A Motor Function for the DEAD-Box RNA Helicase, Gemin3, in Drosophila
Figure 4
Loss of gemin3 disrupts larval locomotion and puparium formation.
(A) Body wall contraction rate of wild-type (y w), gemin3 heteroallelic mutants (1032-GAL4; gemin3R/gemin3W), and rescued gemin3 mutants (1032-GAL4≫UAS-CFP::gemin3; gemin3R/gemin3W) throughout their larval development. Compared to controls, gemin3 transheterozygotes exhibit a significant reduction in body wall contraction at the third instar larval stage. At 25°C, 24 hrs AEL = 1st instar larvae, 48 hrs AEL = 2nd instar larvae, and 72–96 hrs AEL = 3rd instar larvae. Individual bars represent the mean body wall contraction rate ± 1.0 S.E.M. (n = 15–51). (B) Puparia of wild-type, gemin3 heteroallelic mutants and rescued mutants. Mutants form slender and longer puparia compared to wild-type, a defect that was corrected upon expression of gemin3 driven by the constitutive driver, 1032-GAL4. Arrowheads show failure in spiracle eversion. (C) Graph displaying the axial ratios for puparia of the indicated genotype. Compared to wild-type and rescued mutants, axial ratios of mutant puparia were significantly larger. The mean is marked by a horizontal line running through the data points (***p<0.0001; n>31). (D) Wild-type and mutant third instar larval muscle fillets labelled using Alexa Fluor-488-conjugated phalloidin show no apparent disruption in the gross structure of body wall musculature (left panels) and sarcomere organisation (right panels).