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  1. Artikel ; Online: Protocol to study the inheritance and propagation of non-genetically encoded states using barcode decay lineage tracing.

    Shlyakhtina, Yelyzaveta / Bloechl, Bianca / Moran, Katherine L / Portal, Maximiliano M

    STAR protocols

    2024  Band 5, Heft 1, Seite(n) 102809

    Abstract: Here, we present a protocol to perform barcode decay lineage tracing followed by single-cell transcriptome analysis (BdLT-Seq). We describe steps for BdLT-Seq experimental design, building barcoded episome reporters, performing episome transfection, and ... ...

    Abstract Here, we present a protocol to perform barcode decay lineage tracing followed by single-cell transcriptome analysis (BdLT-Seq). We describe steps for BdLT-Seq experimental design, building barcoded episome reporters, performing episome transfection, and barcode retrieval. We then describe procedures for sequencing library construction while providing options for sample multiplexing and data analysis. This BdLT-Seq technique enables the assessment of clonal evolution in a directional manner while preserving isogeneity, thus allowing the comparison of non-genetic molecular features between isogenic cell lineages. For complete details on the use and execution of this protocol, please refer to Shlyakhtina et al. (2023).
    Mesh-Begriff(e) Inheritance Patterns ; Cell Lineage/genetics ; Clonal Evolution ; Cloning, Molecular ; Data Analysis
    Sprache Englisch
    Erscheinungsdatum 2024-01-04
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2023.102809
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: BdLT-Seq as a barcode decay-based method to unravel lineage-linked transcriptome plasticity.

    Shlyakhtina, Yelyzaveta / Bloechl, Bianca / Portal, Maximiliano M

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 1085

    Abstract: Cell plasticity is a core biological process underlying a myriad of molecular and cellular events taking place throughout organismal development and evolution. It has been postulated that cellular systems thrive to balance the organization of meta-stable ...

    Abstract Cell plasticity is a core biological process underlying a myriad of molecular and cellular events taking place throughout organismal development and evolution. It has been postulated that cellular systems thrive to balance the organization of meta-stable states underlying this phenomenon, thereby maintaining a degree of populational homeostasis compatible with an ever-changing environment and, thus, life. Notably, albeit circumstantial evidence has been gathered in favour of the latter conceptual framework, a direct observation of meta-state dynamics and the biological consequences of such a process in generating non-genetic clonal diversity and divergent phenotypic output remains largely unexplored. To fill this void, here we develop a lineage-tracing technology termed Barcode decay Lineage Tracing-Seq. BdLT-Seq is based on episome-encoded molecular identifiers that, supported by the dynamic decay of the tracing information upon cell division, ascribe directionality to a cell lineage tree whilst directly coupling non-genetic molecular features to phenotypes in comparable genomic landscapes. We show that cell transcriptome states are both inherited, and dynamically reshaped following constrained rules encoded within the cell lineage in basal growth conditions, upon oncogene activation and throughout the process of reversible resistance to therapeutic cues thus adjusting phenotypic output leading to intra-clonal non-genetic diversity.
    Mesh-Begriff(e) Transcriptome ; Cell Lineage/genetics ; Genome ; Phenotype
    Sprache Englisch
    Erscheinungsdatum 2023-02-25
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36744-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Genetic and Non-Genetic Mechanisms Underlying Cancer Evolution.

    Shlyakhtina, Yelyzaveta / Moran, Katherine L / Portal, Maximiliano M

    Cancers

    2021  Band 13, Heft 6

    Abstract: Cancer development can be defined as a process of cellular and tissular microevolution ultimately leading to malignancy. Strikingly, though this concept has prevailed in the field for more than a century, the precise mechanisms underlying evolutionary ... ...

    Abstract Cancer development can be defined as a process of cellular and tissular microevolution ultimately leading to malignancy. Strikingly, though this concept has prevailed in the field for more than a century, the precise mechanisms underlying evolutionary processes occurring within tumours remain largely uncharacterized and rather cryptic. Nevertheless, although our current knowledge is fragmentary, data collected to date suggest that most tumours display features compatible with a diverse array of evolutionary paths, suggesting that most of the existing macro-evolutionary models find their avatar in cancer biology. Herein, we discuss an up-to-date view of the fundamental genetic and non-genetic mechanisms underlying tumour evolution with the aim of concurring into an integrated view of the evolutionary forces at play throughout the emergence and progression of the disease and into the acquisition of resistance to diverse therapeutic paradigms. Our ultimate goal is to delve into the intricacies of genetic and non-genetic networks underlying tumour evolution to build a framework where both core concepts are considered non-negligible and equally fundamental.
    Sprache Englisch
    Erscheinungsdatum 2021-03-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13061380
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: The role of non-genetic information in evolutionary frameworks.

    Moran, Katherine L / Shlyakhtina, Yelyzaveta / Portal, Maximiliano M

    Critical reviews in biochemistry and molecular biology

    2021  Band 56, Heft 3, Seite(n) 255–283

    Abstract: The evolution of organisms has been a subject of paramount debate for hundreds of years and though major advances in the field have been made, the precise mechanisms underlying evolutionary processes remain fragmentary. Strikingly, the majority of the ... ...

