Conserved Genes Act as Modifiers of Invertebrate SMN Loss of Function Defects (original) (raw)
Figure 6
Loss of Drosophila Cbp20 or FMRF enhances _Dm_Smn loss of function neuromuscular defects.
For two C. elegans modifier genes, loss of function alleles were available for orthologous Drosophila genes: Cbp20 and FMRF [68]–[70]. Loss of either Drosophila gene enhanced the NMJ defects of _Dm_Smn animals. The number of synaptic boutons in the A2 segment of muscles 6 and 7 was counted in third instar larvae (visualized using Discs large and synaptotagmin immunoreactivity, shown in red and green, respectively). Homozygous loss of _Dm_Smn in _Dm_Smnf1109/_Dm_Smn73Ao animals dramatically decreases bouton number but loss of one copy of _Dm_Smn, Cbp20 or FMRF had little effect. Loss of one copy of either Cbp20 or FMRF in animals heterozygous for either _Dm_Smn allele significantly decreased bouton numbers. This nonallelic noncomplementation suggests a strong genetic interaction between these two conserved modifier genes and _Dm_Smn. Scale bar indicates 10 microns in representative images; S.E.M. is shown in graph; all transheterozygous combinations are significantly different from the corresponding single heterozygous controls with p≤0.05 by ANOVA as indicated with asterisk.