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  • 1. Almuzzaini, Bader
    et al.
    Sarshad, Aishe A.
    Rahmanto, Aldwin S.
    Hansson, Magnus L.
    Von Euler, Anne
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Sangfelt, Olle
    Visa, Neus
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Östlund Farrants, Ann-Kristin
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    In beta-actin knockouts, epigenetic reprogramming and rDNA transcription inactivation lead to growth and proliferation defects2016In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, no 8, p. 2860-2873Article in journal (Refereed)
    Abstract [en]

    Actin and nuclear myosin 1 (NM1) are regulators of transcription and chromatin organization. Using a genome-wide approach, we report here that beta-actin binds intergenic and genic regions across the mammalian genome, associated with both protein-coding and rRNA genes. Within the rDNA, the distribution of beta-actin correlated with NM1 and the other subunits of the B-WICH complex, WSTF and SNF2h. In beta-actin(-/-) mouse embryonic fibroblasts (MEFs), we found that rRNA synthesis levels decreased concomitantly with drops in RNA polymerase I (Pol I) and NM1 occupancies across the rRNA gene. Reintroduction of wild-type beta-actin, in contrast to mutated forms with polymerization defects, efficiently rescued rRNA synthesis underscoring the direct role for a polymerization-competent form of beta-actin in Pol I transcription. The rRNA synthesis defects in the beta-actin(-/-) MEFs are a consequence of epigenetic reprogramming with up-regulation of the repressive mark H3K4me1 (mono-methylation of lys4 on histone H3) and enhanced chromatin compaction at promoter-proximal enhancer (T0 sequence), which disturb binding of the transcription factor TTF1. We propose a novel genome-wide mechanism where the polymerase-associated beta-actin synergizes with NM1 to coordinate permissive chromatin with Pol I transcription, cell growth, and proliferation.

  • 2. Al-Sayegh, M. A.
    et al.
    Mahmood, S. R.
    Abul Khair, S. B.
    Xie, X.
    El Gindi, M.
    Kim, T.
    Almansoori, A.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    β-actin contributes to open chromatin for activation of the adipogenic pioneer factor CEBPA during transcriptional reprograming2020In: Molecular Biology of the Cell, ISSN 1059-1524, E-ISSN 1939-4586, Vol. 31, no 23, p. 2511-2521Article in journal (Refereed)
    Abstract [en]

    Adipogenesis is regulated by a cascade of signals that drive transcriptional reprogramming in adipocytes. Here, we report that nuclear actin regulates the chromatin states that establish tissue- specific expression during adipogenesis. To study the role of beta-actin in adipocyte differentiation, we conducted RNA sequencing on wild-type and beta-actin knockout mouse embryonic fibroblasts (MEFs) after reprograming to adipocytes. We found that beta-actin depletion affects induction of several adipogenic genes during transcriptional reprograming. This impaired regulation of adipogenic genes is linked to reduced expression of the pioneer factor Cebpa and is rescued by reintroducing NLS-tagged beta-actin. ATAC-Seq in knockout MEFs revealed that actin-dependent reduction of Cebpa expression correlates with decreased chromatin accessibility and loss of chromatin association of the ATPase Brg1. This, in turn, impairs CEBPB's association with its Cebpa promoter-proximal binding site during adipogenesis. We propose a role for the nuclear beta-actin pool in maintaining open chromatin for transcriptional reprogramming during adipogenic differentiation.

  • 3. Assadi, Ghazaleh
    et al.
    Vesterlund, Liselotte
    Bonfiglio, Ferdinando
    Mazzurana, Luca
    Cordeddu, Lina
    Schepis, Danika
    Mjösberg, Jenny
    Ruhrmann, Sabrina
    Fabbri, Alessia
    Vukojevic, Vladana
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, United Arab Emirates.
    Salomons, Florian A.
    Laurencikiene, Jurga
    Törkvist, Leif
    Halfvarson, Jonas
    D'Amato, Mauro
    Functional Analyses of the Crohn's Disease Risk Gene LACC12016In: PLOS ONE, E-ISSN 1932-6203, Vol. 11, no 12, article id e0168276Article in journal (Refereed)
    Abstract [en]

