Yersinia enterocolitica is an enterobacterium responsible for gastroin
testinal syndromes. Its pathogenicity depends on the presence of the 7
0-kb pYV plasmid, which directs Yop secretion. The Yop secretion machi
nery, consisting of the YscA-U and LcrD proteins, presents some struct
ural similarity with the flagellum assembly machinery characterized in
other bacteria. Flagellum assembly requires sigma(28), an alternative
sigma factor. The region upstream of the lcrD gene resembles promoter
s recognized by sigma(28), suggesting that the similarity between Yop
secretion and flagellum assembly could extend to their regulation. The
chromosome of Y. enterocolitica also contains pathogenicity determina
nts such as myfA, which encodes the Myf antigen subunit. The promoter
region of myfA also resembles promoters recognized by sigma(28). In an
attempt to clarify; the role of sigma(28) in the expression of lcrD,
myfA, and flagellar genes, we cloned, sequenced, and mutagenized the f
liA gene encoding the sigma(28) homolog in Y. enterocolitica. As is th
e case in other bacteria, fliA was required for motility. However, it
was involved neither in fibrilla synthesis nor in Yop secretion. The f
liA mutant allowed us to monitor the role of motility in pathogenesis.
At least in the mouse model, motility seemed not to be required for Y
. enterocolitica pathogenesis.