Summary: Invertebrate modifiers of SMN loss of function.

The summary table is divided into three sections corresponding to potential Cesmn-1(lf) modifier genes originally identified in humans, Drosophila, or C. elegans (1 in Hs, 40 in Dm, and 4 in Ce, respectively). Species and gene names are listed in the first three columns. The change in gene expression due to Drosophila GAL4-driven transposon insertion lines or C. elegans RNAi knockdown is listed in columns 4 and 5; effect on Drosophila gene function is predicted based solely on transposon insertion sites in some cases. (RNAi: RNAi knockdown; Lof: loss of function; decreased function or antisense; OE: over-expression; ?: unclear; Enh: enhanced SMN loss of function defects; Sup: suppressed SMN loss of function defects, Cmpx: complex genetic interaction; not determined, n.d.). Column 4 includes the C. elegans assay revealing modifier activity (Gr: growth; Pump: pharyngeal pumping.) RNAi knockdown was sufficient to modify pumping rates for T02G5.3 and ncbp-2; mutant alleles of grk-2 exacerbated Cesmn-1(lf) pumping defects. flp-4 loss decreased Cesmn-1(lf) pumping rates in 4 out of 5 trials, but did not reach significance overall. Discordance between Drosophila and C. elegans results is indicated with ≠.