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Biology subjects

Sierra, I.

Publications and source records attributed to Sierra, I..

3 recordsLinked to original sources

Tissue-Specific and NF-kappaB-Independent Xist RNA Localization Patterns in Female Intestinal, Blood, and Muscle Progenitors

X-Chromosome Inactivation (XCI), driven by the expression of Xist RNA and the enrichment of various repressive epigenetic marks, results in the formation of a mostly inactive X chromosome (Xi) to equalize X-linked gene expression between sexes. Unexpectedly, in unstimulated female lymphocytes that are largely quiescent, these epigenetic features are largely absent but are restored by NF-{kappa}B signaling following their activation. To determine whether these epigenetic phenotypes correlate with quiescence or NF-{kappa}B activation in other tissues, we evaluated female progenitor and stem cells from intestine, blood, and muscle. Despite known NF-{kappa}B activation, intestinal progenitors have variable Xist RNA patterns, whereas blood progenitors and neutrophils show a strong correlation between NF-{kappa}B activation status and Xist RNA localization. In contrast, muscle satellite cells (SCs) and myoblasts exhibit Xist RNA accumulation at the Xi without NF-{kappa}B activation. Xist RNA localization patterns in SCs change with age, yet adult SCs have an Xi that is mostly transcriptionally silent while allowing expression of muscle-specific X-linked genes including Dmd. These findings reveal that female somatic cells employ diverse, tissue-specific epigenetic mechanisms to maintain X chromosome inactivation, enabling cell type specific Xi gene expression while preserving chromosome-wide silencing.

genetics↗

B cell stimulation changes the structure and higher-order organization of the inactive X chromosome

X Chromosome Inactivation (XCI) equalizes X-linked gene expression between sexes. B cells exhibit dynamic XCI, with Xist RNA/heterochromatic marks absent on the inactive X (Xi) in naive B cells but returning following mitogenic stimulation. The impact of dynamic XCI on Xi structure and maintenance was previously unknown. Here, we find dosage compensation of the Xi with state-specific XCI escape genes in naive and in vitro activated B cells. Allele-specific OligoPaints indicate similar Xi and Xa territories in B cells that are less compact than in fibroblasts. Allele-specific Hi-C reveals a lack of TAD-like structures on the Xi of naive B cells, and stimulation-induced alterations in TAD-like boundary strength independent of gene expression. Notably, Xist deletion in B cells changes TAD boundaries and large-scale Xi compaction. Altogether, our results uncover B cell-specific Xi plasticity which could underlie sex-biased biological mechanisms.

genetics↗

Remodeling and compaction of the inactive X is regulated by Xist during female B cell activation

X Chromosome Inactivation (XCI) equalizes X-linked gene expression between sexes. B cells exhibit unusually dynamic XCI, as Xist RNA/heterochromatic marks on the inactive X (Xi) are absent in naive B cells, but return following mitogenic stimulation. Xi gene expression analysis supports dosage compensation, but reveals high levels of XCI escape genes in both naive and activated B cells. Allele-specific OligoPaints indicate similar Xi and Xa territories in B cells that is less compact than in fibroblasts. Allele-specific Hi-C maps reveal a lack of TAD-like structures on the Xi of naive B cells, and alterations in TADs and stronger TAD boundaries at Xi escape genes after mitogenic stimulation. Notably, Xist deletion in B cells reduces Xi compaction and changes TAD boundaries, independent of its localization to the Xi. Our findings provide the first evidence that Xi compaction/small scale organization in lymphocytes impact XCI maintenance and female biased X-linked gene expression.

genetics↗