This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Cellular expansion is an absolute necessity during the growth and development of plants and fungi. Expansion relies upon the accumulation of inorganic ions, the resulting water influx creates the hydrostatic pressure (turgor) that causes the cell to expand. Cellular expansion is normally asymmetric. Rather than expanding in all directions, there are localized regions of expansion that result in the well-defined final shape of the cell. The extreme example of anisomorphic cell expansion is tip growth. Here, the machinery of expansion is highly concentrated in a small region such that the cell exhibits tubular growth. How does the cell maintain the turgor that drives expansion? How is expansion controlled spatially? Both aspects of tip growth rely on transport at the plasma membrane. During my most recent visit to the BioCurrents Center (Feb/Mar 2006), I used ion-selective microelectrodes to determine the role ion uptake plays during turgor recovery after hyperosmotic treatment. We had shown that a MAP kinase cascade, homologous to the HOG pathway in yeast, activated ion transport after hyperosmotic treatment, the cause of rapid recovery of the normal high hydrostatic pressure (turgor) . We proposed to examine a novel signal transduction pathway, identified by osmosensitivity of the cut mutant which encodes a defective phosphatase and plays a separate role in osmoresponses.
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