The Role of Actin-specific Bacterial Endoproteases Grimelysin and Protelysin in Serratia Invasion
DOI:
https://doi.org/10.9734/bpi/ramb/v8/11034FKeywords:
Actin proteolysis, metalloproteinases, protease ECP 32, grimelysin, protealysin, bacterial invasionAbstract
This chapter describes the properties of the bacterial proteases grimelysin and protealysin, which are virulence factors in vitro and in vivo, and actin can be a target for these proteases upon their translocation into the host cell.
Bacterial invasion into eukaryotic cells is one of the major areas of research in infection biology, whereby they employ different strategies to invade the host cells. These interactions are highly complex, and the type of interaction depends on the bacterium, host, as well as environmental factors. The single actin polypeptide link, Gly42-Val43, is broken by grimelysin. No other proteases are able to break this link, which results in the reversible loss of actin polymerization. Similar characteristics were shared by protealysin, another bacterial protease. Grimelysin and protealysin are unique tools for studying the functional characteristics of actin because of their characteristics. Furthermore, bacteria Serratia grimesii and Serratia proteamaculans, producing grimelysin and protealysin, invade eukaryotic cells, and the recombinant Escherichia coli expressing the grimelysin or protealysins gene become invasive. Specifically, the grimelysin (ECP 32)-producing bacteria invaded the transformed epithelial and fibroblasts cells A431, HeLa and 3T3-SV40, but they were not found in embryonic fibroblasts, primary human keratinocytes and in cells of poorly transformed 3T3 cell lines. The invasion of eukaryotic cells by S. grimesii has been demonstrated to include the cellular c-Src and RhoA/ROCK signaling pathways, and it has also been proposed that E-cadherin plays a role in the invasion. Furthermore, it was discovered that S. grimesii produces membrane vesicles that contain grimelysin, enter eukaryotic cells, and promote bacterial invasion of these cells. These data indicate that the protease is a virulence factor, and actin can be a target for the protease upon its translocation into the host cell.
