EC Number |
General Information |
Reference |
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3.4.23.43 | malfunction |
the deletion strain DpibD does not exhibit any type IV pilus-like structures. Attachment to surfaces is strongly reduced in the pibD deletion strain and no growth defect is observed |
-, 729693 |
3.4.23.43 | metabolism |
prepilin peptidase cleaves the positively charged peptide anchor on the cytoplasmic face of the transmembrane segment |
754426 |
3.4.23.43 | metabolism |
the enzyme is needed for maturation of preflagellins and other type IV pilin-like proteins |
753673 |
3.4.23.43 | physiological function |
a prepilin peptidase pilD null mutant accumulates an unprocessed form of the major pilin PilA1 and its non-glycosylated derivative. The mutant strain has aberrant membrane ultrastructure and does not grow photoautotrophically because the synthesis of Photosystem II subunits is abolished. Other membrane components such as Photosystem I and ATP synthase are synthesized at levels comparable to the control strain. Proliferation of the pilD mutant strain is rescued by elimination of the pilA1 gene. PilA1 co-immunoprecipitates with the SecY translocase and the YidC insertase, and both of these essential translocon components are degraded in the mutant |
734719 |
3.4.23.43 | physiological function |
pilD mutant is unable to produce pili. PilD deficiency also leads to a nonfunctional type II secretion system. Loss of metal reduction in a PilD mutant is due to a type II secretion deficiency, and therefore the absence of c-cytochromes from the outer surface of MR-1 cells, and not the loss of pili or flagella |
-, 717534 |