Disulfide bonds protect RMAD-4(62–94) from degradation
by serine proteases. Panel A shows the primary amino acid
sequences of RMAD-4(62–94) and the two disulfide variants
(C4/11/31/32/A)-RMAD-4(62–94) and
(6C/A)-RMAD-4(62–94) (see “Experimental
Procedures”). CI-CVI and
CIII-CV disulfide bonds are disrupted in
(C4/11/31/32/A)-RMAD-4(62–94) and all disulfide bonds
CI-CVI, CIII-CV, and
CII-CIV are disrupted in
(6C/A)-RMAD-4(62–94). Mutated Cys positions converted to Ala
are shown in bold font (right panel). In B, the
bactericidal activities of RMAD-4(62–94) disulfide variants
are compared. Exponentially growing bacterial cells were exposed to
(C4/11/31/32A)-RMAD-4(62–94) (-○-),
(6C/A)-RMAD-4(62–94) (-▾-), and native
RMAD-4(62–94) (-•-) for 1 h at 37 °C (see
“Experimental Procedures”). Both disulfide variants have
activities comparable with RMAD-4 against S. typhimurium
ΔphoP (A), E. coli (B), S.
typhimurium JSG 210 (C), L. monocytogenes (D),
and V. cholerae (H). Against S. typhimurium CS022
(E), S. aureus (F), and S. typhimurium
14028s (G), (6C/A)-RMAD-4 has attenuated activity relative to RMAD-4.
C, equal quantities (10 μg) of RMAD-4,
(C4/11/28/29A)-RMAD-4(62–94), and
(6C/A)-RMAD-4(62–94) were digested for 18 h in the presence
of NE, CG, P3, or trypsin, resolved on AU-PAGE, and stained with Coomassie
Blue. Disulfide bonds protect α-defensins from proteolysis during
conversion to active forms.