Fig. 3: Rpd3, Mi-2, and MEP-1 are implicated in TE epigenetic silencing in OSCs. | Nature Communications

Fig. 3: Rpd3, Mi-2, and MEP-1 are implicated in TE epigenetic silencing in OSCs.

From: The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

Fig. 3

a Scatterplots of RNA-seq reads in FPKM (fragments per kilobase of exon per million reads mapped) for 108 annotated D. melanogaster TEs in control knockdown (KD) (siGFP) vs. Piwi-KD (sipiwi) (left), Mi-2 KD (siMi-2) (middle), and Rpd3-KD (siRpd3) (right). TEs for which the expression level differed from control by more than two-fold in Piwi-KD (Piwi–piRNA-targeted TEs) are plotted in orange. Both x-axis and y-axis are a log10 scale. b A browser screenshot shows RNA-seq tracks upon GFP (siGFP), Piwi (sipiwi), Mi-2 (siMi-2), and Rpd3 (siRpd3) knockdown at the expanded (ex) locus. OSC-specific Gypsy insertion site is annotated; ex TSS is indicated with a dashed line. c RT-qPCR fold changes in steady-state RNA levels of three endogenous TEs (Tabor, Gypsy, and mdg1) and of the expanded (ex) gene upon MEP-1 (siMEP-1), Mi-2 (siMi-2), Rpd3 (siRpd3), or Piwi (sipiwi) knockdown using siRNAs. Dots show RNA values quantified relative to Rpl32 and normalized to control knockdown for n = 3 biologically independent samples, lines represent mean values ± SD (log2). d–f H3K9me3 (d), H3 (e), or H3K9ace (f) quantified by ChIP-qPCR at mdg1 and Gypsy TE genomic loci, as well as on the expanded (ex) and krimper (krimp) genes after knockdown using the indicated siRNA. Values relative to a positive control (1360-element for H3K9me3 or RpL32 for H3 and H3K9ace) were normalized to input (mean ± SD from n = 3 independent biological replicates). Source data for c–f: Supplementary Data set 3.

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