Ana Cláudia Raposo

TL;DR: It is proposed that this novel SETD2-dependent role provides a chromatin bookmarking instrument that facilitates signaling and repair of DSBs and may afford an alternative mechanism for the inactivation of the p53-mediated checkpoint without the need for additional genetic mutations in TP53.

TL;DR: It is reported that downregulation of SETD2 in human cells leads to intragenic transcription initiation in at least 11% of active genes, and activity modulates FACT recruitment and nucleosome dynamics, thereby repressing cryptic transcription initiation.

TL;DR: It is found that transcriptional silencing can be largely uncoupled from Polycomb repressive complex 1 and complex 2 (PRC1/2) recruitment, which requires B and C repeats, which suggests distinct modules within the Xist RNA are involved in the convergence of independent chromatin modification and gene repression pathways.

TL;DR: Overall, it is shown that hierarchy of imprinting control in donor cells might not apply to iPSCs, accounting for their spectrum of imprinted alterations, and differences in imprinting regulation should be taken into consideration for the use of i PSCs in disease modeling.

TL;DR: It is found that transcriptional silencing can be largely uncoupled from Polycomb repressive complex 1 and 2 (PRC1/2) recruitment, which requires repeats B and C, and distinct modules within the Xist RNA are involved in the convergence of independent chromatin modification and gene repression pathways.