Mutation of the cytosolic ribosomal protein-encoding <it>RPS10B</it> gene affects shoot meristematic function in Arabidopsis

<p>Abstract</p> <p>Background</p> <p>Plant cytosolic ribosomal proteins are encoded by small gene families. Mutants affecting these genes are often viable, but show growth and developmental defects, suggesting incomplete functional redundancy within the families. Dormancy to growth transitions, such as the activation of axillary buds in the shoot, are characterised by co-ordinated upregulation of ribosomal protein genes.</p> <p>Results</p> <p>A recessive mutation in <it>RPS10B,</it> one of three Arabidopsis genes encoding the eukaryote-specific cytoplasmic ribosomal protein S10e, was found to suppress the excessive shoot branching mutant <it>max2-1</it>. <it>rps10b-1</it> mildly affects the formation and separation of shoot lateral organs, including the shoot axillary meristems. Axillary meristem defects are enhanced when <it>rps10b-1</it> is combined with mutations in <it>REVOLUTA</it>, <it>AUXIN-RESISTANT1</it>, <it>PINOID</it> or another suppressor of <it>max2-1</it>, <it>FAR-RED ELONGATED HYPOCOTYL3</it>. In some of these double mutants, the maintenance of the primary shoot meristem is also affected. In contrast, mutation of <it>ALTERED MERISTEM PROGRAMME1</it> suppresses the <it>rps10b-1</it>axillary shoot defect. Defects in both axillary shoot formation and organ separation were enhanced by combining <it>rps10b-1</it> with <it>cuc3,</it> a mutation affecting one of three Arabidopsis NAC transcription factor genes with partially redundant roles in these processes. To assess the effect of <it>rps10b-1</it> on bud activation independently from bud formation, axillary bud outgrowth on excised cauline nodes was analysed. The outgrowth rate of untreated buds was reduced only slightly by <it>rps10b-1</it> in both wild-type and <it>max2-1</it> backgrounds. However, <it>rps10b-1</it> strongly suppressed the auxin resistant outgrowth of <it>max2-1</it> buds. A developmental phenotype of <it>rps10b-1</it>, reduced stamen number, was complemented by the cDNA of another family member, <it>RPS10C</it>, under the <it>RPS10B</it> promoter.</p> <p>Conclusions</p> <p><it>RPS10B</it> promotes shoot branching mainly by promoting axillary shoot development. It contributes to organ boundary formation and leaf polarity, and sustains <it>max2-1</it> bud outgrowth in the presence of auxin. These processes require the auxin response machinery and precise spatial distribution of auxin. The correct dosage of protein(s) involved in auxin-mediated patterning may be <it>RPS10B</it>-dependent. Inability of other <it>RPS10</it> gene family members to maintain fully S10e levels might cause the <it>rps10b-1</it> phenotype, as we found no evidence for unique functional specialisation of either <it>RPS10B</it> promoter or RPS10B protein.</p>