Author Correction: Varying levels of X chromosome coalescence in female somatic cells alters the balance of X-linked dosage compensation and is implicated in female-dominant systemic lupus erythematosus.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Varying levels of X chromosome coalescence in female somatic cells alters the balance of X-linked dosage compensation and is implicated in female-dominant systemic lupus erythematosus.

The three-dimensional organization of the genome in mammalian interphase nuclei is intrinsically linked to the regulation of gene expression. Whole chromosome territories and their encoded gene loci occupy preferential positions within the nucleus that changes according to the expression profile of a given cell lineage or stage. To further illuminate the relationship between chromosome organization, epigenetic environment, and gene expression, here we examine the functional organization of chromosome X and corresponding X-linked genes in a variety of healthy human and disease state X diploid (XX) cells.

Clinical Epigenetic Therapies Disrupt Sex Chromosome Dosage Compensation in Human Female Cells.

Sex chromosome gene dosage compensation is required to ensure equivalent levels of X-linked gene expression between males (46, XY) and females (46, XX). To achieve similar expression, X-chromosome inactivation (XCI) is initiated in female cells during early stages of embryogenesis. Within each cell, either the maternal or paternal X chromosome is selected for whole chromosome transcriptional silencing, which is initiated and maintained by epigenetic and chromatin conformation mechanisms.

Myc binds the pluripotency factor Utf1 through the basic-helix-loop-helix leucine zipper domain.

In order to elucidate the function of Myc in the maintenance of pluripotency and self-renewal in mouse embryonic stem cells (mESCs), we screened for novel ESC-specific interactors of Myc by mass spectrometry. Undifferentiated embryonic cell transcription factor 1 (Utf1) was identified in the screen as a putative Myc binding protein in mESCs. We found that Myc and Utf1 directly interact.

Utf1: Goldilocks for ESC bivalency.

Recently in Cell, Jia et al. (2012) reported novel Utf1-controlled mechanisms of maintaining pluripotency and self-renewal in embryonic stem cells (ESCs). Utf1 buffers bivalent gene expression by competitive binding with polycomb repressive complex 2 and initiation of mRNA degradation.

Sodium/calcium exchangers selectively regulate calcium signaling in mouse taste receptor cells.

Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete taste stimuli. Some taste stimuli activate G protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified.

Sodium-calcium exchangers contribute to the regulation of cytosolic calcium levels in mouse taste cells.

Taste cells use multiple signalling mechanisms to generate unique calcium responses to distinct taste stimuli. Some taste stimuli activate G-protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). We recently demonstrated that a constitutive calcium influx exists in taste cells that is regulated by mitochondrial calcium transport and that the magnitude of this calcium influx correlates with the signalling mechanisms used by the taste cells.