TY - JOUR AB - Environment-epigenome interactions are emerging as contributors to disease risk and health outcomes. In fact, organisms outside of the laboratory are constantly exposed to environmental changes that can influence chromatin regulation at multiple levels, potentially impacting on genome function. In this review, we will summarize recent findings on how major external cues impact on 3D chromatin organization in different experimental systems. We will describe environment-induced 3D genome alterations ranging from chromatin accessibility to the spatial distribution of the genome and discuss their role in regulating gene expression. AU - Pudelko, L AU - Cabianca, D.S. C1 - 70108 C2 - 55427 CY - 84 Theobalds Rd, London Wc1x 8rr, England TI - The influencers' era: How the environment shapes chromatin in 3D. JO - Curr. Opin. Genet. Dev. VL - 85 PB - Current Biology Ltd PY - 2024 SN - 0959-437X ER - TY - JOUR AB - In mammals, cells acquire totipotency at fertilization. Embryonic genome activation (EGA), which occurs at the 2-cell stage in the mouse and 4- to 8-cell stage in humans, occurs during the time window at which embryonic cells are totipotent and thus it is thought that EGA is mechanistically linked to the foundations of totipotency. The molecular mechanisms that lead to the establishment of totipotency and EGA had been elusive for a long time, however, recent advances have been achieved with the establishment of new cell lines with greater developmental potential and the application of novel low-input high-throughput techniques in embryos. These have unveiled several principles of totipotency related to its epigenetic makeup but also to characteristic features of totipotent cells. In this review, we summarize and discuss current views exploring some of the key drivers of totipotency from both in vitro cell culture models and embryogenesis in vivo. AU - Nakatani, T. AU - Torres-Padilla, M.E. C1 - 68137 C2 - 54615 CY - 84 Theobalds Rd, London Wc1x 8rr, England TI - Regulation of mammalian totipotency: A molecular perspective from in vivo and in vitro studies. JO - Curr. Opin. Genet. Dev. VL - 81 PB - Current Biology Ltd PY - 2023 SN - 0959-437X ER - TY - JOUR AB - A central question of biology is the basis of stable cell fates. Cell fates are formed during development, where the zygote progresses from totipotency to terminal differentiation. Each step of lineage commitment involves establishment of stable states encoding-specific developmental commitments that can be faithfully transmitted to daughter cells — a ‘memory’ of cell fate is acquired. However, this cell-fate memory is reversible and can be changed when experimental reprogramming procedures such as nuclear transfer to eggs or transcription factor overexpression are used. The ability to reprogram cell fates impacts regenerative medicine, as progress in understanding underlying molecular mechanisms of cell-fate changes can allow the generation of any cell type needed for cell replacement therapies. Given its potential, studies are currently aiming at improving the low efficiency of cell-fate conversion. In recent years, epigenetic mechanisms suggested to promote stable cell-fate memory emerged as factors that cause resistance to cell-fate conversions during nuclear reprogramming. In this review, we highlight the latest work that has characterised epigenetic barriers to reprogramming which, during normal development, help to maintain the stable differentiation status of cells. AU - Hörmanseder, E. C1 - 62169 C2 - 50674 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - 24-31 TI - Epigenetic memory in reprogramming. JO - Curr. Opin. Genet. Dev. VL - 70 PB - Current Biology Ltd PY - 2021 SN - 0959-437X ER - TY - JOUR AB - The skin is home to a collection of fibroblastic cell types from varying embryonic origins. These varying fibroblastic lineages display unique genetic programs and in vivo functions. Studying the diversity of fibroblastic cells is emerging as an important area for cutaneous biology, wound repair and regenerative medicine. In this mini-review we discuss the distinct embryonic origins, microenvironments, and transcriptomic profiles of fibroblastic lineages, and how these varying lineages shape the skin's wound response across injury depths, anatomic locations, and developmental time to promote either scarring or regeneration. We outline how the development of single cell sequencing has led to our improved understanding of fibroblastic lineages at the molecular level and discuss existing challenges and future outlook on developing regenerative therapies that are based on this emerging field of eclectic fibroblasts. AU - Jiang, D. AU - Rinkevich, Y. C1 - 62082 C2 - 50637 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - 7-14 TI - Distinct fibroblasts in scars and regeneration. JO - Curr. Opin. Genet. Dev. VL - 70 PB - Current Biology Ltd PY - 2021 SN - 0959-437X ER - TY - JOUR AU - Stricker, S.H. AU - Berninger, B.