Abstract
The uppermost internode is one of the fastest elongating organs in rice, and is expected to require an adequate supply of cell-wall materials and enzymes to the cell surface to enhance mechanical strength. Although it has been reported that the phenotype of shortened uppermost internode 1 (sui1) is caused by mutations in PHOSPHATIDYLSERINE SYNTHASE (OsPSS), the underlying mechanism remains unclear. Here we show that the OsPSS-1, as a gene expressed predominantly in elongating cells, regulates post-Golgi vesicle secretion to intercellular spaces. Mutation of OsPSS-1 leads to compromised delivery of CESA4 and secGFP towards the cell surface, resulting in weakened intercellular adhesion and disorganized cell arrangement in parenchyma. The phenotype of sui1-4 is caused largely by the reduction in cellulose contents in the whole plant and detrimental delivery of pectins in the uppermost internode. We found that OsPSS-1 and its potential product PS (phosphatidylserine) localized to organelles associated with exocytosis. These results together suggest that OsPSS-1 plays a potential role in mediating cell expansion by regulating secretion of cell wall components.
Highlights
Cell division and anisotropic cell expansion determine the final size and shape of plant organs
Similar JIM7-labeled pectin clumps were observed in the outermost regions of the cell wall of sui1-4 plants (S3E and S3F Fig), suggesting that the uppermost internodes were defective in pectin secretion and deposition
To determine if any soluble proteins or cell-wall-synthesis related enzymes have defective transport to the plasma membrane (PM) in sui1-4, we investigated trafficking of vesicles carrying OsCESA4, a member of the cellulose synthesis complex, which is believed to be synthesized in the endoplasmic reticulum (ER) and transported to PM via the trans Golgi network (TGN) [37,38]
Summary
Cell division and anisotropic cell expansion determine the final size and shape of plant organs. Role of OsPSS-1 in Plant Development cellulose synthase genes result in altered cellulose contents and inhibition of cell elongation. Mutations of PSS in Schizosaccharomyces pombe (pps1Δ) and the fungus Candida albicans (cho1Δ/Δ) lead to slow growth due to cell-wall defects [19,20]. These results imply an unidentified role of PSS in regulation of cell expansion. We showed that mutation in OsPSS-1 in rice leads to defected cell expansion and compromised cell wall biosynthesis. Our results revealed a potential role of OsPSS-1 in cell wall component trafficking
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