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Communicated by A. Dale Kaiser, Stanford University School of Medicine, Stanford, CA (received for review December 3, 1996)
Abstract
The complex prokaryote, Myxococcus xanthus, undergoes a program of multicellular development when starved for nutrients, culminating in sporulation. M. xanthus makes MglA, a 22-kDa, soluble protein that is required for both multicellular development and gliding motility. MglA is similar in sequence to the Saccharomyces cerevisiae SAR1 protein, a member of the Ras/Rab/Rho superfamily of small eukaryotic GTPases. The SAR1 gene, when integrated into the M. xanthus genome, complements the sporulation defect of a ΔmglA strain. A forward, second-site mutation on the M. xanthus chromosome, rpm, in combination with SAR1, restores fruiting body morphogenesis and gliding motility to a ΔmglA strain. The result that the rpm mutation suppresses the substitution of SAR1 for mglA suggests that Sar1p interacts with other M. xanthus proteins to control the motility-dependent aggregation of cells during development.
ABBREVIATIONS
- CTPM,
- 1% casitone/10 mM Tris/4 mM MgSO4/1 mM potassium phosphate, at a final pH of 7.5;
- TPM,
- CTPM with the casitone omitted
- Received December 3, 1996.
- Accepted July 1, 1997.
- Copyright © 1997, The National Academy of Sciences of the USA
Complementation of sporulation and motility defects in a prokaryote by a eukaryotic GTPase
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