Translocase and major signal peptidase malfunctions affect aerial mycelium formation in Streptomyces lividans

Deficiency in the translocase complex (SecG mutant strain) or in the major type I signal peptidase (SipY mutant strain) function in Streptomyces lividans resulted, as expected, in a drastic reduction of secretory protein production and in a bald phenotype. The transcriptional profiling of both strains showed that the expression of a set of genes involved in the morphological differentiation process was down regulated in both mutant strains (bldG, bldN and bldM), whereas bldA and bldH were only down-regulated in the SipY mutant strain. Consistently, low temperature scanning electron microscopy revealed that the disruption of sipY had a more noticeable effect in the growth/morphological aspect of the mycelium than that of secG, suggesting that in the sipY mutant, the blockage of the export process might have more severe consequences than in the secG mutant. In both cases, the likely degradation of the proteins that cannot be secreted might provide nutrients that might be responsible for the lack of induction of the bald cascade, which is thought to be triggered under conditions of nutritional limitation.

► Streptomyces lividans major type I SPase and translocase mutants are deficient in sporulation.
► Proteomic analyses showed deficiency in secretory protein production in both mutants.
► Transcription of the same developmental genes was similarly affected in both mutants.
► The sporulation process was dissimilarly affected in each mutant strain.
► Regulatory networks of a different structure may take place in each mutant.