* AU - Götz, M. C1 - 62867 C2 - 50991 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - III-V TI - Editorial overview: Fluidity of cell fates - from reprogramming to repair. JO - Curr. Opin. Genet. Dev. VL - 70 PB - Current Biology Ltd PY - 2021 SN - 0959-437X ER - TY - JOUR AB - Multicellular organisms develop from a single cell, the zygote. This feature is referred to as totipotency. In the mouse, only the zygote and the 2-cell stage embryo display this attribute. Cells resembling the embryonic 2-cell stage blastomeres were identified in embryonic stem (ES) cell cultures as ‘2-cell-like cells’ (2CLCs). This discovery brought the first cellular model with the possibility to investigate some features of the totipotent embryo and the molecular mechanisms regulating totipotency in vitro. In this article, we discuss the latest advancements on the research on 2CLCs, which have uncovered an intricate reprogramming process regulated by proteins as well as metabolites and ncRNAs. These recent findings have shed light on the combinatorial regulation of 2-cell-like cell emergence and the nature of their unique attributes. AU - Iturbide Martinez De Albeniz, A. AU - Torres-Padilla, M.E. C1 - 59537 C2 - 48872 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - 26-30 TI - A cell in hand is worth two in the embryo: Recent advances in 2-cell like cell reprogramming. JO - Curr. Opin. Genet. Dev. VL - 64 PB - Current Biology Ltd PY - 2020 SN - 0959-437X ER - TY - JOUR AB - Over the last decade, our understanding of how the genome is packaged in three dimension within the nucleus has grown considerably. This is largely due to advances in high-throughput genomics assays to study higher order chromatin organization. Our knowledge of the structures adopted by the chromatin has far preceded our understanding of function and mechanism. An outstanding question has been how are such structures established. Recently, a suite of genomics assays has been adapted for low-input material, making it possible to apply them to the pre-implantation mammalian embryo. For the first time, chromatin topology and associations with the nuclear lamina have been described in the earliest stages of murine development. These studies have revealed the dynamics with which higher-order chromatin architecture is established in vivo. Additionally, they have yielded some intriguing findings that will pave the way for futures studies into the mechanisms underlying the establishment of three dimensional genome organization. Here, we discuss findings on how embryonic chromatin is dynamically organized within the nucleus throughout preimplantation development, and the outline a number of outstanding questions that will be exciting to address in the future. AU - Jansz, N. AU - Torres-Padilla, M.E. C1 - 56153 C2 - 46857 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - 52-58 TI - Genome activation and architecture in the early mammalian embryo. JO - Curr. Opin. Genet. Dev. VL - 55 PB - Current Biology Ltd PY - 2019 SN - 0959-437X ER - TY - JOUR AB - Cell replacement therapies aim at reestablishment of neuronal circuits after brain injury, stroke or neurodegeneration. Recently, direct reprogramming of resident glial cells into the affected neuronal subtypes has become a feasible and promising option for central nervous system regeneration. Direct reprogramming relies on the implementation of a new transcriptional program defining the desired neuronal identity in fully differentiated glial cells implying the more or less complete down-regulation of the program for the former identity of the glial cell. Despite the enormous progress achieved in this regard with highly efficient in vivo reprogramming after injury, a number of hurdles still need to be resolved. One way to further improve direct neuronal reprogramming is to understand the molecular hurdles which we discuss with the focus on chromatin states of the starting versus the reprogrammed cells. AU - Ninkovic, J. AU - Götz, M. C1 - 53663 C2 - 44936 CY - 84 Theobalds Rd, London Wc1x 8rr, England SP - 65-69 TI - Understanding direct neuronal reprogramming - from pioneer factors to 3D chromatin. JO - Curr. Opin. Genet. Dev. VL - 52 PB - Current Biology Ltd PY - 2018 SN - 0959-437X ER - TY - JOUR AU - Wienberg, J. C1 - 2919 C2 - 22136 SP - 657-666 TI - The evolution of eutherian chromosomes. JO - Curr. Opin. Genet. Dev. VL - 14 PY - 2004 SN - 0959-437X ER -