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Heterochromatin Protein ERH represses alternative cell fates during early mammalian differentiation [CUT&RUN]

ABSTRACT: We investigate the role of ERH in the regulation of H3K9me3 domains which impede transcription factor binding and gene activation in mouse preimplantation, human ESC differentiation, and human fibroblast reprogramming.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268961 | GEO | 2025/06/01

REPOSITORIES: GEO

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Heterochromatin Protein ERH represses alternative cell fates during early mammalian differentiation [RNA-Seq]

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Heterochromatin Protein ERH represses alternative cell fates during early mammalian differentiation [CUT&RUN]

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [3]

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post-transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post-transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

2024-08-22 | GSE274071 | GEO

ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [4]

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [2]

2024-08-22 | GSE274070 | GEO

ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [1]

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post- transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

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