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The plant embryo is supported by a lifeline known as a suspensor that acts like an umbilical cord, connecting the embryo to surrounding tissues in the seed and ferrying in vital nutrients and growth factors. Although scientists have for a century known that the suspensor is a temporary organ, the molecular trigger for its demise was unknown. Now Meng-xiang Sun at Wuhan University in China and his colleagues have uncovered one key way this programmed cell death is controlled — a pair of proteins that antagonistically balance each other, with one spurring death and the other preventing it.
After a plant egg cell is fertilized, it divides to become what is called a proembryo, which possesses two kinds of daughter cells with profoundly different fates. One, the smaller cell sitting at its tip, becomes the embryo, while the other, the larger cell resting at its base, develops into the suspensor that anchors the embryo to the parent plant. The suspensor, which occurs in a dazzling variety of shapes and sizes in the plant kingdom, is required only in the early stages of embryonic development — the disintegration of suspensor cells marks the earliest instance of programmed cell death in a plant's life.
To help solve the mystery behind the suspensor's downfall, researchers experimented with tobacco plants, whose suspensors are relatively easy to study, made up as they are of just simple columns of about four cells that develop through a well-known, precisely timed sequence of cell divisions. The suspensor begins to die once the embryo reaches the 32-celled stage, with death beginning at its base and progressing up to its tip, with all the contents of its cells slowly digested from within.
The scientists focused on a tobacco gene they named
The researchers discovered the natural onset of suspensor degeneration coincided with a steady decrease in
The scientists discovered that overexpressing
It remains a puzzle as to what molecule or molecules naturally set off the rapid decrease of NtCYS activity that kills off suspensors. Since the ephemeral organ's programmed cell death starts at its base, the signal might come from cells at the micropyle, the opening through which the pollen tube penetrates into the ovule, the female part of the plant. Alternatively, the signal might come from the embryo itself, a possibility supported by the fact that suspensor programmed cell death always starts when the embryo reaches a very specific point in its life, its 32-celled stage.
In addition to analyzing what controls the activity of NtCYS and NtCP14, future research can also pinpoint what they control. The investigators discovered that increasing NtCP14 activity in the two-celled proembryo correspondingly increased the activity of molecules similar to caspases, enzymes linked with programmed cell death in animals.