enterocolitica are not transmitted by fleas and cause enteric disease in humans [1–3]. Several Y. pestis genes have been found to be required to infect and be transmitted by fleas. These include the murine toxin gene (ymt), the hemin storage (hmsHFRS) genes, the diguanylate cyclases encoded by y3730 and hmsT, and gmhA. The y3730, hms, and gmhA genes are needed for bis-(3′-5′)-cyclic dimeric GMP (c-di-GMP) metabolism, formation of an extracellular polysaccharide and a lipopolysaccharide core modification, respectively, that are necessary for biofilm
formation and blockage of the flea proventriculus [4–7]. The murine toxin (ymt) gene, which encodes a phospholipase D, is required for survival of Y. pestis within the flea midgut [8]. However, additional genes may MK5108 also be important for survival and replication of Y. pestis within the flea or play a role in transmission to and survival within the mammalian host. Recent microarray data indicate that a number of genes are differentially regulated by Y. pestis during infection of the flea compared to in vitro culture at the same temperature [9]. Among these
were a group of upregulated genes that share homology with insect toxin genes of the Toxin complex (Tc) family. First identified in Photorhabdus luminescens, which maintains a symbiotic relationship with entomopathogenic nematodes of the family Heterorhabditidae [10, 11], Tc protein homologues are also found in PRT062607 nmr a number of other bacteria including Y. enterocolitica and Y. pseudotuberculosis[12]. In P. luminescens, Tc genes are found at four loci which have a high degree of similarity and can be grouped into three basic genetic elements (tcdA/tcaAB/tccAB [type A], tcdB/tcaC [type B], and tccC [type C]) [11]. The P. luminescens toxins are upregulated in the insect host [13], interact with each other to form large active toxin complexes and are highly insecticidal [14, 15]. Furthermore, they have been shown to disrupt the actin cytoskeleton of NIH 3T3 Swiss mouse fibroblast cells [15, 16]. More recently, P. luminescens toxin complexes were
found to ADP-ribosylate actin 17-DMAG (Alvespimycin) HCl and Rho GTPases, respectively, which caused actin polymerization and clustering in human HeLa cells and resulted in altered phagocytosis by Galleria mellonella hemocytes [17]. Tc protein homologues are found in all sequenced Y. pestis strains available to date (Figure 1A). Y. pestis Tc proteins are termed YitA (TcaA-like), YitB (TcaB-like), YitC (TcaC-like), and YipA and YipB (TccC- like) and are found within a single locus in the chromosome (Figure 1A) [18]. selleck products Although their sequences are highly conserved, Y. pestis strains CO92, A1122, D106004, D182038, and Z176003 have an apparent frameshift mutation in yitB (missing a single adenosine [A] from a string of seven A’s), and strain Antiqua has an eleven nucleotide deletion resulting in a frameshift mutation in yitA. Additionally, Y. pestis Angola has a frameshift mutation in the C-terminus of yipA (Figure 1A).
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