CTX phi is a lysogenic filamentous bacteriophage that encodes cholera toxin
. Filamentous phages that infect Escherichia coli require both a pilus and
the products of tolQRA in order to enter host cells. We have previously sho
wn that toxin-coregulated pilus (TGP), a type IV pilus that is an essential
Vibrio cholerae intestinal colonization factor, serves as a receptor for C
TX phi. To test whether CTX phi also depends upon tol gene products to infe
ct V. cholerae, we identified and inactivated the V. cholerae tolQRAB ortho
logues. The predicted amino acid sequences of V. cholerae TolQ, TolR, TolA,
and TolB showed significant similarity to the corresponding E. coil sequen
ces. V. cholerae strains with insertion mutations in tolQ, tolR, or tolA we
re reduced in their efficiency of CTX phi uptake by 4 orders of magnitude,
whereas a strain with an insertion mutation in tolB showed no reduction in
CTX phi entry. We could detect CTX phi infection of TCP- V. cholerae, albei
t at very low frequencies. However, strains with mutations in both tcpA and
either tolQ, tolR, or tolA were completely resistant to CTX phi infection.
Thus, CTX phi, like the E. coli filamentous phages, uses both a pilus and
TolQRA to enter its host. This suggests that the pathway for filamentous ph
age entry into cells is conserved between host bacterial species.