneef, 1981), several of which appear to be confined to the epidermal cell layer of different tissues. ttg1 mutants have a glabrous phenotype, possessing none of the leaf or stem hairs (trichomes) that normally are derived from the meristematic L1 cell layer. Purple anthocyanin pigments are absent from the ttg1 seed coat, causing the transparent testa phenotype in which the yellow cotyledons are visible through the testa. In wild-type plants, anthocyanins are present in the hypocotyl of seedlings and in the stem and leaves of plants as they age, and they are inducible by many forms of stress, including high light, poor nutrients, or water stress. ttg1 mutants completely lack anthocyanins in the epidermis and in subepidermal layers of leaves and stems. Mucilage normally found in the cell wall of the seed coat is absent in ttg1 mutants. Seeds of ttg1 plants do not require drying and cold treatments to germinate and therefore exhibit an altered seed dormancy when compared with ecotypes, such as Landsberg erecta (L er ;Koornneef, 1981;Léon-Kloosterziel et al., 1994). This characteristic of ttg1 mutants may be linked to an altered seed coat structure. The TTG1 gene appears to have the opposite effect on root hair formation when compared with its effect on leaf hair initiation. In Arabidopsis, root hairs extend from root epidermal cells only in files of cells that contact two underlying cortical cells, whereas in ttg1 mutants, extra root hairs occur in the atrichoblast cell files (Galway et al., 1994). Under laboratory growth conditions, mutations at the ttg1 locus do not greatly affect the viability of the plants.In ttg1 mutants, the anthocyanin biosynthetic pathway is blocked at the dihydroflavonol-4-reductase (DFR) step, because DFR-encoding transcripts have not been detected in these mutants (Shirley et al., 1995). By contrast, transcripts of the chalcone synthase and chalcone isomerase genes are unaffected. The point of regulation of the pathway by TTG1 was confirmed by the clon...

Appendage formation is organized by signals from discrete sources that presumably act upon downstream genes to control growth and patterning. The Drosophila vestigial gene is selectively required for wing-cell proliferation, and is sufficient to induce outgrowths of wing tissue from eyes, legs and antennae. Different signals activate separate enhancers to control vestigial expression: first, in the dorsal/ventral organizer through the Notch pathway, and subsequently, in the developing wing blade by decapentaplegic and a signal from the dorsal/ventral organizer. Signal integration must be a general feature of genes like vestigial, that regulate growth or patterning along more than one axis.

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