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First published online January 16, 2004
doi: 10.1242/10.1242/dev.00939
1 Department of Molecular and Human Genetics, Baylor College of Medicine, One
Baylor Plaza, Houston, Texas 77030, USA
2 Summer Medical and Research Training (SMART) Program, Baylor College of
Medicine, One Baylor Plaza, Houston, Texas 77030, USA
3 MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
* Authors for correspondence (e-mail: crt{at}bcm.tmc.edu and gadi{at}bcm.tmc.edu)
Accepted 22 October 2003
The intermingled differentiation and sorting out of Dictyostelium prestalk-O and prespore cells requires the diffusible signaling molecule DIF-1, and provides an example of a spatial information-independent patterning mechanism. To further understand this patterning process, we used genetic selection to isolate mutants in the DIF-1 response pathway. The disrupted gene in one such mutant, dimA–, encodes a bZIP/bRLZ transcription factor, which is required for every DIF-1 response investigated. Furthermore, the dimA– mutant shows strikingly similar developmental defects to the dmtA– mutant, which is specifically defective in DIF-1 synthesis. However, key differences exist: (1) the dmtA– mutant responds to DIF-1 but does not produce DIF-1; (2) the dimA– mutant produces DIF-1 but does not respond to DIF-1; and (3) the dimA– mutant exhibits cell autonomous defects in cell type differentiation. These results suggest that dimA encodes the key transcriptional regulator required to integrate DIF-1 signaling and subsequent patterning in Dictyostelium.
Key words: Dictyostelium, DIF-1, Pattern formation, Prestalk O cells, dimA, dmtA
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