|ISBN: 0486241386 ISBN: 0486241386 ISBN: 0486241386 ISBN: 0486241386|
Dictyostelium feeds as single, amoeboid cells on bacteria. When the food source is exhausted, cells stop vegetative growth (cell division) and enter a developmental cycle. They secrete cAMP which serves as a signal for the cells to stream together and form aggregates of approx. 100.000 individuals. In the aggregates, cells eventually differentiate into non-viable stalk- and dormant spore-cells.
To investigate the transition from growth to multicellular differentiation,we have chosen the discoidin gene family as a molecular marker.
The discoidins are cytoplasmic proteins which are not essential for growth or development (under laboratory conditions) but appear to be involved in cell shape changes at the onset of development: during growth, cells are more or less round, when starved, they elongate and obtain a pronounced anterior-posterior polarity. Strains which do not express discoidins have problems with the organization of migration streams towards aggregation centers.
Discoidins are expressed several generations before the food source is exhausted. Gene expression is induced at low levels by a secreted factor (PSF) which enables the cells to measure their own density in relation to the available food supply.
A second boost of induction (developmental induction) begins approximately 2 hours after starvation.
At about 6 hours of development, discoidin expression is downregulated by cAMP.
Using mutants in known signal transduction components, the following pathways have been established:
Thus there is the interesting situation that intracellular cAMP can stimulate while extracellular cAMP can represses discoidin expression. Circumstantial evidence suggests, however, that PKA may be induced by other signal molecules in addition to cAMP.
To fill in the gaps in this signalling cascad and in order to understand the
mechanisms controlling the growth-development-transition (GDT), we have generated
a number of mutants by REMI (restriction
enzyme mediated integration) which misregulate discoidin expression. We
have identified several mutants which display no or weak discoidin expression
and others which show dramatic overexpression.
This web site is a part of the project StudyPaper.com.
We are grateful to C. Zeng, C. Anjard and W. Nellen for contributing this article.
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