Figure 2

Figure 2

Samhd1 deficiency results in the spontaneous activation of nuclear factor kappa B (NF-κB) and hyperresistance to infection with Salmonella enterica serovar Typhimurium (STM). (A) Real-time visualization of NF-κB activation in Samhd1-deficient zebrafish larvae. The nfkb:eGFP reporter zebrafish line injected with gRNA (samhd1 or STD)/Cas9 complexes were analyzed using fluorescence microscopy and quantified. Each dot represents a larva, and the mean ± SEM for each experimental group is also shown. (B) Representative images of whole larvae are shown, and the region of interest (ROI) used to quantify the fluorescence in the nfkb:eGFP reporter line is indicated as a dot line in the images. (C) Zebrafish one-cell embryos were injected with gRNA (samhd1 or STD)/Cas9 complexes, dechorionated, and infected at 2 days post-fertilization via the yolk sac with STM at a multiplicity of infection (MOI) of 10 or phosphate-buffered saline (PBS), with the number of surviving larvae counted daily during the next 5 days. A total number of >100 specimens/treatment. P-values were calculated using Student’s t test in (A) and long-range test in (C). **p ≤ 0.01, ****p ≤ 0.0001.