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Scripps research scientists identify new regulatory mechanism for critical protein signaling domain

ling in many cells, because it generates the secondary messenger molecules IP3 and DAG (diacylglycerol). We found that ItpkB deficient double positive cells have reduced PLCg1 activity and cannot make normal amounts of DAG. Without the IP4 or DAG messengers, which are essential for positive selection of T cells, these ItpkB-deficient T cells cannot develop into mature, functional cells."

Positive selection of T cells is disrupted by this lack of IP4 and DAG in the mutant mice, the study noted. Quite remarkably, the authors could rescue several aspects of positive selection by treating ItpkB deficient cells with a DAG analog, PMA. DAG is well known for helping to mediate T cell receptor signaling by activating the Ras/Erk pathway, a key signal pathway whose misregulation is often involved in cancer. It is still too early to tell if IP4 plays a broader role in Ras regulation in other cells, Sauer said.

"This is something we stumbled into-the possibility of regulating the Ras pathway with IP4 at the level of DAG production through PLCg1," he said. "In the immature, double positive T cells, this circuitry is essential for positive selection. If you prevent IP4 production, you can never get positive selection-unless you provide a DAG analog like PMA-and that is a very provocative discovery."


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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
5-Apr-2007


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