Project description:To verify ZNF417 and ZNF587 knock out whether leads to HERV-K element reactivation, we performed RNA-seq on ZNF417/ZNF587 double knock out (DKO) K562 cell lines. We observed a dozen of genes were upregulated in KO cells, and some of them possessed PBS-Lys sites near their promoters that can be directly targeted by ZNF417 and ZNF587, such as MS4A clusters. We also measured the expression levels of repetitive elements in ZNF417 ZNF587 dKO cells, which exhibited only some ERVs reactivation indirectly.
Project description:To verify Znf417 and Znf587 knock out whether leads to HERV-K element reactivation, we performed RNA-seq on Znf417/Znf587 double knock out (DKO) 293T cell lines. We did not find any significant changes in HERVK expression.
Project description:The ChIP-seq experiments using GFP antibody on ZNF417/ZNF587-GFP overexpressing 293T cells revealed that ZNF417/ZNF587 preferred to bind a PBS-Lys-containing HERVs. Further motif calling analysis showed that both ZNF417 and ZNF587 bind to HERVK PBS-resembled motif.
Project description:Combined depletion of H1.2 and H1.4 has a strong deleterious effect in the cancer cells examined, and induces a strong interferon (IFN) response with up-regulation of many IFN-stimulated genes (ISGs), which is not seen in individual H1 knock-downs. Although H1 participates to repress ISG promoters, its activation upon H1 KD is mainly generated by the activation of the IFN response through cytosolic nucleic acids receptors, IFN synthesis and JAK-STAT pathway activation. The IFN response may be triggered by the expression of noncoding dsRNAs generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. H1 KD promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats.
Project description:Combined depletion of H1.2 and H1.4 has a strong deleterious effect in the cancer cells examined, and induces a strong interferon (IFN) response with up-regulation of many IFN-stimulated genes (ISGs), which is not seen in individual H1 knock-downs. Although H1 participates to repress ISG promoters, its activation upon H1 KD is mainly generated by the activation of the IFN response through cytosolic nucleic acids receptors, IFN synthesis and JAK-STAT pathway activation. The IFN response may be triggered by the expression of noncoding dsRNAs generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. H1 KD promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats.