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A novel RHH family transcription factor aCcr1 and its viral homologs dictate cell cycle progression in archaea [Synchronization RNA-seq]

ABSTRACT: Cell cycle regulation is of paramount importance for all forms of life. Here we report that a conserved and essential cell cycle-specific transcription factor (designated as aCcr1) and its viral homologs control cell division in Sulfolobales. We show that the transcription level of accr1 reaches peak during active cell division (D-phase) subsequent to the expression of CdvA, an archaea-specific cell division protein. Cells over-expressing the 58-aa-long RHH (ribbon-helix-helix) family cellular transcription factor as well as the homologs encoded by large spindle-shaped viruses Acidianus two-tailed virus (ATV) and Sulfolobus monocaudavirus 3 (SMV3) display significant growth retardation and cell division failure, manifested as enlarged cells with multiple chromosomes. aCcr1 over-expression results in downregulation of 17 genes (>4-folds) including cdvA. A conserved motif, aCcr1-box, located between the TATA-binding box and the translation initiation site in the promoters of 13 out of the 17 highly repressed genes, is critical for aCcr1 binding. The aCcr1-box is present in the promoters of cdvA genes across Sulfolobales, suggesting that aCcr1-mediated cdvA repression is an evolutionarily conserved mechanism by which archaeal cells dictate cytokinesis progression, whereas their viruses take advantage of this mechanism to manipulate the host cell cycle.

ORGANISM(S): Sulfolobus islandicus

PROVIDER: GSE220819 | GEO | 2023/03/08

REPOSITORIES: GEO

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A novel RHH family transcription factor aCcr1 and its viral homologs dictate cell cycle progression in archaea [ChIP-seq]

Project description:Cell cycle regulation is of paramount importance for all forms of life. Here we report that a conserved and essential cell cycle-specific transcription factor (designated as aCcr1) and its viral homologs control cell division in Sulfolobales. We show that the transcription level of accr1 reaches peak during active cell division (D-phase) subsequent to the expression of CdvA, an archaea-specific cell division protein. Cells over-expressing the 58-aa-long RHH (ribbon-helix-helix) family cellular transcription factor as well as the homologs encoded by large spindle-shaped viruses Acidianus two-tailed virus (ATV) and Sulfolobus monocaudavirus 3 (SMV3) display significant growth retardation and cell division failure, manifested as enlarged cells with multiple chromosomes. aCcr1 over-expression results in downregulation of 17 genes (>4-folds) including cdvA. A conserved motif, aCcr1-box, located between the TATA-binding box and the translation initiation site in the promoters of 13 out of the 17 highly repressed genes, is critical for aCcr1 binding. The aCcr1-box is present in the promoters of cdvA genes across Sulfolobales, suggesting that aCcr1-mediated cdvA repression is an evolutionarily conserved mechanism by which archaeal cells dictate cytokinesis progression, whereas their viruses take advantage of this mechanism to manipulate the host cell cycle.

2023-03-08 | GSE218790 | GEO

A novel RHH family transcription factor aCcr1 and its viral homologs dictate cell cycle progression in archaea [RNA-seq]

2023-03-08 | GSE218792 | GEO

Illumina sequencing of CRAC data obtained with Ylr419w

Project description:27 years after the yeast genome sequencing, the function of many ORFs remain unknown. Despite the evolutionary distance between human and yeast, homology with the conserved DEAD-box helicase domains allowed us to list DHX29, DHX36 and DHX57 as three putative homologs of the yeast Ylr419w. Functional studies first linked the Ylr419w protein to the translating ribosome, and cross-linking and analysis of cDNA (CRAC) experiments determined the precise region of Ylr419w in contact with the ribosome. It corresponds to the loop of the h16 helix in the 18S rRNA designing the translation initiation factor DHX29, as the functional homolog of Ylr419w.