    Background Genetic variation in the Laccase (multicopper oxidoreductase) domain-containing 1 (LACC1) gene has been shown to affect the risk of Crohn's disease, leprosy and, more recently, ulcerative colitis and juvenile idiopathic arthritis. LACC1 function appears to promote fatty-acid oxidation, with concomitant inflammasome activation, reactive oxygen species production, and anti-bacterial responses in macrophages. We sought to contribute to elucidating LACC1 biological function by extensive characterization of its expression in human tissues and cells, and through preliminary analyses of the regulatory mechanisms driving such expression. Methods We implemented Western blot, quantitative real-time PCR, immunofluorescence microscopy, and flow cytometry analyses to investigate fatty acid metabolism-immune nexus (FAMIN; the LACC1 encoded protein) expression in subcellular compartments, cell lines and relevant human tissues. Gene-set enrichment analyses were performed to initially investigate modulatory mechanisms of LACC1 expression. A small-interference RNA knockdown in vitro model system was used to study the effect of FAMIN depletion on peroxisome function. Results FAMIN expression was detected in macrophage-differentiated THP-1 cells and several human tissues, being highest in neutrophils, monocytes/macrophages, myeloid and plasmacytoid dendritic cells among peripheral blood cells. Subcellular co-localization was exclusively confined to peroxisomes, with some additional positivity for organelle endomembrane structures. LACC1 co-expression signatures were enriched for genes involved in peroxisome proliferator-activated receptors (PPAR) signaling pathways, and PPAR ligands downregulated FAMIN expression in in vitro model systems. Conclusion FAMIN is a peroxisome-associated protein with primary role(s) in macrophages and other immune cells, where its metabolic functions may be modulated by PPAR signaling events. However, the precise molecular mechanisms through which FAMIN exerts its biological effects in immune cells remain to be elucidated.

  • 4. Bajusz, Csaba
    et al.
    Kristó, Ildikó
    Abonyi, Csilla
    Venit, Tomáš
    Vedelek, Viktor
    Lukácsovich, Tamás
    Farkas, Attila
    Borkuti, Peter
    Kovács, Zoltán
    Bajusz, Izabella
    Marton, Annamária
    Vizler, Csaba
    Lipinszki, Zoltán
    Sinka, Rita
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, UAE.
    Vilmos, Peter
    The nuclear activity of the actin-binding Moesin protein is necessary for gene expression in Drosophila2021In: The FEBS Journal, ISSN 1742-464X, E-ISSN 1742-4658, Vol. 288, no 16, p. 4812-4832Article in journal (Refereed)
    Abstract [en]

    Ezrin-Radixin-Moesin (ERM) proteins play an essential role in the cytoplasm by cross-linking actin filaments with plasma membrane proteins. Research has identified the nuclear localization of ERMs, as well as the involvement of a single Drosophila ERM protein, Moesin, in nuclear mRNA exports. However, the question of how important the nuclear activity of ERM proteins are for the life of an organism has so far not been explored. Here, we present the first attempt to reveal the in vivo relevance of nuclear localization of Moesin in Drosophila. With the help of a nuclear export signal, we decreased the amount of Moesin in the nuclei of the animals. Furthermore, we observed various developmental defects, demonstrating the importance of ERM function in the nucleus for the first time. Transcriptome analysis of the mutant flies revealed that the lack of nuclear Moesin function leads to expression changes in nearly 700 genes, among them heat-shock genes. This result together with additional findings revealed that in Drosophila the expression of protein chaperones requires the nuclear functions of Moesin.

