Figure 1.
Salmonella Typhimurium DT104 kills C. elegans significantly faster when MDR genes are present.
L4 stage hermaphrodite SS104 worms were exposed to wild type Salmonella Typhimurium DT104 (--●--),SNS12, a ΔMDR isogenic mutant of DT104 (--■--), and E. coli OP 50 (--▲--). P<0.001.
Figure 2.
Salmonella Typhimurium DT104 colonization in C. elegans intestine is enhanced due to MDR genes.
L1 stage N2 worms were exposed to DT104 (--●--) and SNS12 (--■--), and the extent of colonization was determined every 24 hours. Each data point represents the colony forming unit per worm (CFU worm-1) from a pool of 10 infected worms. Horizontal bar indicates the cumulative geometric mean of three independent experiments.
Figure 3.
Colonization of the C. elegans intestine by Salmonella Typhimurium DT104.
Confocal microscopy images of representative worms exposed to DT104, SNS12, and E. coli OP 50. White arrow shows the grinder of the pharynx, and yellow line shows extent of intestinal distention.
Figure 4.
Ced-1 mutant C. elegans worms are more sensitive to killing by DT104.
Ced-1 loss-of-function mutant worms [ced-1(e1735)] die significantly faster (P=0.0085) than wild type N2 worms, when exposed to Salmonella Typhimurium DT104. L4 stage wild type N2 (--●--) and ced-1 (e1735) (--■--) worms were exposed to DT104 and assayed daily for survival.
Figure 5.
Antimicrobial response to wild type Salmonella Typhimurium DT104.
Expression of (A) pqn-54, (B) abu-1, (C) abf-2 and (D) abu-11 genes of N2 worms as determined by qRT-PCR at one hour, 24-hour and 48-hour exposure. Relative expression levels (DT104 or SNS12 over OP 50) are shown as fold changes (mean ± std. err.).