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Figure 5 | Epigenetics & Chromatin

Figure 5

From: Drosophila linker histone H1 coordinates STAT-dependent organization of heterochromatin and suppresses tumorigenesis caused by hyperactive JAK-STAT signaling

Figure 5

STAT92E contributes to H1-dependent heterochromatin formation. Polytene chromosomes of salivary gland cells from L3 larvae were analyzed by indirect immunofluorescence (IF) staining with antibodies against HP1 or H1 (red) and STAT92E (green). DNA was stained with DAPI (blue). Scale bar represents 10 μm. (A) Polytene chromosome structure in wild type larvae (top), H1-depleted larvae (middle), and H1-depleted larvae that overexpress nonphosphorylatable STAT, STAT92E(Y704F) (bottom). HP1 signal is strongly enriched in a single chromocenter region in the wild type. The chromocenter is not discernable (DAPI), and HP1 staining is dispersed in multiple foci upon H1 depletion (see also Figure 1A). The phenotype is partially rescued by STAT92E(Y704F) expression. (B) STAT92E(Y704F) overexpressed in H1-depleted larvae, co-localizes with residual H1 in polytene chromosomes (top). Ectopically overexpressed transgenic wild type (WT) STAT92E fails to restore the single chromocenter and does not co-localize with residual H1 (bottom).

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