Degradation of active C 19 -gibberellins (GAs) by dioxygenases through 2 ␤ -hydroxylation yields inactive GA products. We identified two genes in Arabidopsis ( AtGA2ox7 and AtGA2ox8 ), using an activation-tagging mutant screen, that encode 2 ␤ -hydroxylases. GA levels in both activation-tagged lines were reduced significantly, and the lines displayed dwarf phenotypes typical of mutants with a GA deficiency. Increased expression of either AtGA2ox7 or AtGA2ox8 also caused a dwarf phenotype in tobacco, indicating that the substrates for these enzymes are conserved. AtGA2ox7 and AtGA2ox8 are more similar to each other than to other proteins encoded in the Arabidopsis genome, indicating that they may constitute a separate class of GA-modifying enzymes. Indeed, enzymatic assays demonstrated that AtGA2ox7 and AtGA2ox8 both perform the same GA modification: 2 ␤ -hydroxylation of C 20 -GAs but not of C 19 -GAs. Lines containing increased expression of AtGA2ox8 exhibited a GA dose-response curve for stem elongation similar to that of the biosynthetic mutant ga1-11 . Double loss-of-function Atga2ox7 Atga2ox8 mutants had twofold to fourfold higher levels of active GAs and displayed phenotypes associated with excess GAs, such as early bolting in short days, resistance to the GA biosynthesis inhibitor ancymidol, and decreased mRNA levels of AtGA20ox1 , a gene in the GA biosynthetic pathway.

SummaryThe HUA2 gene acts as a repressor of floral transition. Lesions in hua2 were identified through a study of natural variation and through two mutant screens. An allele of HUA2 from Landsberg erecta (Ler) contains a premature stop codon and acts as an enhancer of early flowering 4 (elf4) mutants. hua2 single mutants, in the absence of the elf4 lesion, flower earlier than wild type under short days. hua2 mutations partially suppress late flowering in FRIGIDA (FRI )-containing lines, autonomous pathway mutants, and a photoperiod pathway mutant. hua2 mutations suppress late flowering by reducing the expression of several MADS genes that act as floral repressors including FLOWERING LOCUS C (FLC ) and FLOWERING LOCUS M (FLM ).

SummaryEARLY FLOWERING 5 (ELF5) is a single-copy gene involved in¯owering time regulation in Arabidopsis. ELF5 encodes a nuclear-targeted protein that is related to the human nuclear protein containing a WW domain (Npw)38-binding protein (NpwBP). Lesions in ELF5 cause early¯owering in both long days and short days. elf5 mutations partially suppress the late¯owering of both autonomous-pathway mutants and FRIGIDA (FRI)-containing lines by reducing the expression of FLOWERING LOCUS C (FLC), a¯oral repressor upon which many of the¯owering pathways converge. elf5 mutations also partially suppress photoperiodpathway mutants, and this, along with the ability of elf5 mutations to cause early¯owering in short days, indicates that ELF5 also affects¯owering independently of FLC.

Seeds of rapid-cycling Brassica oleracea were mutagenized with the chemical mutagen, ethylmethane sul fonate. The reverse genetics technique, TILLING, was used on a sample population of 1,000 plants, to determine the mutation proWle. The spectrum and frequency of mutations induced by ethylmethane sulfonate was similar to that seen in other diploid species such as Arabidopsis thaliana. These data indicate that the mutagenesis was eVective and demonstrate that TILLING represents an eYcient reverse genetic technique in B. oleracea that will become more valuable as increasing genomic sequence data become available for this species. The extensive duplication in the B. oleracea genome is believed to result in the genetic redundancy that has been important for the evolution of morphological diversity seen in today's B. oleracea crops (broccoli, Brussels sprouts, cauliXower, cabbage, kale and kohlrabi). However, our forward genetic screens identiWed 120 mutants in which some aspect of development was