Elucidating the mechanism of cell division during plant self-healing

When the stem of a plant is injured, the surrounding cells proliferate to repair and fuse the damaged tissue, eventually restoring function. This self-healing property is utilized in grafting techniques to propagate fruit and vegetable plants.

Prior research on this process has mainly concentrated on the initiation of cell proliferation. However, few studies have explored the inhibitory mechanisms that act as a brake on proliferation.

In a new study, researchers studying Arabidopsis demonstrated that At2-MMP, a proteolytic enzyme, is vital to inhibit cell proliferation to repair severed flowering stems. The findings are published in the journal Plant And Cell Physiology.

By comparing tissue repair in Arabidopsis mutants lacking the At2-MMP gene (mutant at2-mmp) with wild-type plants, researchers found that the mutants exhibited abnormal cell proliferation at the injury site.

In severed wild-type Arabidopsis flowering stems, cell proliferation begins in pith cells (the center of the root and stem) approximately three days after cutting. At2-MMP transcripts gradually increase from day 0 to day 5 and decrease by day 7 to complete tissue repair.

However, image analysis revealed abnormal cell division in at2-mmp mutants. Conversely, when At2-MMP was overexpressed, normal wound healing similar to that in wild-type plants was observed.

Overall, these findings indicate that At2-MMP contributes to tissue repair by suppressing cell division at the cleavage site and preventing abnormal cell proliferation. This process may reflect a survival strategy developed by immobile plants to enhance their self-healing ability.