In Arabidopsis, the DET1, COP and FUS proteins are thought to be global repressors of photomorphogenesis — changes in growth and development in response to light. Although DET1 is known to encode a nuclear protein that regulates gene expression, its precise function has remained unclear. Now, however, reporting in Science, Joanne Chory and colleagues provide insights into the function of DET1 by isolating suppressors of the det1 phenotype.

The authors called these suppressors ted mutants, and found that the ted3 mutant is a dominant suppressor of the det1 phenotype. They mapped and sequenced the TED3 gene and used database searches to show that TED3 is homologous to PEX2 in yeast and mammals. PEX2 is involved in peroxisome assembly and matrix-enzyme import, and peroxisomes are single-membrane-bound organelles that perform many metabolic functions. Using a TED3–green fluorescent protein fusion construct, the authors confirmed the peroxisomal localization of TED3.

Chory and co-workers showed that the phenotype of the homozygous TED3 knockout is embryonic lethal, and also that transgenic plants containing the antisense TED3 transcript are dwarfed, pale and sterile. Because they found that TED3 is ubiquitously expressed throughout development and showed that it is expressed at high levels in seeds, pollen, ovules and cotyledons, the authors propose that it is essential for Arabidopsis reproduction and development.

Because ted3 is localized to peroxisomes, the authors investigated whether peroxisomal activities are disrupted in det1 plants and restored in det1 ted3 plants. Germination on a sugar-free medium requires active peroxisomes, and they found that det1 seeds could not fully develop on such a medium unless ted3 came to the rescue. In addition, glyoxysomes (specialized peroxisomes) can convert indole-3-butyric acid (IBA) to indole-3-acetic acid, an auxin that inhibits root elongation, and they showed that IBA affected root elongation to a lesser extent in det1 plants than in wild-type or det1 ted3 plants.

When the authors compared the levels of glyoxysomal enzymes in det1 and det1 ted3 plants, they found that the levels were much higher in the latter. They also compared wild-type and ted3 seedlings, and found that, although RNA levels were similar, protein levels were higher in ted3 plants. The data therefore indicate that det1 seedlings have defective peroxisomes that can be rescued by the ted3 gain-of-function mutation, and that ted3 might act by stabilizing peroxisomal proteins.

Finally, Chory and colleagues used an Arabidopsis oligonucleotide array containing ∼8,300 genes to compare gene-expression profiles in wild-type, ted3 and det1 ted3 plants. They showed that, in both light- and dark-grown seedlings, a large proportion of the genes that are misregulated in det1 plants are restored, or partially restored, by ted3. In addition, they found that several peroxisome-related genes were underexpressed in det1 plants.

The authors have therefore found that “increased peroxisomal function can suppress the numerous ... defects caused by mutations in DET1”. Because they also found that ted3 partially suppresses the effects of cop1 , they propose that peroxisomes, whose roles still remain largely unknown, have an important function in a photomorphogenetic pathway that is negatively regulated by DET1 and COP. This newly discovered link between peroxisomes and the response to light should open up new avenues in understanding how plants respond to environmental variation.