2024-01-08 | GSE252043 | GEO

Identification of genes regulated by the transcription factor RFX1 (CR_06110C) in the yeast Candida albicans

Project description:The regulatory factor X (RFX) gene family comprises a functionally diverse group of transcription factors characterized by a highly conserved and unique winged-helix DNA binding domain. The RFX proteins control a variety of processes ranging from genome integrity and cell cycle in model yeasts to immune functions and tissue differentiation in higher eukaryotes. The yeast Candida albicans encodes two RFX homologs, one of which (CR_06110C, termed RFX1) remains uncharacterized. In this study we employed RNA-seq to identify downstream targets of the transcriptional regulator Rfx1 in C. albicans.

2023-12-15 | GSE249927 | GEO

CdrL ChIP-seq data for the paper "CdrS is required for cell division site placement but not elongation in hypersaline-adapted archaea"

Project description:Precise control of the cell cycle is central to the physiology of all cells. In prior work we demonstrated that archaeal cells maintain a constant cell size; however, the regulatory mechanisms underlying the cell cycle remain unexplored in this domain of life. In this study we use genetics, functional genomics, and quantitative imaging to identify and characterize the CdrSL gene regulatory network in a model species of archaea. We demonstrate the central role of these ribbon-helix-helix family transcription factors in the regulation of cell division. In this GEO series related to this study, we use ChIP-seq analysis to demonstrate the binding of CdrL to the upstream region of the cdrS-ftsZ2 locus. We conclude that the CdrSL-Z2 transcriptional network is required to coordinate cell division with cell growth in archaea.

2020-04-04 | GSE148065 | GEO

A conserved abundant cytoplasmic long noncoding RNA modulates repression of mRNAs by Pumilio proteins in human cells

Project description:Thousands of long noncoding RNA (lncRNA) genes are encoded in the human genome, and hundreds of them are evolutionary conserved, but their functions and modes of action remain largely obscure. Particularly enigmatic lncRNAs are those that are exported to the cytoplasm, including NORAD - an abundant and highly conserved cytoplasmic lncRNA. Most of the sequence of NORAD is comprised of repetitive units that together contain at least 17 functional binding sites for the two Pumilio homologs in mammals. Through binding to PUM1 and PUM2, NORAD modulates the mRNA levels of their targets, which are enriched for genes involved in chromosome segregation during cell division. Our results suggest that some cytoplasmic lncRNAs function by modulating the activities of RNA binding proteins, an activity which positions them at key junctions of cellular signaling pathways.

2016-07-11 | GSE79804 | GEO

Genome-wide analyses in neuronal cells reveal that USF transcription factors regulate lysosomal gene expression [ChIP-chip]

Project description:The upstream stimulating factors (USFs) USF1 and USF2 are ubiquitously expressed transcription factors characterized by a conserved basic helix-loop-helix leucine zipper DNA-binding domain. They form homo- or heterodimers and recognize E-box motifs to modulate gene expression. They are known to regulate diverse cellular functions including the cell cycle, immune response and glucose-lipid metabolism, but their roles in neuronal cells remain to be clarified. Here, we performed chromatin immunoprecipitation of USF1 from mouse brain cortex preparations. Subsequent promoter array analysis (ChIP-chip) indicated that USF1 exclusively bound to the CACGTG E-box motifs in the proximal promoter regions. Importantly, functional annotation of the USF1-binding targets revealed an enrichment of genes related to lysosomal functions. Gene expression arrays using a neuronal cell line subsequently revealed that knockdown of USFs deregulated lysosomal gene expression. Altered expression was validated by quantitative RT-PCR, supporting the conclusion that USFs regulate lysosomal gene expression. Furthermore, USFs knockdown slightly increased LysoTracker staining, implying a role for USFs in modulating lysosomal homeostasis. Together, our comprehensive, genome-scale analyses identified lysosomal genes as targets of USFs in neuronal cells, suggesting a potential additional pathway of lysosomal regulation. ChIP-chip analysis of USF1 and NF-Y in mouse brain cortex. To identify downstream targets of USF1 and NF-Y in neuronal cells, they were chromatin-immunoprecipitated from mouse brain cortical lysates. The obtained chromatin DNAs were labeled with biotin and hybridized on Affymetrix Mouse Promoter 1.0R Array.

