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Biology subjects

Halasz, H.

Publications and source records attributed to Halasz, H..

4 recordsLinked to original sources

Phase transition drives bacterial single-stranded DNA binding (SSB) protein mobilization during stress response and metabolic adaptation

Single-stranded DNA-binding proteins (SSBs) are ubiquitous factors of genome metabolism, recently recognized for their ability to undergo liquid-liquid phase separation (LLPS). While Escherichia coli SSB (EcSSB) has emerged as a model for bacterial LLPS in vitro, its phase behavior and functional dynamics in vivo have remained largely unexplored. Here, we define the subcellular organization of EcSSB under diverse physiological and stress conditions using super-resolution microscopy coupled with newly developed image analysis tools. We show that EcSSB forms dynamic intracellular assemblies during exponential growth, which partially dissolve in response to DNA damage, oxidative stress, antibiotic exposure, and metabolic adaptation. In contrast, these dynamic reorganizations are attenuated in stationary phase cells. Moreover, we show that EcSSB foci exhibit limited overlap with nucleoid regions under stress-free conditions, whereas stress induction is accompanied by increased DNA association. These in vivo observations are consistent with stress- and growth-phase dependent modulation of EcSSB organization and together with biophysical characterization of EcSSB condensation in vitro suggest a role for LLPS-based dynamic storage and mobilization in response to physiological demands. Our work provides a quantitative framework for analyzing the cellular organization of bacterial proteins and the spatial regulation of genome maintenance factors in changing environments. This knowledge may also support future strategies targeting SSB organization pathways for antimicrobial development.

biochemistry↗

CRISPRi screens identify the lncRNA, LOUP, as a multifunctional locus regulating macrophage differentiation epigenetically and inflammatory signaling through a short, encoded peptide

Long non-coding RNAs (lncRNAs) account for the largest portion of RNA from the transcriptome, yet most of their functions remain unknown. Here we performed two independent high-throughput CRISPRi screens to understand the role of lncRNAs in monocyte function and differentiation. The first was a reporter-based screen to identify lncRNAs that regulate TLR4-NFkB signaling in human monocytes and the second screen identified lncRNAs involved in monocyte to macrophage differentiation. We successfully identified numerous novel non-coding and protein-coding genes that can positively or negatively regulate inflammation and differentiation. To understand the functional roles of lncRNAs in both processes, we chose to further study the lncRNA LOUP (lncRNA originating from upstream regulatory element of SPI1 [also known as PU.1]), as it emerged as a top hit in both screens. Not only does LOUP regulate its neighboring gene, the myeloid fate determining factor SPI1, thereby affecting monocyte to macrophage differentiation, but knockdown of LOUP leads to a broad upregulation of NFkB-targeted genes at baseline and upon TLR4-NFkB activation. LOUP also harbors three small open reading frames (sORFs) capable of being translated and are responsible for LOUPs ability to negatively regulate TLR4/NFkB signaling. This work emphasizes the value of high-throughput screening to rapidly identify functional lncRNAs in the innate immune system.

immunology↗

LincRNA-Cox2 functions to regulate inflammation in alveolar macrophages during acute lung injury.

The respiratory system exists at the interface between our body and the surrounding non-sterile environment; therefore, it is critical for a state of homeostasis to be maintained through a balance of pro- and anti- inflammatory cues. An appropriate inflammatory response is vital for combating pathogens, while an excessive or uncontrolled inflammatory response can lead to the development of chronic diseases. Recent studies show that actively transcribed noncoding regions of the genome are emerging as key regulators of biological processes, including inflammation. LincRNA-Cox2 is one such example of an inflammatory inducible long noncoding RNA functioning to control immune response genes. Here using bulk and single cell RNA-seq, in addition to florescence activated cell sorting, we show that lincRNA-Cox2 is most highly expressed in the lung, particularly in alveolar macrophages where it functions to control immune gene expression following acute lung injury. Utilizing a newly generated lincRNA-Cox2 transgenic overexpressing mouse, we show that it can function in trans to control genes including Ccl3, 4 and 5. This work greatly expands our understanding of the role for lincRNA-Cox2 in host defense and sets in place a new layer of regulation in RNA-immune-regulation of genes within the lung.

immunology↗

Epigenomic reprogramming of repetitive noncoding RNAs and IFN-stimulated genes by mutant KRAS

RAS genes are the most frequently mutated oncogenes in cancer. However, the effects of oncogenic RAS signaling on the noncoding transcriptome are unclear. We analyzed the transcriptomes of human airway epithelial cells transformed with mutant KRAS to define the landscape of KRAS-regulated noncoding RNAs. We found that oncogenic KRAS upregulates noncoding transcripts throughout the genome, many of which arise from transposable elements. These repetitive noncoding RNAs exhibit differential RNA editing in single cells, are released in extracellular vesicles, and are known targets of KRAB zinc-finger proteins, which are broadly down-regulated in mutant KRAS cells and lung adenocarcinomas. Moreover, mutant KRAS induces IFN-stimulated genes through both epigenetic and RNA-based mechanisms. Our results reveal that mutant KRAS remodels the noncoding transcriptome through epigenomic reprogramming, expanding the scope of genomic elements regulated by this fundamental signaling pathway and revealing how mutant KRAS induces an intrinsic IFN-stimulated gene signature often seen in ADAR-dependent cancers.

genomics↗