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Slower translation elongation rescues the targeting defect of sub-optimal SRP substrate proteins in vivo. Failures in the efficient SRP-dependent targeting of FtsQ-PSBT (A), PhoA-Avi (B), and EspP-PSBT (C) were detected by their biotinylation in the cytoplasm, as described in the text, in wild-type (arabinose, +) and SRP-depleted (arabinose, −) cells and in the presence and absence of the translation elongation inhibitor tetracyclin.
