| Summary: | <p>Abstract</p> <p>Background</p> <p>The <it>EXO </it>(<it>EXORDIUM</it>) gene was identified as a potential mediator of brassinosteroid (BR)-promoted growth. It is part of a gene family with eight members in Arabidopsis. <it>EXO </it>gene expression is under control of BR, and <it>EXO </it>overexpression promotes shoot and root growth. In this study, the consequences of loss of <it>EXO </it>function are described.</p> <p>Results</p> <p>The <it>exo </it>loss of function mutant showed diminished leaf and root growth and reduced biomass production. Light and scanning electron microscopy analyses revealed that impaired leaf growth is due to reduced cell expansion. Epidermis, palisade, and spongy parenchyma cells were smaller in comparison to the wild-type. The <it>exo </it>mutant showed reduced brassinolide-induced cotyledon and hypocotyl growth. In contrast, <it>exo </it>roots were significantly more sensitive to the inhibitory effect of synthetic brassinolide. Apart from reduced growth, <it>exo </it>did not show severe morphological abnormalities. Gene expression analyses of leaf material identified genes that showed robust EXO-dependent expression. Growth-related genes such as <it>WAK1</it>, <it>EXP5</it>, and <it>KCS1</it>, and genes involved in primary and secondary metabolism showed weaker expression in <it>exo </it>than in wild-type plants. However, the vast majority of BR-regulated genes were normally expressed in <it>exo</it>. HA- and GFP-tagged EXO proteins were targeted to the apoplast.</p> <p>Conclusion</p> <p>The <it>EXO </it>gene is essential for cell expansion in leaves. Gene expression patterns and growth assays suggest that EXO mediates BR-induced leaf growth. However, EXO does not control BR-levels or BR-sensitivity in the shoot. EXO presumably is involved in a signalling process which coordinates BR-responses with environmental or developmental signals. The hypersensitivity of <it>exo </it>roots to BR suggests that EXO plays a diverse role in the control of BR responses in the root.</p>
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