Fig. 6

Co-expression with wild-type full-length MyD88 partially rescues the ability of the recurrent bacterial infection disease-associated point mutants to polymerise. a GFP brightness histogram of the mCherry-tagged wild-type MyD88 co-expressed with disease-associated mutants (simulating heterozygous expression in patients), as well as L93P, R196C or L252P mutant proteins co-expressed with themselves (i.e. homozygous protein expression) and wild-type MyD88 alone as a control. GFP brightness from mutants and WT measured. b–d Fluorescence time-traces of the disease-associated mutants co-expressed with mCherry-tagged WT MyD88. The recurrent bacterial infection disease-associated point mutation, L93P (b) and R196C (c), co-expression rescue experiments contrast with the continuously oligomerising L252P mutant whereby (d) L252P is not rescued and exists as its own separate population. Values are mean ± SD from six independent experiments (a) with representative traces from these experiments shown in (b–d). NS > 0.9999, ***P = 0.0001, ****P < 0.0001