Transverse Lattice QCD in 2+1 Dimensions

Following a suggestion due to Bardeen and Pearson, we formulate an effective light-front Hamiltonian for large-N gauge theory in (2+1)-dimensions. Two space-time dimensions are continuous and the remaining space dimension is discretised on a lattice. Eguchi-Kawai reduction to a (1+1)-dimensional theory takes place. We investigate the string tension and glueball spectrum, comparing with Euclidean Lattice Monte Carlo data.Comment: 4 pages LaTeX with 2 Postscript figures, uses boxedeps.tex and e spcrc2.sty. Poster session contribution to LATTICE96(poster). Minor changes in new versio

MAX1and MAX2 control shoot lateral branching in Arabidopsis

Plant shoots elaborate their adult form by selective control over the growth of both their primary shoot apical meristem and their axillary shoot meristems. We describe recessive mutations at two loci in Arabidopsis, MAX1 and MAX2, that affect the selective repression of axillary shoots. All the first order (but not higher order) axillary shoots initiated by mutant plants remain active, resulting in bushier shoots than those of wild type. In vegetative plants where axillary shoots develop in a basal to apical sequence, the mutations do not clearly alter node distance, from the shoot apex, at which axillary shoot meristems initiate but shorten the distance at which the first axillary leaf primordium is produced by the axillary shoot meristem. A small number of mutant axillary shoot meristems is enlarged and, later in development, a low proportion of mutant lateral shoots is fasciated. Together, this suggests that MAX1 and MAX2 do not control the timing of axillary meristem initiation but repress primordia formation by the axillary meristem. In addition to shoot branching, mutations at both loci affect leaf shape. The mutations at MAX2 cause increased hypocotyl and petiole elongation in light-grown seedlings. Positional cloning identifies MAX2 as a member of the F-box leucine-rich repeat family of proteins. MAX2 is identical to ORE9, a proposed regulator of leaf senescence (Woo, H. R., Chung, K. M., Park, J.-H., Oh, S. A., Ahn, T., Hong, S. H., Jang, S. K. and Nam, H. G. (2001) Plant Cell 13, 1779-1790). Our results suggest that selective repression of axillary shoots involves ubiquitinmediated degradation of as yet unidentified proteins that activate axillary growth