After fertilization, the endosperm develops into a coenocyte, which accumulates osmolytes. The osmotic influx of water generates a turgor pressure that acts on the cell walls of the testa surrounding the coenocytic endosperm. These cell walls are elastic to some degree, allowing the seed to expand in response to the increased turgor. However, it is also known that cell wall elasticity can be modified, for example by changing the status of methyl-esterification of the most abundant pectin, homogalacturonan. Completely demethylesterified homogalacturonan increases cell wall stiffness by forming calcium-dependent cross-links; it was hypothesized that this could contribute to diminishing seed growth. However, it was unknown how this cell wall modification relates to endosperm turgor, and was thought that reduced turgor restricts growth, just as increased turgor initiates growth.
The researchers tested the new model using Arabidopsis iku2 mutants, which have smaller seeds than the wild type. Despite this, endosperm turgor was found to be higher in these mutants than in the wild type throughout seed growth. This finding clearly falsifies the idea that restriction of seed growth is caused by reduced endosperm turgor. Instead, the model predicts that seed growth restriction is indirectly caused by turgor-induced cell wall stiffening. Indeed, the researchers find that the iku2 mutants have more demethylesterified homogalacturonan in the testa cell walls. Interestingly, it was found that iku2 mutants have a higher expression of the mechanosensitive ELA1 gene, suggesting that the increased endosperm turgor causes a cell wall stress signal that leads to precocious cell wall stiffening, which is ultimately the cause for the earlier restriction of seed growth.
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