| 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. |