  • 5. Fukuda, Nanaho
    et al.
    Fukuda, Tomoyuki
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, UAE.
    Oda, Kanako
    Takei, Nobuyuki
    Czaplinski, Kevin
    Touhara, Kazushige
    Yoshihara, Yoshihiro
    Sasaoka, Toshikuni
    Axonal mRNA binding of hnRNP A/B is crucial for axon targeting and maturation of olfactory sensory neurons2023In: Cell Reports, E-ISSN 2211-1247, Vol. 42, no 5, article id 112398Article in journal (Refereed)
    Abstract [en]

    Spatiotemporal control of gene expression is important for neural development and function. Here, we show that heterogeneous nuclear ribonucleoprotein (hnRNP) A/B is highly expressed in developing olfactory sensory neurons (OSNs), and its knockout results in reduction in mature OSNs and aberrant targeting of OSN axons to the olfactory bulb. RNA immunoprecipitation analysis reveals that hnRNP A/B binds to a group of mRNAs that are highly related to axon projections and synapse assembly. Approximately 11% of the identified hnRNP A/B targets, including Pcdha and Ncam2, encode cell adhesion molecules. In Hnrnpab knockout mice, PCDHA and NCAM2 levels are significantly reduced at the axon terminals of OSNs. Furthermore, deletion of the hnRNP A/B-recognition motif in the 3′ UTR of Pcdha leads to impaired PCDHA expression at the OSN axon terminals. Therefore, we propose that hnRNP A/B facilitates OSN maturation and axon projection by regulating the local expression of its target genes at axon terminals.

  • 6. Gallardo-Dodd, Carlos J.
    et al.
    Oertlin, Christian
    Record, Julien
    Galvani, Romulo G.
    Sommerauer, Christian
    Kuznetsov, Nikolai V.
    Doukoumopoulos, Evangelos
    Ali, Liaqat
    Oliveira, Mariana M. S.
    Seitz, Christina
    Percipalle, Mathias
    Nikic, Tijana
    Sadova, Anastasia A.
    Shulgina, Sofia M.
    Shmarov, Vjacheslav A.
    Kutko, Olga V.
    Vlasova, Daria D.
    Orlova, Kseniya D.
    Rykova, Marina P.
    Andersson, John
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Center for Genomics and Systems Biology, NYUAD, Abu Dhabi, United Arab Emirates.
    Kutter, Claudia
    Ponomarev, Sergey A.
    Westerberg, Lisa S.
    Exposure of volunteers to microgravity by dry immersion bed over 21 days results in gene expression changes and adaptation of T cells2023In: Science Advances, E-ISSN 2375-2548, Vol. 9, no 34, article id eadg1610Article in journal (Refereed)
    Abstract [en]

    The next steps of deep space exploration are manned missions to Moon and Mars. For safe space missions for crew members, it is important to understand the impact of space flight on the immune system. We studied the effects of 21 days dry immersion (DI) exposure on the transcriptomes of T cells isolated from blood samples of eight healthy volunteers. Samples were collected 7 days before DI, at day 7, 14, and 21 during DI, and 7 days after DI. RNA sequencing of CD3(+) T cells revealed transcriptional alterations across all time points, with most changes occurring 14 days after DI exposure. At day 21, T cells showed evidence of adaptation with a transcriptional profile resembling that of 7 days before DI. At 7 days after DI, T cells again changed their transcriptional profile. These data suggest that T cells adapt by rewiring their transcriptomes in response to simulated weightlessness and that remodeling cues persist when reexposed to normal gravity.

  • 7. Gjorgjieva, Tamara
    et al.
    Xie, Xin
    Commins, Patrick
    Pasricha, Renu
    Mahmood, Syed Raza
    Gunsalus, Kristin C.
    Naumov, Pance
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Loss of beta-Actin Leads to Accelerated Mineralization and Dysregulation of Osteoblast-Differentiation Genes during Osteogenic Reprogramming2020In: Advanced Science, E-ISSN 2198-3844, Vol. 7, no 23, article id 2002261Article in journal (Refereed)
    Abstract [en]