2016-01-08 | E-GEOD-76616 | biostudies-arrayexpress

Genome-wide analyses in neuronal cells reveal that USF transcription factors regulate lysosomal gene expression [Expression analysis]

Project description:The upstream stimulating factors (USFs) USF1 and USF2 are ubiquitously expressed transcription factors characterized by a conserved basic helix-loop-helix leucine zipper DNA-binding domain. They form homo- or heterodimers and recognize E-box motifs to modulate gene expression. They are known to regulate diverse cellular functions including the cell cycle, immune response and glucose-lipid metabolism, but their roles in neuronal cells remain to be clarified. Here, we performed chromatin immunoprecipitation of USF1 from mouse brain cortex preparations. Subsequent promoter array analysis (ChIP-chip) indicated that USF1 exclusively bound to the CACGTG E-box motifs in the proximal promoter regions. Importantly, functional annotation of the USF1-binding targets revealed an enrichment of genes related to lysosomal functions. Gene expression arrays using a neuronal cell line subsequently revealed that knockdown of USFs deregulated lysosomal gene expression. Altered expression was validated by quantitative RT-PCR, supporting the conclusion that USFs regulate lysosomal gene expression. Furthermore, USFs knockdown slightly increased LysoTracker staining, implying a role for USFs in modulating lysosomal homeostasis. Together, our comprehensive, genome-scale analyses identified lysosomal genes as targets of USFs in neuronal cells, suggesting a potential additional pathway of lysosomal regulation. Gene expression profiling of neuro2a cells knocking down USFs. To screen USFs-downstream genes, mouse neuro2a cells were transfected with vectors for USFs miR RNAi or an empty vector, and then subjected to microarray analysis using Affymetrix Mouse Gene 1.0 ST Array.

2016-01-08 | E-GEOD-76615 | biostudies-arrayexpress

Role of BHLHE40 in shaping macrophage inflammatory response

Project description:BHLHE40 is a member of basic helix-loop-helix family transcription factors and highly conserved across mammalian species. Structurally, BHLHE40 consists of an N-terminal basic DNA binding domain, a helix-loop-helix dimerization domain, and a protein interacting orange domain. BHLHE40 is known to regulate a wide variety of essential cellular processes, including cell cycle, cellular proliferation, programmed cell death, cellular development and differentiation, and circadian rhythm. Here we isolated thioglycollate-elicited peritoneal macrophages (PMs) from 3 mice per group (Lyz2cre and Lyz2cre:BHLHE40Fl/Fl). These cells were stimulated with 100ng/ml LPS for 4 hours. Total RNA was isolated and subjected to RNAseq analyses.

2021-09-24 | GSE176174 | GEO

An organelle-tethering mechanism couples flagellation to cell division in bacteria

Project description:In both free-living and pathogenic bacteria, problems in the synthesis and assembly of early flagellar components invariably lead to cell division defects. However, the mechanism that fine-tunes the cell division cycle with the flagellar biogenesis is poorly understood. Herein, we report the role of the conserved regulator MadA in coupling flagellar biogenesis to cell division in Caulobacter crescentus. We demonstrate that MadA is required to induce the flagellar specific type III export component FlhA to release and activate FliX, which in-turn is required to license the conserved σ54-activator, FlbD. In the absence of MadA, FliX is tethered to FlhA, inhibiting FlbD activation and crippling completion of flagellar biogenesis and cell division. Furthermore, we demonstrate that MadA exploits a divisome-stoichiometric to control cell division. We propose that MadA has a sentinel-type function that warrants progression of the flagellar biogenesis, and the cell division cycle, once early flagellar structures are properly assembled.

2021-02-18 | GSE153968 | GEO

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