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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE153749 | GEO | 2021/08/04

REPOSITORIES: GEO

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties [RNA-seq]

Project description:ILC2s from different tissues manifest distinct properties. To investigate the molecular mechanisms regulating tissue features of ILC2s, we performed single cell RNA-seq on purified ILC2s from 5 different tissues.

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties [ATAC-seq]

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

Project description:Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties [RNA-seq]

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Nuclear export of mRNA is an essential process for eukaryotic gene expression. The TREX complex couples gene expression from transcription and splicing to mRNA export. Sub2, a core component of the TREX complex in yeast, has diversified in humans to two closely related RNA helicases, UAP56 and URH49. Here, we show that URH49 forms a novel URH49-CIP29 complex, termed the AREX (alternative mRNA export) complex, whereas UAP56 forms the human TREX complex. The mRNAs regulated by these helicases are different at the genome-wide level. The two sets of target mRNAs contain distinct subsets of key mitotic regulators. Consistent with their target mRNAs, depletion of UAP56 causes mitotic delay and sister chromatid cohesion defects, whereas depletion of URH49 causes chromosome arm resolution defects and failure of cytokinesis. In addition, depletion of the other human TREX components or CIP29 causes mitotic defects similar to those observed in UAP56- or URH49-depleted cells, respectively. Taken together, the two closely related RNA helicases have evolved to form distinct mRNA export machineries, which regulate mitosis at different steps.

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Macrophages regulate lung ILC2 activation via Pla2g5-dependent mechanisms.

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