    Actin plays fundamental roles in both the cytoplasm and the cell nucleus. In the nucleus, beta-actin regulates neuronal reprogramming by consolidating a heterochromatin landscape required for transcription of neuronal gene programs, yet it remains unknown whether it has a role in other differentiation models. To explore the potential roles of beta-actin in osteogenesis, beta-actin wild-type (WT) and beta-actin knockout (KO) mouse embryonic fibroblasts (MEFs) are reprogrammed to osteoblast-like cells using small molecules in vitro. It is discovered that loss of beta-actin leads to an accelerated mineralization phenotype (hypermineralization), accompanied with enhanced formation of extracellular hydroxyapatite microcrystals, which originate in the mitochondria in the form of microgranules. This phenotype is a consequence of rapid upregulation of mitochondrial genes including those involved in oxidative phosphorylation (OXPHOS) in reprogrammed KO cells. It is further found that osteogenic gene programs are differentially regulated between WT and KO cells, with clusters of genes exhibiting different temporal expression patterns. A novel function for beta-actin in osteogenic reprogramming through a mitochondria-based mechanism that controls cell-mediated mineralization is proposed.

  • 8. Hari-Gupta, Yukti
    et al.
    Fili, Natalia
    dos Santos, Ália
    Cook, Alexander W.
    Gough, Rosemarie E.
    Reed, Hannah C. W.
    Wang, Lin
    Aaron, Jesse
    Venit, Tomas
    Wait, Eric
    Grosse-Berkenbusch, Andreas
    Gebhardt, J. Christof M.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Chew, Teng-Leong
    Martin-Fernandez, Marisa
    Toseland, Christopher P.
    Myosin VI regulates the spatial organisation of mammalian transcription initiation2022In: Nature Communications, E-ISSN 2041-1723, Vol. 13, article id 1346Article in journal (Refereed)
    Abstract [en]

    During transcription, RNA Polymerase II (RNAPII) is spatially organised within the nucleus into clusters that correlate with transcription activity. While this is a hallmark of genome regulation in mammalian cells, the mechanisms concerning the assembly, organisation and stability remain unknown. Here, we have used combination of single molecule imaging and genomic approaches to explore the role of nuclear myosin VI (MVI) in the nanoscale organisation of RNAPII. We reveal that MVI in the nucleus acts as the molecular anchor that holds RNAPII in high density clusters. Perturbation of MVI leads to the disruption of RNAPII localisation, chromatin organisation and subsequently a decrease in gene expression. Overall, we uncover the fundamental role of MVI in the spatial regulation of gene expression.

  • 9. Hunashal, Yamanappa
    et al.
    Percipalle, Mathias
    Molnár, Tamás
    Kardos, Jòzsef
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, United Arab Emirates.
    Esposito, Gennaro
    Approaching Protein Aggregation and Structural Dynamics by Equilibrium and Nonequilibrium Paramagnetic Perturbation2022In: Analytical Chemistry, ISSN 0003-2700, E-ISSN 1520-6882, Vol. 94, no 31, p. 10949-10958Article in journal (Refereed)
    Abstract [en]

    PENELOP (Paramagnetic Equilibrium vs Nonequilibrium magnetization Enhancement or LOss Perturbation) is the presented nuclear magnetic resonance (NMR) approach to identify at once the location of proteins' exposed surface, hindered accessibility, and exchange processes occurring on a mu s-ms time scale. In addition to mapping the protein surface accessibility, the application of this method under specific conditions makes it possible to distinguish conformational mobility and chemical exchange processes, thereby providing an alternative to characterization by more demanding techniques (transverse relaxation dispersion, saturation transfer, and high-pressure NMR). Moreover, its high sensitivity enables studying samples at low, physiologically more relevant concentrations. Association, dynamics, and oligomerization are addressed by PENELOP for a component of SARS-CoV-2 replication transcription complex and an amyloidogenic protein.

  • 10. Mahmood, Syed Raza
    et al.
    El Said, Nadine Hosny
    Gunsalus, Kristin C.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    β-actin mediated H3K27ac changes demonstrate the link between compartment switching and enhancer-dependent transcriptional regulation2023In: Genome Biology, ISSN 1465-6906, E-ISSN 1474-760X, Vol. 24, article id 18Article in journal (Refereed)
    Abstract [en]

    Background: Recent work has demonstrated that three-dimensional genome organization is directly affected by changes in the levels of nuclear cytoskeletal proteins such as β-actin. The mechanisms which translate changes in 3D genome structure into changes in transcription, however, are not fully understood. Here, we use a comprehensive genomic analysis of cells lacking nuclear β-actin to investigate the mechanistic links between compartment organization, enhancer activity, and gene expression.

