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Lovell, C. D.

Publications and source records attributed to Lovell, C. D..

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↗

Xist Deletion in B Cells Results in Systemic Lupus Erythematosus Phenotypes

Systemic lupus erythematosus (SLE) is an autoimmune disease preferentially observed in females. X-linked gene expression in XX females is normalized to that of XY males by X-Chromosome Inactivation (XCI). However, B cells from female SLE patients and mouse models of SLE exhibit mislocalization of Xist RNA, a critical regulator of XCI, and aberrant expression of X-linked genes, suggesting that impairment of XCI may contribute to disease. Here, we find that a subset of female mice harboring a conditional deletion of Xist in B cells ("Xist cKO") spontaneously develop SLE phenotypes, including expanded activated B cell subsets, disease-specific autoantibodies, and glomerulonephritis. Moreover, pristane-induced SLE-like disease is more severe in Xist cKO mice. Activated B cells from Xist cKO mice with SLE phenotypes have increased expression of proinflammatory X-linked genes implicated in SLE. Together, this work indicates that impaired XCI maintenance in B cells directly contributes to the female-bias of SLE.

immunology↗

Quantitative sub-cellular acyl-CoA analysis reveals distinct nuclear regulation

Quantitative sub-cellular metabolomic measurements can yield crucial insights into the roles of metabolites in cellular processes, but are subject to multiple confounding factors. We developed Stable Isotope Labeling of Essential nutrients in cell Culture - Sub-cellular Fractionation (SILEC-SF), which uses isotope labeled internal standard controls that are present throughout fractionation and processing to quantify acyl-Coenzyme A thioesters in sub-cellular compartments by liquid chromatography-mass spectrometry. We tested SILEC-SF in a range of sample types and examined the compartmentalized responses to oxygen tension, cellular differentiation, and nutrient availability. Application of SILEC-SF to the challenging analysis of the nuclear compartment revealed a nuclear acyl-CoA profile distinct from that of the cytosol, with notable nuclear enrichment of propionyl-CoA. Using isotope tracing we identified the branched chain amino acid (BCAA) isoleucine as a major metabolic source of nuclear propionyl-CoA and histone propionylation, thus revealing a new mechanism of crosstalk between metabolism and the epigenome.

biochemistry↗