A STAT-regulated, stress-induced signalling pathway in Dictyostelium

Tsuyoshi Araki, Masatsune Tsujioka, Tomoaki Abe, Masashi Fukuzawa, Marcel Meima, Pauline Schaap, Takahiro Morio, Hideko Urushihara, Mariko Katoh, Mineko Maeda, Yoshimasa Tanaka, Ikuo Takeuchi, Jeffrey G. Williams

    Research output: Contribution to journalArticlepeer-review

    39 Citations (Scopus)


    The Dictyostelium stalk cell inducer differentiation-inducing factor (DIF) directs tyrosine phosphorylation and nuclear accumulation of the STAT (signal transducer and activator of transcription) protein Dd-STATc. We show that hyperosmotic stress, heat shock and oxidative stress also activate Dd-STATc. Hyperosmotic stress is known to elevate intracellular cGMP and cAMP levels, and the membrane-permeant analogue 8-bromo-cGMP rapidly activates Dd-STATc, whereas 8-bromo-cAMP is a much less effective inducer. Surprisingly, however, Dd-STATc remains stress activatable in null mutants for components of the known cGMP-mediated and cAMP-mediated stress-response pathways and in a double mutant affecting both pathways. Also, Dd-STATc null cells are not abnormally sensitive to hyperosmotic stress. Microarray analysis identified two genes, gapA and rtoA, that are induced by hyperosmotic stress. Osmotic stress induction of gapA and rtoA is entirely dependent on Dd-STATc. Neither gene is inducible by DIF but both are rapidly inducible with 8-bromo-cGMP. Again, 8-bromo-cAMP is a much less potent inducer than 8-bromo-cGMP. These data show that Dd-STATc functions as a transcriptional activator in a stress-response pathway and the pharmacological evidence, at least, is consistent with cGMP acting as a second messenger.
    Original languageEnglish
    Pages (from-to)2907-2915
    Number of pages9
    JournalJournal of Cell Science
    Issue number14
    Publication statusPublished - Jul 2003


    • Dictyostelium
    • DIF
    • STAT
    • Stress response


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