    Abstract The evolution of organisms has been a subject of paramount debate for hundreds of years and though major advances in the field have been made, the precise mechanisms underlying evolutionary processes remain fragmentary. Strikingly, the majority of the core principles accepted across the many fields of biology only consider genetic information as the major - if not exclusive - biological information carrier and thus consider it as the main evolutionary avatar. However, the real picture appears far more complex than originally anticipated, as compelling data suggest that nongenetic information steps up when highly dynamic evolutionary frameworks are explored. In light of recent evidence, we discuss herein the dynamic nature and complexity of nongenetic information carriers, and their emerging relevance in the evolutionary process. We argue that it is possible to overcome the historical arguments which dismissed these carriers, and instead consider that they are indeed core to life itself as they support a sustainable, continuous source of rapid adaptation in ever-changing environments. Ultimately, we will address the intricacies of genetic and non-genetic networks underlying evolutionary models to build a framework where both core biological information concepts are considered non-negligible and equally fundamental.
    Mesh-Begriff(e) Biological Evolution ; Models, Biological
    Sprache Englisch
    Erscheinungsdatum 2021-05-10
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review ; Video-Audio Media
    ZDB-ID 1000977-2
    ISSN 1549-7798 ; 1381-3455 ; 1040-9238
    ISSN (online) 1549-7798
    ISSN 1381-3455 ; 1040-9238
    DOI 10.1080/10409238.2021.1908949
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Asymmetric Inheritance of Cell Fate Determinants: Focus on RNA.

    Shlyakhtina, Yelyzaveta / Moran, Katherine L / Portal, Maximiliano M

    Non-coding RNA

    2019  Band 5, Heft 2

    Abstract: During the last decade, and mainly primed by major developments in high-throughput sequencing technologies, the catalogue of RNA molecules harbouring regulatory functions has increased at a steady pace. Current evidence indicates that hundreds of ... ...

    Abstract During the last decade, and mainly primed by major developments in high-throughput sequencing technologies, the catalogue of RNA molecules harbouring regulatory functions has increased at a steady pace. Current evidence indicates that hundreds of mammalian RNAs have regulatory roles at several levels, including transcription, translation/post-translation, chromatin structure, and nuclear architecture, thus suggesting that RNA molecules are indeed mighty controllers in the flow of biological information. Therefore, it is logical to suggest that there must exist a series of molecular systems that safeguard the faithful inheritance of RNA content throughout cell division and that those mechanisms must be tightly controlled to ensure the successful segregation of key molecules to the progeny. Interestingly, whilst a handful of integral components of mammalian cells seem to follow a general pattern of asymmetric inheritance throughout division, the fate of RNA molecules largely remains a mystery. Herein, we will discuss current concepts of asymmetric inheritance in a wide range of systems, including prions, proteins, and finally RNA molecules, to assess overall the biological impact of RNA inheritance in cellular plasticity and evolutionary fitness.
    Sprache Englisch
    Erscheinungsdatum 2019-05-09
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2813993-8
    ISSN 2311-553X ; 2311-553X
    ISSN (online) 2311-553X
    ISSN 2311-553X
    DOI 10.3390/ncrna5020038
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Dual role of DR5 in death and survival signaling leads to TRAIL resistance in cancer cells.

    Shlyakhtina, Yelyzaveta / Pavet, Valeria / Gronemeyer, Hinrich

    Cell death & disease

    2017  Band 8, Heft 8, Seite(n) e3025

    Abstract: Besides its tumor-selective apoptotic activity, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes pro-survival, proliferative or migratory signaling (NF-κB, PI3K/Akt, MAPK and JNK; referred to as 'non-apoptotic' cascades). Indeed, ... ...

    Abstract Besides its tumor-selective apoptotic activity, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes pro-survival, proliferative or migratory signaling (NF-κB, PI3K/Akt, MAPK and JNK; referred to as 'non-apoptotic' cascades). Indeed, apoptosis and non-apoptotic signaling can be activated in clonal populations of cancer cells in response to treatment and, as a result, only a part of the initial cellular population dies while a fraction survives and develops resistance to TRAIL-induced apoptosis (referred to as 'fractional survival'). Notably, the molecular characterization of the protein platforms streaming into tumoricidal versus tumor-promoting cascades that control fractional survival remained elusive. Here we demonstrate that, in the context of DR4-DR5-DcR2 hetero-oligomeric complexes, a single death receptor (DR5) suffices to assemble composite plasma membrane-proximal pro-apoptotic/pro-survival platforms that propagate TRAIL signaling to both death and survival pathways in clonal populations of cancer cells. Moreover, we show that while all members of TRAIL-induced complexes support survival, none of them acted exclusively pro-apoptotic. Indeed, key apoptotic proteins as FADD and procaspase-8 were also involved in transducing non-apoptotic signaling in response to this cytokine. Collectively, this study reveals the Janus faces of DR5, and the contributions of other death complex components in fractional survival that foster the generation of resistance. Our data highlight a new level of complexity in TRAIL signaling and point to an improved therapeutic rationale in view of hitherto disappointing results.
    Mesh-Begriff(e) Apoptosis/drug effects ; Apoptosis/genetics ; Caspase 8/genetics ; Caspase 8/metabolism ; Cell Line, Transformed ; Cell Survival/drug effects ; Clone Cells ; Drug Resistance, Neoplasm/genetics ; Fas-Associated Death Domain Protein/genetics ; Fas-Associated Death Domain Protein/metabolism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Mitogen-Activated Protein Kinases/genetics ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand/genetics ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Tumor Necrosis Factor Decoy Receptors/genetics ; Tumor Necrosis Factor Decoy Receptors/metabolism
    Chemische Substanzen FADD protein, human ; Fas-Associated Death Domain Protein ; NF-kappa B ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Recombinant Proteins ; TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10A protein, human ; TNFRSF10B protein, human ; TNFRSF10D protein, human ; TNFSF10 protein, human ; Tumor Necrosis Factor Decoy Receptors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Caspase 8 (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2017-08-31
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/cddis.2017.423
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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