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. 2010 Aug 9;190(3):407–425. doi: 10.1083/jcb.200911020

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© 2010 Velichkova et al.

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Figure 7. — mtm interacts with both class II Pi3K68D and class III Vps34 for PI(3)P homeostasis. (A) PI(3)P distribution, as detected by mCherry:2xFYVE in single hemocyte for genotypes as shown, was expanded (IR-mtm), depleted (IR-Pi3K68D or Vps34-KD), or restored (bottom; IRmtm with IR-Pi3K68D or Vps34-KD). (B) Depletion of Pi3K68D or Vps34 transcripts in RNAi-treated Kc₁₆₇ cells (left) and purified hemocytes (right; Pxn-GAL4/UAS-IR-Pi3K68D). Pi3K68D:GFP (bottom; anti-GFP) in RNAi-treated Kc₁₆₇ cells. WB, Western blot. (C) GFP:2xFYVE area in RNAi-treated Kc₁₆₇ cells (Fig. S4 C) normalized per cell number. Single-kinase RNAi (gray) or mtm coRNAi (black). (D) Percent PI(3)P of total myo-inositol from RNAi-treated Kc₁₆₇ cells. Similar trends were found across two experiments. (E) Pi3K68D:GFP expression expanded PI(3)P detected by mCherry:2xFYVE. Error bars indicate SEM.