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Several models for the transport of proteins across membranes predict a role for lipids. If these models are correct, then alterations in lipid metabolism may affect protein export and vice versa. We are investigating this possibility by studying Escherichia coli K-12 mutants with defects in protein export or phospholipid metabolism. A temperature-sensitive secA mutant, which is defective in protein export at 42 degrees C, exhibited severe pleiotropic effects on membrane biogenesis. Incubation of this strain at 42 degrees C resulted in the appearance of intracytoplasmic membranes, in alterations in lipopolysaccharide structure and in decreased cardiolipin and C18:1 fatty acid content. On the other hand, a pgsA mutant which is defective in the synthesis of acidic phospholipids, exhibited a protein export defect when studied in vivo or in vitro. These results are in agreement with a postulated role of membrane lipids in protein export.
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Tommassen et al. (1989) studied this question.
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