Substrates of the Plasminogen Activator Protease of Yersinia pestis

Genome-Wide Analysis of Small RNAs Expressed by Yersinia pestis Identifies a Regulator of the Yop-Ysc Type III Secretion System

“…Binding of the YopDLcrH complex to target transcripts requires two specific AU-rich regions of mRNA common to many, but not all, yop transcripts, and the distance of the AU-rich regions from the RBS seems to affect the affinity of YopD for the transcript, suggesting a mechanism for a hierarchy of translation (17). Additionally, Y. pestis can degrade extracellular and/or mistargeted T3SS proteins via the activity of the Y. pestis-specific plasminogen activator protease Pla, thus providing a posttranslational layer of regulation to the T3SS in this species (18,19).…”

Identification of host factors required for Yersinia pestis macrophage intracellular survival and their impact on vacuole maturation, acidification and trafficking.

“…To highlight this, the Plasminogen activator, pla, is protease that is capable of cleaving C3 complement and degrading T3SS effector Yersinia outer membrane proteins (Yops). These functions allow for Y. pestis dissemination throughout the host, and dampening of Yop activation of innate immune responses [30][31][32][33][34]. Pla is encoded on pPCP [1,16,18,19,35,36].…”

Characterizing the virulence factor YapE in Yersinia pestis.

“…pla was identified as one of the most exceedingly expressed genes in Y. pestis isolated from bubos of infected rats [46,47]. Pla is a member of the omptin family of proteases that has evolved specifically for bubonic and pneumonic forms of plague [48]. Pla is able to convert plasminogen to plasmin allowing for the degradation of extracellular matrices permitting Y. pestis to quickly invade the host and migrate to draining lymph nodes [17,[49][50][51].…”

“…Pla is able to convert plasminogen to plasmin allowing for the degradation of extracellular matrices permitting Y. pestis to quickly invade the host and migrate to draining lymph nodes [17,[49][50][51]. During subdermal or subcutaneous infection, Y. pestis expressing Pla had wide-spread bacterial foci with minimal recruitment of inflammatory cells [48,52]. Conversely, when Pla was not expressed, it resulted in an accumulation of bacteria at site of infection, causing an inability to disseminate and thereby increasing the recruitment of immune cells [48].…”

“…During subdermal or subcutaneous infection, Y. pestis expressing Pla had wide-spread bacterial foci with minimal recruitment of inflammatory cells [48,52]. Conversely, when Pla was not expressed, it resulted in an accumulation of bacteria at site of infection, causing an inability to disseminate and thereby increasing the recruitment of immune cells [48]. Unlike the bubonic (subcutaneous) model, Pla is not necessary for the dissemination from the initial site of infection for primary pneumonic plague.…”