Figure 3: Tctp is genetically antagonistic to brm.
(a) Genetic interaction of overexpressed Brm and Tctp. (Top) ap-Gal4/+, ap>Tctp and ap>TctpE12V do not affect wing veins. Below each wing, regions of L2 vein and posterior crossvein (PCV) are shown at a higher magnification. (Bottom) ap>brm causes ectopic veins near the L2 vein and the posterior crossvein. Co-expression of Tctp and Brm (ap>brm, Tctp) considerably suppresses the Brm overexpression phenotype. Overexpression of mutated TctpE12V fails to suppress the Brm phenotype. (Histogram) Quantification of genetic interactions in percent flies. L2: extra veins in L2 vein. PCV: extra veins in the posterior crossvein. L2+PCV: extra veins in both. n=260-330 flies. Scale bar, 500 μm. (b) Genetic interaction between brm and Tctp mutations. Extra PCV (black arrowhead) phenotype in adult TctpEY/h59 transheterozygotes is suppressed by brm2/+ mutation (white arrowhead). (Histogram) Quantification of extra PCV phenotype in female adult flies. Scale bar, 500 μm. n=number of flies. (c) Antagonistic genetic interaction in wing shape. (Top) ptc-Gal4/+, ptc-Gal4/+; brm2/+ and ptc>brm show normal straight wings. (Bottom) ptc>Tctp-i flies show partial curled-up wings (black arrow). This phenotype is suppressed (asterisk) or enhanced (white arrow, curled-up wing) by brm reduction or overexpression, respectively. (Histogram) Quantification of curled wing phenotype in adult flies (mean±s.d.). n=163–237 flies. (d) Genetic interaction between Tctp-knockdown and dominant-negative Brm with catalytically inactive ATPase (BrmDN). (Top) vg-Gal4/+, vg>brmDN, and vg>ISWIDN show normal straight wings. (Bottom) Downward-kinked adult wing phenotype of vg>Tctp-i flies (black arrowhead) was suppressed by coexpressing BrmDN (white arrow), but not by ISWIDN (black arrow). ISWI is an ATPase subunit for other chromatin remodelers such as ACF, CHRAC, and NURF. (Histogram) Quantification of downward-kinked wing phenotype in adult flies. n=number of flies.
