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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites

ABSTRACT: SATB1, a nuclear matrix-associated protein, has long been proposed to function as a global chromatin loop organizer in T cells. However, the precise roles of SATB1 in chromatin organization remain elusive. Here we show that the depletion of SATB1 in immortalized T cells led to pronounced changes in gene expression, particularly for genes involved in cell proliferation and T cell activation, as well as 3D genome architecture at multiple scales, including the A/B compartment, topologically associating domains (TADs), and loops. Importantly, SATB1 extensively colocalizes with CTCF throughout the genome. Depletion of SATB1 led to increased association among the SATB1/CTCF co-occupied sites, as well as increased chromatin contacts across these sites, thereby altering the genome-wide chromatin loop landscape. SATB1 does not regulate genome architecture by modulating CTCF occupancy. Rather, the topological effects imposed by SATB1 may be attributed to SATB1-dependent anchoring of CTCF to the salt extraction-resistant nuclear matrix. Together, our findings suggest that the functional interplay between nuclear matrix and CTCF plays a critical role in orchestrating 3D genome organization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE199006 | GEO | 2023/03/05

REPOSITORIES: GEO

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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites

Project description:SATB1, a nuclear matrix-associated protein, has long been proposed to function as a global chromatin loop organizer in T cells. However, the precise roles of SATB1 in chromatin organization remain elusive. Here we show that the depletion of SATB1 in immortalized T cells led to pronounced changes in gene expression, particularly for genes involved in cell proliferation and T cell activation, as well as 3D genome architecture at multiple scales, including the A/B compartment, topologically associating domains (TADs), and loops. Importantly, SATB1 extensively colocalizes with CTCF throughout the genome. Depletion of SATB1 led to increased association among the SATB1/CTCF co-occupied sites, as well as increased chromatin contacts across these sites, thereby altering the genome-wide chromatin loop landscape. SATB1 does not regulate genome architecture by modulating CTCF occupancy. Rather, the topological effects imposed by SATB1 may be attributed to SATB1-dependent anchoring of CTCF to the salt extraction-resistant nuclear matrix. Together, our findings suggest that the functional interplay between nuclear matrix and CTCF plays a critical role in orchestrating 3D genome organization.

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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites [Hi-C]

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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites [RNA-seq]

Project description:Spatial genome organization is critical for precise gene regulation during development. Special AT-rich sequence binding protein 1 (SATB1) has long been proposed to act as a global chromatin loop organizer in T cells. However, the exact functions of SATB1 in genome organization remain elusive. Here we show that the depletion of SATB1 in human and murine T cells led to transcriptional dysregulation for genes involved in T cell activation, as well as alterations of 3D genome architecture at multiple scales, including the A/B compartment, topologically associating domains (TADs), and loops. Importantly, SATB1 extensively colocalizes with CTCF throughout the genome. Depletion of SATB1 led to increased chromatin contacts among and across the SATB1/CTCF co-occupied sites, thereby affecting the transcription of critical genes involved in T cell activation. The loss of SATB1 did not affect the genome-wide occupancy of CTCF, but significantly reduced the retention of CTCF in the nuclear matrix. Collectively, our data reveal that SATB1 constrains chromatin topology surrounding CTCF-binding sites by tethering CTCF to the nuclear matrix, and suggest that the functional interplay between SATB1 and CTCF contributes to 3D genome organization.

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The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 2]

Project description:Here we show that HNRNPU, the major nuclear matrix attachment factor, is necessary to maintain proper nuclear architecture in mouse hepatocytes. Upon HNRNPU depletion, the interactions between chromatin and nuclear lamina have been changed dramatically；chromatin organization is globally changed; boundaries of topologically associating domains (TADs) become weaker; inter-TAD interactions are increased; thousands of genes are significantly altered coincident with 3D chromatin changes. Mechanically, HNRNPU interacts with CTCF and RAD21, which affects the binding of RAD21 to the chromatin significantly, whereas CTCF bindings are almost unchanged, what’ more, the decrease of binding strengths are highly correlated with the weakness of loop bounded by Rad21. Taken together, we identify HNRNPU as a key regulator of chromatin architecture, and our data suggest the importance of nuclear matrix associating factors in 3D genome organization.

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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites

Project description:SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites

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SATB1 Regulates 3D Genome Architecture in T cells by Constraining Chromatin Interactions surrounding CTCF-binding sites

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