At least two genes have been shown to be required for the expression of the antiphagocytic M protein molecule in group A streptococci. Evidence for phage involvement in the expression of M protein is that: (a) M- cultures of bacteria can be converted to the M+ state (resistant to phagocytosis) upon lysogenization with appropriate bacteriophages; (b) without those bacteriophages the M- recipient culture could not be detected to revert to the M+ state, even under our most stringent selective conditions; and (c) stable M+ lysogens cured of their bacteriophages returned to the M- state. Immunochemical analysis of lysogenically converted M+ strains demonstrated that they contain precipitating and antiphagocytic determinants of the parental M-76 strain (CS110) rather than M-12 determinants expressed by the phage donor strain. This information strongly suggests that the M- strain CS112 possesses the structural gene for M protein, but that it remains predominantly unexpressed. Quantitation of the M antigen produced by these strains supports the observation that the M- phage-recipient strain possesses a small amount of extractable M antigen and that phage activates its synthesis by some unknown mechanism. Various possibilities to account for the phage requirement in M protein synthesis and its role in the transition between M+ and M- states are discussed.
Skip Nav Destination
Article navigation
1 November 1980
Article|
November 01 1980
Bacteriophage control of antiphagocytic determinants in group A streptococci.
J G Spanier
P P Cleary
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1980) 152 (5): 1393–1406.
Citation
J G Spanier, P P Cleary; Bacteriophage control of antiphagocytic determinants in group A streptococci.. J Exp Med 1 November 1980; 152 (5): 1393–1406. doi: https://doi.org/10.1084/jem.152.5.1393
Download citation file:
Sign in
Don't already have an account? Register
Client Account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Sign in via your Institution
Sign in via your InstitutionSuggested Content
Email alerts
Advertisement