    Results: Using HiC-Seq, ATAC-Seq, and RNA-Seq, we first demonstrate that transcriptional and chromatin accessibility changes observed upon β-actin loss are highly enriched in compartment-switching regions. Accessibility changes within compartment switching genes, however, are mainly observed in non-promoter regions which potentially represent distal regulatory elements. Our results also show that β-actin loss induces widespread accumulation of the enhancer-specific epigenetic mark H3K27ac. Using the ABC model of enhancer annotation, we then establish that these epigenetic changes have a direct impact on enhancer activity and underlie transcriptional changes observed upon compartment switching. A complementary analysis of fibroblasts undergoing reprogramming into pluripotent stem cells further confirms that this relationship between compartment switching and enhancer-dependent transcriptional change is not specific to β-actin knockout cells but represents a general mechanism linking compartment-level genome organization to gene expression.

    Conclusions: We demonstrate that enhancer-dependent transcriptional regulation plays a crucial role in driving gene expression changes observed upon compartment-switching. Our results also reveal a novel function of nuclear β-actin in regulating enhancer function by influencing H3K27 acetylation levels.

  • 11. Mahmood, Syed Raza
    et al.
    Xie, Xin
    El Said, Nadine Hosny
    Venit, Tomas
    Gunsalus, Kristin C.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    β-actin dependent chromatin remodeling mediates compartment level changes in 3D genome architecture2021In: Nature Communications, E-ISSN 2041-1723, Vol. 12, no 1, article id 5240Article in journal (Refereed)
    Abstract [en]

    β-actin is a crucial component of several chromatin remodeling complexes that control chromatin structure and accessibility. The mammalian Brahma-associated factor (BAF) is one such complex that plays essential roles in development and differentiation by regulating the chromatin state of critical genes and opposing the repressive activity of polycomb repressive complexes (PRCs). While previous work has shown that β-actin loss can lead to extensive changes in gene expression and heterochromatin organization, it is not known if changes in β-actin levels can directly influence chromatin remodeling activities of BAF and polycomb proteins. Here we conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) using ATAC-Seq, HiC-seq, RNA-Seq and ChIP-Seq of various epigenetic marks. We demonstrate that β-actin levels can induce changes in chromatin structure by affecting the complex interplay between chromatin remodelers such as BAF/BRG1 and EZH2. Our results show that changes in β-actin levels and associated chromatin remodeling activities can not only impact local chromatin accessibility but also induce reversible changes in 3D genome architecture. Our findings reveal that β-actin-dependent chromatin remodeling plays a role in shaping the chromatin landscape and influences the regulation of genes involved in development and differentiation.

  • 12. Neriec, Nathalie
    et al.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, United Arab Emirates.
    Sorting mRNA Molecules for Cytoplasmic Transport and Localization2018In: Frontiers in Genetics, E-ISSN 1664-8021, Vol. 9, article id 510Article, review/survey (Refereed)
    Abstract [en]

    In eukaryotic cells, gene expression is highly regulated at many layers. Nascent RNA molecules are assembled into ribonucleoprotein complexes that are then released into the nucleoplasmic milieu and transferred to the nuclear pore complex for nuclear export. RNAs are then either translated or transported to the cellular periphery. Emerging evidence indicates that RNA-binding proteins play an essential role throughout RNA biogenesis, from the gene to polyribosomes. However, the sorting mechanisms that regulate whether an RNA molecule is immediately translated or sent to specialized locations for translation are unclear. This question is highly relevant during development and differentiation when cells acquire a specific identity. Here, we focus on the RNA-binding properties of heterogeneous nuclear ribonucleoproteins (hnRNPs) and how these mechanisms are believed to play an essential role in RNA trafficking in polarized cells. Further, by focusing on the specific hnRNP protein CBF-A/hnRNPab and its naturally occurring isoforms, we propose a model on how hnRNP proteins are capable of regulating gene expression both spatially and temporally throughout the RNA biogenesis pathway, impacting both healthy and diseased cells.

