Restricting flow can be beneficial in some instances, such as when damaged parts need to be closed off or virus-infected cells need to be quarantined. But flow blockage can be fatal too, especially when it happens in meristems.
"Meristems that are blocked and thereby starved of nutrients won't give rise to daughter cells and spawn new organs, thus stunting the plant's growth," explains Jackson. "What we've found now is probably the mechanism that normally prevents blockages from occurring in these stem cells."
Jackson's team has found that plants stave off callose accumulation and keep the channels open by turning on the GAT1 gene in their stem cells. Seeds in which this gene failed to work were observed by the CSHL team to give rise to seedlings that barely survived more than two weeks, despite forming intact roots and an intact phloem the main transport artery that carries nutrients and other supplies to the meristems.
The mutants even had intact meristems that had developed the required numbers of transport channels. These channels, however, were functionally defective, as the pile-up of callose narrowed them, making the passage of nutrient molecules impossible. The CSHL scientists were able to reverse this defect by re-introducing a functional GAT1 gene into mutant plants. When the GAT1 gene was turned on, the production and accumulation of callose decreased.
GAT1 counters oxidative stress
One of the distress signals that spur cells to synthesize callose are oxygen free radicals the same cell-damaging molecules that have gained notoriety as a major cause of cell death and aging. In mutant plant seeds that lack a functional GAT1 gene, stem cells brim with high levels of these free radicals and other toxic ions, collectively known as reactive oxygen species (ROS).
This ROS threat, according to Jackson's team, is normally counter-bala
|Contact: Hema Bashyam|
Cold Spring Harbor Laboratory