Tissue-specific pectin methylesterification and pectin methylesterase activities play a role in lettuce seed germination

Abstract

Cell wall mechanical strength is partially controlled by the degree of pectin methylesterification that is mediated through the action of pectin methylesterases (PMEs). Changes in cell wall mechanical strength are involved in the endosperm cap weakening and radicle elongation growth during the germination of some endospermic seeds. However, little is known about the roles of the status of pectin methylesterification and PME activities during seed germination, especially in lettuce, a traditional model plant for seed germination research. In the present study, we demonstrated that the rupture of lettuce endosperm cap during seed germination was caused by cell rupture, not by cell separation as formerly reported in other species. Next, we investigated the status of pectin methylesterification of the endosperm cap and radicle during germination, using immunolabeling by specific monoclonal antibodies against methyl-esterified pectins and calcium bridges. We also analyzed the expression patterns of PME activities and an encoding gene LsPME/PMEI51 in the endosperm cap and radicle. It was found that cell walls of the endosperm cap comprise more methyl-esterified pectins than radicle, while PME activities and the abundance of LsPME/PMEI51 transcripts in the endosperm cap are lower than those in the radicle. In addition, the status of pectin methylesterification and PME expression patterns changed during seed germination. Low PME activities and high pectin methylesterification in the endosperm cap is hypothesized to be the reason of why endosperm does not rupture by cell separation. It is concluded that tissue-specific pectin methylesterification and PME activities play a role in lettuce seed germination.