  • 13.
    Percipalle, Piergiorgio
    et al.
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi, United Arab Emirates.
    Vartiainen, Maria
    Cytoskeletal proteins in the cell nucleus: a special nuclear actin perspective2019In: Molecular Biology of the Cell, ISSN 1059-1524, E-ISSN 1939-4586, Vol. 30, no 15, p. 1781-1785Article in journal (Refereed)
    Abstract [en]

    The emerging role of cytoskeletal proteins in the cell nucleus has become a new frontier in cell biology. Actin and actin-binding proteins regulate chromatin and gene expression, but importantly they are beginning to be essential players in genome organization. These actin-based functions contribute to genome stability and integrity while affecting DNA replication and global transcription patterns. This is likely to occur through interactions of actin with nuclear components including nuclear lamina and subnuclear organelles. An exciting future challenge is to understand how these actin-based genome-wide mechanisms may regulate development and differentiation by interfering with the mechanical properties of the cell nucleus and how regulated actin polymerization plays a role in maintaining nuclear architecture. With a special focus on actin, here we summarize how cytoskeletal proteins operate in the nucleus and how they may be important to consolidate nuclear architecture for sustained gene expression or silencing.

  • 14. Record, Julien
    et al.
    Saeed, Mezida B.
    Venit, Tomas
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Westerberg, Lisa S.
    Journey to the Center of the Cell: Cytoplasmic and Nuclear Actin in Immune Cell Functions2021In: Frontiers in Cell and Developmental Biology, E-ISSN 2296-634X, Vol. 9, article id 682294Article, review/survey (Refereed)
    Abstract [en]

    Actin cytoskeletal dynamics drive cellular shape changes, linking numerous cell functions to physiological and pathological cues. Mutations in actin regulators that are differentially expressed or enriched in immune cells cause severe human diseases known as primary immunodeficiencies underscoring the importance of efficienct actin remodeling in immune cell homeostasis. Here we discuss recent findings on how immune cells sense the mechanical properties of their environement. Moreover, while the organization and biochemical regulation of cytoplasmic actin have been extensively studied, nuclear actin reorganization is a rapidly emerging field that has only begun to be explored in immune cells. Based on the critical and multifaceted contributions of cytoplasmic actin in immune cell functionality, nuclear actin regulation is anticipated to have a large impact on our understanding of immune cell development and functionality.

  • 15. Venit, Tomas
    et al.
    Dowaidar, Moataz
    Stockholm University, Faculty of Science, Department of Biochemistry and Biophysics.
    Gestin, Maxime
    Stockholm University, Faculty of Science, Department of Biochemistry and Biophysics.
    Raza Mahmood, Syed
    Langel, Ülo
    Stockholm University, Faculty of Science, Department of Biochemistry and Biophysics. University of Tartu, Estonia.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), UAE.
    Transcriptional Profiling Reveals Ribosome Biogenesis, Microtubule Dynamics and Expression of Specific lncRNAs to be Part of a Common Response to Cell-Penetrating Peptides2020In: Biomolecules, E-ISSN 2218-273X, Vol. 10, no 11, article id 1567Article in journal (Refereed)
    Abstract [en]

    Cell-penetrating peptides (CPPs) are short peptides that are able to efficiently penetrate cellular lipid bilayers. Although CPPs have been used as carriers in conjugation with certain cargos to target specific genes and pathways, how rationally designed CPPs per se affect global gene expression has not been investigated. Therefore, following time course treatments with 4 CPPs-penetratin, PepFect14, mtCPP1 and TP10, HeLa cells were transcriptionally profiled by RNA sequencing. Results from these analyses showed a time-dependent response to different CPPs, with specific sets of genes related to ribosome biogenesis, microtubule dynamics and long-noncoding RNAs being differentially expressed compared to untreated controls. By using an image-based high content phenotypic profiling platform we confirmed that differential gene expression in CPP-treated HeLa cells strongly correlates with changes in cellular phenotypes such as increased nucleolar size and dispersed microtubules, compatible with altered ribosome biogenesis and cell growth. Altogether these results suggest that cells respond to different cell penetrating peptides by alteration of specific sets of genes, which are possibly part of the common response to such stimulus.

