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. Author manuscript; available in PMC: 2017 Dec 5.
Published in final edited form as: Dev Cell. 2016 Dec 5;39(5):560–571. doi: 10.1016/j.devcel.2016.11.004

Figure 4. Long Oskar and its N-terminal domain are both necessary and sufficient to trap and retain mitochondria at the cortex. Arrows indicate mitochondrial accumulation.

Figure 4

(A) Loss of oskar, but not tudor nor vasa, prevents posterior mitochondrial accumulation. 0 to 1 hour old embryos from wild-type, oskar null mutant (oskA87/Df(3R)p-XT103), tudor null mutant (tudortux46/Df(tudor)), or Vasa knockdown (nosgal4::VP16, mito-EYFP/uas-vasa RNAi) mothers were immunostained with α-ATP synthase α. See also Figure S3.

(B) Loss of long, but not short, oskar prevents posterior mitochondrial accumulation. 0 to 1 hour old embryos from wild-type mothers, oskar null mutant mothers (oskA87/Df(3R)p-XT103), or oskar null mutant mothers transgenically expressing either Long Oskar (short osk−/−; oskM139L (go M2-12)/+; oskA87/Df(3R)p-XT103) or Short Oskar (long osk−/− ;oskM1L(go M1-7)/+;oskA87/Df(3R)p-XT103) were immunostained with α-ATP synthase α and α-Oskar.

(C) The N-terminal domain is sufficient to trap mitochondria at the anterior when it is expressed there. Left, 0 to 1 hour old embryos from wild-type mothers were immunostained with α-ATP synthase α and α-Oskar. Right, 0 to 1 hour old embryos from mothers expressing the N-terminus of Long Oskar fused to mCherry, FLAG, and HA at the anterior using the bcd 3’UTR (N-term osk-bcd 3’UTR: uas-osk N-term::mCherry::3xFLAGHA/+; nosgal4::VP16, mito-EYFP/+) were imaged with EYFP (mitochondria) and mCherry (N-term. Oskar). See also Figure S4.