Methylation and demethylation of the Arabidopsis genome.

The primary sequence of the genome is broadly constant and superimposed upon that constancy is the postreplicative modification of a small number of cytosine residues to 5-methylcytosine. The pattern of methylation is non-random; some sequence contexts are frequently methylated and some rarely methylated and some regions of the genome are highly methylated and some rarely methylated. Once established, methylation is not static: it can potentially change in response to developmental or environmental cues and this may result in correlated changes in gene expression. Changes can occur passively owing to a failure to maintain DNA methylation through rounds of DNA replication, or actively, through the action of enzymes with DNA glycosylase activity. Recent advances in genetic analyses and the generation of high resolution, genome-wide methylation maps are revealing in unprecedented detail the patterns and dynamic changes of DNA methylation in plants.

MAX2 participates in an SCF complex which acts locally at the node to suppress shoot branching.

The Arabidopsis gene ORE9/MAX2 encodes an F-box leucine-rich repeat protein. F-box proteins function as the substrate-recruiting subunit of SCF-type ubiquitin E3 ligases in protein ubiquitination. One of several phenotypes of max2 mutants, the highly branched shoot, is identical to mutants at three other MAX loci. Reciprocal grafting, double mutant analysis and gene cloning suggest that all MAX genes act in a common pathway, where branching suppression depends on MAX2 activity in the shoot, in response to an acropetally mobile signal that requires MAX3, MAX4 and MAX1 for its production. Here, we further investigate the site and mode of action of MAX2 in branching. Transcript analysis and a translational MAX2-GUS fusion indicate that MAX2 is expressed throughout the plant, most highly in developing vasculature, and is nuclear-localized in many cell types. Analysis of cell autonomy shows that MAX2 acts locally, either in the axillary bud, or in adjacent stem or petiole tissue. Expression of MAX2 from the CaMV 35S promoter complements the max2 mutant, does not affect branching in a wild-type background and partially rescues increased branching in the max1, max3 and max4 backgrounds. Expression of mutant MAX2, lacking the F-box domain, under the CaMV 35S promoter does not complement max2, and dominant-negatively affects branching in the wild-type background. Myc-epitope-tagged MAX2 interacts with the core SCF subunits ASK1 and AtCUL1 in planta. We conclude that axillary shoot growth is controlled locally, at the node, by an SCF(MAX2), the action of which is enhanced by the mobile MAX signal.