Table 1.
Functional group | Protein implicated in invasion |
Internalization a (%) |
p-valueb | Normalized internalizationc |
Hit shared with other screensd |
---|---|---|---|---|---|
--- | untreated control cells | 54 ± 10 | --- | 1 ± 0.09 | --- |
Rho family GTPase | Rac1 | 37 ± 17 | 0.0021 | 0.84 ± 0.5 | 4,5,7,10 |
Rac2 | 37 ± 8 | 0.002 | 0.77 ± 0.09 | 3,4,5,10 | |
Rac1 + Cdc42 | 34 ± 5 | 0.0003 | 0.68 ± 0.11 | --- | |
Rac1 + Rac2 | 39 ± 18 | 0.0031 | 0.84 ± 0.46 | --- | |
Actin filament nucleator | ARP2 | 29 ± 9 | <0.0001 | 0.59 ± 0.15 | 2,3,9 |
ARP3 | 34 ± 9 | 0.0002 | 0.67 ± 0.07 | 2,3,4,6,9 | |
ARPC1 (p41) | 33 ± 16 | 0.0013 | 0.66 ± 0.25 | ||
ARPC2 (p34) | 30 ± 9 | <0.0001 | 0.63 ± 0.21 | 2,3 | |
ARPC4 (p20) | 36 ± 12 | 0.001 | 0.61 ± 0.22 | 1,2,3,4,5,6,7,8,10 | |
ARPC5 (p16) | 25 ± 6 | <0.0001 | 0.5 ± 0.04 | 2,3,4,5,10 | |
Actin nucleation promoting factor | WAVE (SCAR) | 18 ± 6 | <0.0001 | 0.38 ± 0.08 | 1,4,5,6,7,8,9,10 |
WAVE complex member, regulator | Abi | 17 ± 10 | <0.0001 | 0.34 ± 0.18 | 1,2,3,4,5,7,8 |
Kette HEM-protein | 31 ± 9 | <0.0001 | 0.57 ± 0.24 | 1,7,8 | |
Sra-1 | 35 ± 6 | 0.0027 | 0.55 ± 0.07 | 1,4,6,7 | |
WASP binding, regulator | WIP veroprolin | 38 ± 16 | 0.005 | 0.78 ± 0.34 | |
Myosin motor protein | Myosin IA | 28 ± 12 | <0.0001 | 0.62 ± 0.37 | 10 |
Myosin II (zipper) | 33 ± 6 | 0.0002 | 0.72 ± 0.27 | 1 | |
Endocytic / phagocytic adapter | Hip1R | 35 ± 7 | 0.0005 | 0.74 ± 0.17 | 10 |
Membrane-cytoskeleton linker | MIM homolog | 33 ± 8 | 0.0001 | 0.69 ± 0.21 | 9 |
Myoblast city | 38 ± 4 | 0.0089 | 0.87 ± 0.11 | 7 | |
Actin filament bundling/organizing | α-actinin | 34 ± 14 | 0.0004 | 0.71 ± 0.19 | 7,8,10 |
Fimbrin | 38 ± 6 | 0.0078 | 0.86 ± 0.05 | 7,10 | |
Actin monomer dynamics | Cofilin (twinstar) | 40 ± 12 | 0.0088 | 0.8 ± 0.09 | 1,7,10 |
Percent of R. parkeri internalized 15 mins after infection in cells treated with dsRNA targeting the indicated protein(s). The data presented are the mean ± SD of at least three independent experiments.
Determined by pairwise comparison with the untreated control using the Student’s t-test. p<0.01 was considered statistically significant.
Data were adjusted with the mean percent internalization of matched untreated control cells (duplicate samples) for each day’s experiment set as 1 (100%).
RNAi targeting this protein was also found to 1reduce lamella formation (Rogers et al., 2003); 2Listeria monocytogenes and/or 3Mycobacterium fortuitum infection (Agaisse et al., 2005); 4Candida albicans, 5E. coli or 6latex bead phagocytosis (Stroschein-Stevenson et al., 2005); 7Chlamydia trachomatis infection (Elwell et al., 2008); 8Pseudomonas aeruginosa internalization (Pielage et al., 2008); 9Rickettsia parkeri infection, or 10R. parkeri actin tail formation (Serio et al., 2010).