Inhibiting MAP kinase activity prevents calcium transients and mitosis entry in early sea urchin embryos.

A transient calcium increase triggers nuclear envelope breakdown (mitosis entry) in sea urchin embryos. Cdk1/cyclin B kinase activation is also known to be required for mitosis entry. More recently, MAP kinase activity has also been shown to increase during mitosis.

The effects of manipulating phospholipase C on guard cell ABA-signalling.

Studies using stably transformed tobacco plants containing very low levels of PI-PLC in their guard cells show that this enzyme plays a role in the events associated with the inhibition of stomatal opening by ABA, but not in the cellular reactions that are responsible for ABA-induced stomatal closure. However, Commelina communis guard cells microinjected with the InsP3 antagonist, heparin, fail to close on addition of ABA. There are three possible explanations for this apparent data mismatch.

Phospholipase C is required for the control of stomatal aperture by ABA.

The calcium-releasing second messenger inositol 1,4,5-trisphosphate is involved in the regulation of stomatal aperture by ABA. In other signalling pathways, inositol 1,4,5-trisphosphate is generated by the action of phospholipase C. We have studied the importance of phospholipase C in guard cell ABA-signalling pathways.

Calcium-based signalling systems in guard cells.

Calcium is a ubiquitous intracellular signal responsible for controlling numerous cellular processes in both plants and animals. As an example, Ca has been shown to be a second messenger in the signal transduction pathways by which stomatal guard cells respond to external stimuli. Regulated increases in the cytosolic concentration of free calcium ions ([Ca ] ) in guard cells have been observed to be a common intermediate in many of the pathways leading to either opening or closing of the stomatal pore.