  • 16. Venit, Tomas
    et al.
    El Said, Nadine Hosny
    Mahmood, Syed Raza
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    A dynamic actin-dependent nucleoskeleton and cell identity2021In: Journal of Biochemistry (Tokyo), ISSN 0021-924X, E-ISSN 1756-2651, Vol. 169, no 3, p. 243-257Article, review/survey (Refereed)
    Abstract [en]

    Actin is an essential regulator of cellular functions. In the eukaryotic cell nucleus, actin regulates chromatin as a bonafide component of chromatin remodelling complexes, it associates with nuclear RNA polymerases to regulate transcription and is involved in co-transcriptional assembly of nascent RNAs into ribonucleoprotein complexes. Actin dynamics are, therefore, emerging as a major regulatory factor affecting diverse cellular processes. Importantly, the involvement of actin dynamics in nuclear functions is redefining the concept of nucleoskeleton from a rigid scaffold to a dynamic entity that is likely linked to the three-dimensional organization of the nuclear genome. In this review, we discuss how nuclear actin, by regulating chromatin structure through phase separation may contribute to the architecture of the nuclear genome during cell differentiation and facilitate the expression of specific gene programs. We focus specifically on mitochondrial genes and how their dysregulation in the absence of actin raises important questions about the role of cytoskeletal proteins in regulating chromatin structure. The discovery of a novel pool of mitochondrial actin that serves as 'mitoskeleton' to facilitate organization of mtDNA supports a general role for actin in genome architecture and a possible function of distinct actin pools in the communication between nucleus and mitochondria.

  • 17. Venit, Tomas
    et al.
    Mahmood, S. Raza
    Endara-Coll, Martin
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Nuclear actin and myosin in chromatin regulation and maintenance of genome integrity2020In: Actin Cytoskeleton in Cancer Progression and Metastasis - Part A / [ed] Clément Thomas, Lorenzo Galluzzi, Cambridge: Academic Press, 2020, 1, Vol. 355, p. 67-108Chapter in book (Refereed)
    Abstract [en]

    Cytoskeletal proteins are beginning to be considered as key regulators of nuclear function. Among them, actin and myosin have been implicated in numerous tasks, including chromatin regulation, transcription and assembly of nascent ribonucleoprotein complexes. We also know from work performed by several labs that influx of actin and myosin into the nucleus and out of the nucleus is tightly regulated. In particular, in the case of actin, its nucleocytoplasmic import/export cycle is controlled by the importin/exportin system and it correlates with the transcriptional state of the cell. These basic molecular functions of both actin and myosin seem to impact key cellular functions, including development and differentiation as well as the cellular response to DNA damage by directly affecting transcriptional reprograming. These observations are beginning to suggest that actin and myosin could play an important role in consolidating the organization of the mammalian genome and that loss of actin and myosin likely leads to a general instability of the genome. In this chapter, we provide a general background on evidence that actin and myosin are important in key nuclear functions. Following this, we will focus on evidence supporting of a role in genome organization and finally we will discuss increasingly striking results on the role of actin and myosin in the maintenance of genome integrity.

