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Identification of an association of ALADIN and
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Knockdown of CK2α+β elicits ectopic mc’s on the scutellum and wing ON-01910 akin to h mutants
While RNAi against CK2α or CK2β elicited ectopic MC’s, these flies did not exhibit ectopic mc’s as in h1/h1 animals (compare Fig. 3B, F, and G). We thus tested whether RNAi against CK2α+β would elicit ectopic mc’s on the scutellum and the L2 vein, and mimic h1/h1 ( Fig. 4 and Fig. 2), but not h2/h2, h2/Tm3 or h1/Tm3 flies ( Fig. 4B and inset). Similar to h1/h1 flies, RNAi against CK2α+β elicited ectopic mc’s on the scutellum and wing veins ( Fig. 4C–E). Moreover, these flies displayed mc’s along the L2 and L5 veins, both also affected in h41/Tik trans-heterozygous flies ( Fig. 2 and Fig. 4F). Thus, knockdown of CK2α+β elicits ectopic mc’s on the scutellum and along the L2 and L5 wing veins, phenotypes that closely mimic mutations in h. Together, these results provide strong evidence that attenuated levels of CK2 elicits phenotypes that mimic h loss of function in vivo.





 
 
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