Founder Cell

Founder cell is a term that has been used to describe an aspect in the initiation of aggregation in slime molds, especially Dictyostelium. These organisms are normally single cells, but when environmental conditions become unfavorable, they aggregate to form a composite. One cell in a population, the founder cell, will begin signaling to the others by secreting pulses of a chemoattractant. Dictyostelium discoideum uses the normally intracellular second-messenger molecule cyclic AMP (cAMP) as its chemoattractant. Other species use a variety of chemoattractants, such as pterin derivatives and small peptides. Cells in the immediate area of the founding cell respond in two ways. They first migrate toward the chemoattractant source, and then they secrete additional cAMP signal. An extracellular phosphodiesterase degrades the cAMP between the waves. The resulting temporal and spatial waves of the chemoattractant flow through the environment. As the cells respond, they move together, then pause and move again, until almost all the cells in an area are in a central aggregate. The timing of the pulses and the rate of motility, combined with the enzymatic rates of signal degradation and secretion, determine the size and shape of the aggregate (1).

Exactly what causes a single cell in a population of apparent equals to become a founder cell is unknown, but it must be tightly regulated for the aggregates to end up with an optimum number of cells. Allowing cells to divide to increase the size of the aggregate is not an option, because cell-cycle arrest occurs very early in the developmental program. Once a cell adjacent to a founder responds, that cell cannot itself become a founder. There are some data that suggest that the differentiation events that occur in the founder cell do so before neighboring cells become competent for chemotaxis. Perhaps a diffusible factor secreted from the founder is involved in that process (2).

References

1. E. Palsson et al. (1977) Proc. Natl. Acad. Sci. USA 94, 13719–13723.

2. R. K. Raman (1976) J. Cell Sci. 20, 497–512.