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Evolution of a transcriptional regulator from a transmembrane nucleoporin

ABSTRACT: Evolution of a transcriptional regulator from a transmembrane nucleoporin

PROVIDER: PRJNA326730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3707264.fastq.gz	Fastqsanger.gz
	SRR3707265.fastq.gz	Fastqsanger.gz
	SRR3707266.fastq.gz	Fastqsanger.gz
	SRR3707267.fastq.gz	Fastqsanger.gz
	SRR3707268.fastq.gz	Fastqsanger.gz

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Evolution of a transcriptional regulator from a transmembrane nucleoporin.

Project description:Nuclear pore complexes (NPCs) emerged as nuclear transport channels in eukaryotic cells ∼1.5 billion years ago. While the primary role of NPCs is to regulate nucleo-cytoplasmic transport, recent research suggests that certain NPC proteins have additionally acquired the role of affecting gene expression at the nuclear periphery and in the nucleoplasm in metazoans. Here we identify a widely expressed variant of the transmembrane nucleoporin (Nup) Pom121 (named sPom121, for "soluble Pom121") that arose by genomic rearrangement before the divergence of hominoids. sPom121 lacks the nuclear membrane-anchoring domain and thus does not localize to the NPC. Instead, sPom121 colocalizes and interacts with nucleoplasmic Nup98, a previously identified transcriptional regulator, at gene promoters to control transcription of its target genes in human cells. Interestingly, sPom121 transcripts appear independently in several mammalian species, suggesting convergent innovation of Nup-mediated transcription regulation during mammalian evolution. Our findings implicate alternate transcription initiation as a mechanism to increase the functional diversity of NPC components.

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Evolution of a transcriptional regulator from a transmembrane nucleoporin

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Evolution of a transcriptional regulator from a transmembrane nucleoporin

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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

Project description:Nucleoporin Seh1 has been involved in gene regulation. To dissect nucleoporin's direct regulated genes, we performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for nucleoporin Seh1 in neural stem cells.

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Project description:Cystic fibrosis, the most commonly inherited lethal pulmonary disorder in Caucasians, is caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR). To identify genomic responses to the presence or absence of CFTR in pulmonary tissues in vivo, microarray analyses of lung mRNAs were performed on whole lung tissue from mice lacking (CFTR(-)) or expressing mouse CFTR (CFTR(+)). Whereas the histology of lungs from CFTR(-) and CFTR(+) mice was indistinguishable, statistically significant increases in the relative abundance of 29 and decreases in 25 RNAs were identified by RNA microarray analysis. Of RNAs whose expression was consistently altered by the absence of CFTR, functional classes of genes influencing gene transcription, inflammation, intracellular trafficking, signal transduction, and ion transport were identified. RNAs encoding the transcription factor CCAAT enhancer-binding protein (CEBP) delta and interleukin (IL) 1beta, both known to regulate CFTR expression, were induced, perhaps indicating adaptation to the lack of CFTR. RNAs mediating lung inflammation including calgranulin-S100 family members, IL-1beta and IL-4, were increased. Likewise, expression of several membrane transport proteins that interact directly with CFTR were increased, suggesting that CFTR-protein complexes initiate genomic responses. Absence of CFTR influenced the expression of genes modulating diverse pulmonary cell functions that may ameliorate or contribute to the pathogenesis of CF. Keywords: Genotype comparison

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