Plant and Cell Physiology Advance Access published online on November 4, 2009
Plant and Cell Physiology, doi:10.1093/pcp/pcp152
Suppression of Peroxisome Biogenesis Factor 10 Reduces Cuticular Wax Accumulation by Disrupting the ER Network in Arabidopsis thaliana
1Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
2Department of Molecular Biomechanics, School of Life Science, The Graduate University for Advanced Studies (SOKENDAI), Okazaki, 444-8585, Japan
* Corresponding author: Mikio Nishimura Department of Cell Biology National Institute for Basic Biology, Okazaki 444-8585, Japan Phone number: +81-564-55-7500 Fax number: +81-564-55-7505 E-mail: mikosome{at}nibb.ac.jp
| Abstract |
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Peroxisome biogenesis factor 10 (PEX10) is a component of the peroxisomal matrix protein import machinery. To analyze the physiological function of PEX10, we used transgenic AtPEX10i Arabidopsis plants that had suppressed expression of the PEX10 gene due to RNA interference. AtPEX10i plants had patches of paleness on leaves, and abnormal floral organs that were typical of cuticular wax-deficient mutants. Quantitative analysis of cuticular wax revealed that the amount of wax in AtPEX10i plants was indeed lower than that in control plants. This result was confirmed by toluidine blue staining and scanning electron microscopic analysis of AtPEX10i. The CER1, CER4, WAX2 and SHN1 genes are known to be responsible for wax biosynthesis in Arabidopsis. Of these, CER1, CER4 and WAX2 were found to be localized on the ER. In AtPEX10i plants, the expression of these genes was down-regulated, and CER1, CER4 and WAX2 were mislocalized to the cytosol. We also found that AtPEX10i plants had defects in ER morphology. Based on these results, we propose that PEX10 is essential for the maintenance of ER morphology and for the expression of CER1, CER4, WAX2 and SHN1 genes, which contribute to the biosynthesis of cuticular wax.
Keywords: Arabidopsis - cuticle - endoplasmic reticulum - glyoxysome - peroxisome - wax
(Received September 16, 2009; Accepted October 20, 2009)
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