ArticleGenes & development2015
A monoallelic-to-biallelic T-cell transcriptional switch regulates GATA3 abundance.
Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
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- X-Chromosome Inactivation and Autosomal Random Monoallelic Expression as "Faux Amis".Frontiers in cell and developmental biology · 2021Review
- Novel, Non-Gene-Destructive Knock-In Reporter Mice Refute the Concept of MonoallelicJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Order by chance: origins and benefits of stochasticity in immune cell fate control.Current opinion in systems biology · 2019Article
- Human IL12RB1 expression is allele-biased and produces a novel IL12 response regulator.Genes and immunity · 2019Article
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- Protective effects of astragaloside IV against ovalbumin-induced allergic rhinitis are mediated by T-box protein expressed in T cells/GATA-3 and forkhead box protein 3/retinoic acid-related orphan nuclear receptor γt.Molecular medicine reports · 2017Article
- GATA3 Abundance Is a Critical Determinant of T Cell Receptor β Allelic Exclusion.Molecular and cellular biology · 2017Article
- Gata3 restrains B cell proliferation and cooperates with p18INK4c to repress B cell lymphomagenesis.Oncotarget · 2016Article
- Hematopoiesis and T-cell specification as a model developmental system.Immunological reviews · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Protein abundance must be precisely regulated throughout life, and nowhere is the stringency of this requirement more evident than during T-cell development: A twofold increase in the abundance of transcription factor GATA3 results in thymic lymphoma, while reduced GATA3 leads to diminished T-cell production. GATA3 haploinsufficiency also causes human HDR (hypoparathyroidism, deafness, and renal dysplasia) syndrome, often accompanied by immunodeficiency. Here we show that loss of one Gata3 allele leads to diminished expansion (and compromised development) of immature T cells as well as aberrant induction of myeloid transcription factor PU.1. This effect is at least in part mediated transcriptionally: We discovered that Gata3 is monoallelically expressed in a parent of origin-independent manner in hematopoietic stem cells and early T-cell progenitors. Curiously, half of the developing cells switch to biallelic Gata3 transcription abruptly at midthymopoiesis. We show that the monoallelic-to-biallelic transcriptional switch is stably maintained and therefore is not a stochastic phenomenon. This unique mechanism, if adopted by other regulatory genes, may provide new biological insights into the rather prevalent phenomenon of monoallelic expression of autosomal genes as well as into the variably penetrant pathophysiological spectrum of phenotypes observed in many human syndromes that are due to haploinsufficiency of the affected gene.
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