Publications by authors named "Wade T Nottingham"

Macro long non-coding RNAs (lncRNAs) play major roles in gene silencing in inprinted gene clusters. Within the imprinted cluster, the paternally expressed lncRNA downregulates its sense counterpart . To explore the mechanism of action of , we generated two new knock-in alleles to truncate upstream and downstream of the promoter.

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Transcription factors such as Scl/Tal1, Lmo2, and Runx1 are essential for the development of hematopoietic stem cells (HSCs). However, the precise mechanisms by which these factors interact to form transcriptional networks, as well as the identity of the genes downstream of these regulatory cascades, remain largely unknown. To this end, we generated an Scl(-/-) yolk sac cell line to identify candidate Scl target genes by global expression profiling after reintroduction of a TAT-Scl fusion protein.

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The transcription factor Runx1/AML1 is an important regulator of hematopoiesis and is critically required for the generation of the first definitive hematopoietic stem cells (HSCs) in the major vasculature of the mouse embryo. As a pivotal factor in HSC ontogeny, its transcriptional regulation is of high interest but is largely undefined. In this study, we used a combination of comparative genomics and chromatin analysis to identify a highly conserved 531-bp enhancer located at position + 23.

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Genomic imprinting results in allele-specific silencing according to parental origin. Silencing is brought about by imprinting control regions (ICRs) that are differentially marked in gametogenesis. The group of imprinted transcripts in the mouse Gnas cluster (Nesp, Nespas, Gnasxl, Exon 1A and Gnas) provides a model for analyzing the mechanisms of imprint regulation.

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Article Synopsis
  • Genomic imprinting leads to the silencing of specific gene alleles based on whether they come from the mother or the father, regulated by special regions that can affect nearby genes significantly.
  • Researchers have identified two important regions that control imprinting in the Gnas gene cluster on mouse chromosome 2, finding that one region affects the expression of Gnas itself while the other may influence related transcripts.
  • A study showed that deleting a specific methylation region linked to paternal expression of Gnas can reverse certain abnormalities in mice with a maternal Gnas mutation, indicating a complex control system for this gene and its neighbors.
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