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. 2014 Aug 15;28(16):1772–1785. doi: 10.1101/gad.245738.114

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© 2014 Hayashi et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0.

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Figure 1. — The EJC is required for transposon silencing in ovarian soma and the germline. (A,B) Cartoons of Drosophila egg chambers to illustrate the tissue-specific gene depletions in germline (A) or somatic (B) cells. The affected cell types (colored), knockdown strategies, TE reporters, and marker TEs expressed in the respective tissues are indicated. (C,D) The results of the TE reporter assays upon germline (C) or soma (D) knockdown of EJC factors. Defective TE silencing is reflected by lacZ expression (blue). The depletion of EJC core factors mago and tsu, but not btz, as well as the depletion of peripheral factors RnpS1 or Acn consistently leads to lacZ expression in both soma and the germline. Stained egg chambers of representative phenotypes are shown: white for no staining, tsu for strong staining but abnormal morphology, and Acn for strong staining and no morphological defects. Knockdown of piRNA biogenesis factor armi served as control. (E,F) Fold changes in steady-state RNA levels of endogenous TEs in ovaries upon depletion of the indicated genes in the germline (E) or soma (F). RNA levels are normalized to rp49 levels, and values indicate averages of three biological replicates relative to control knockdowns; error bars indicate standard deviation. The depletion of EJC core factors (mago and tsu) and peripheral factors (RnpS1 and Acn) causes strong TE derepression almost comparable with armi depletions.