  • 18. Venit, Tomas
    et al.
    Sapkota, Oscar
    Abdrabou, Wael Said
    Loganathan, Palanikumar
    Pasricha, Renu
    Mahmood, Syed Raza
    El Said, Nadine Hosny
    Sherif, Shimaa
    Thomas, Sneha
    Abdelrazig, Salah
    Amin, Shady
    Bedognetti, Davide
    Idaghdour, Youssef
    Magzoub, Mazin
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice2023In: Nature Communications, E-ISSN 2041-1723, Vol. 14, article id 6328Article in journal (Refereed)
    Abstract [en]

    Metabolic reprogramming is one of the hallmarks of tumorigenesis. Here, we show that nuclear myosin 1 (NM1) serves as a key regulator of cellular metabolism. NM1 directly affects mitochondrial oxidative phosphorylation (OXPHOS) by regulating mitochondrial transcription factors TFAM and PGC1α, and its deletion leads to underdeveloped mitochondria inner cristae and mitochondrial redistribution within the cell. These changes are associated with reduced OXPHOS gene expression, decreased mitochondrial DNA copy number, and deregulated mitochondrial dynamics, which lead to metabolic reprogramming of NM1 KO cells from OXPHOS to aerobic glycolysis.This, in turn, is associated with a metabolomic profile typical for cancer cells, namely increased amino acid-, fatty acid-, and sugar metabolism, and increased glucose uptake, lactate production, and intracellular acidity. NM1 KO cells form solid tumors in a mouse model, suggesting that the metabolic switch towards aerobic glycolysis provides a sufficient carcinogenic signal. We suggest that NM1 plays a role as a tumor suppressor and that NM1 depletion may contribute to the Warburg effect at the onset of tumorigenesis.

  • 19. Venit, Tomas
    et al.
    Semesta, Khairunnisa
    Farrukh, Sannia
    Endara-Coll, Martin
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), UAE.
    Havalda, Robert
    Hozak, Pavel
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), UAE.
    Nuclear myosin 1 activates p21 gene transcription in response to DNA damage through a chromatin-based mechanism2020In: Communications biology, E-ISSN 2399-3642, Vol. 3, no 1, article id 115Article in journal (Refereed)
    Abstract [en]

    Nuclear myosin 1 (NM1) has been implicated in key nuclear functions. Together with actin, it has been shown to initiate and regulate transcription, it is part of the chromatin remodeling complex B-WICH, and is responsible for rearrangements of chromosomal territories in response to external stimuli. Here we show that deletion of NM1 in mouse embryonic fibroblasts leads to chromatin and transcription dysregulation affecting the expression of DNA damage and cell cycle genes. NM1 KO cells exhibit increased DNA damage and changes in cell cycle progression, proliferation, and apoptosis, compatible with a phenotype resulting from impaired p53 signaling. We show that upon DNA damage, NM1 forms a complex with p53 and activates the expression of checkpoint regulator p21 (Cdkn1A) by PCAF and Set1 recruitment to its promoter for histone H3 acetylation and methylation. We propose a role for NM1 in the transcriptional response to DNA damage response and maintenance of genome stability. Venit et al. demonstrate a role for Nuclear myosin 1 (NM1) in the DNA Damage Response by affecting the expression of the p53 target, p21, through chromatin remodeling. They used embryonic fibroblasts from mouse model, high content phenotypic profiling and cell assays, RNA-Seq and ChIP-Seq and pull-down assays and show that NM1 is required for the recruitment of PCAF and SET1 to the p21 gene in response to etoposide.

  • 20. Xie, Xin
    et al.
    Almuzzaini, Bader
    Drou, Nizar
    Kremb, Stephan
    Yousif, Ayman
    Östlund Farrants, Ann-Kristin
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Gunsalus, Kristin
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    beta-Actin-dependent global chromatin organization and gene expression programs control cellular identity2018In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 32, no 3, p. 1296-1314Article in journal (Refereed)
    Abstract [en]

    During differentiation and development, cell fate and identity are established by waves of genetic reprogramming. Although the mechanisms are largely unknown, during these events, dynamic chromatin reorganization is likely to ensure that multiple genes involved in the same cellular functions are coregulated, depending on the nuclear environment. In this study, using high-content screening of embryonic fibroblasts from a beta-actin knockout (KO) mouse, we found major chromatin rearrangements and changes in histone modifications, such as methylated histone (H)3-lysine-(K)9. Genome-wide H3K9 trimethylation-(Me)3 landscape changes correlate with gene up-and down-regulation in beta-actin KO cells. Mechanistically, we found loss of chromatin association by the Brahma-related gene (Brg)/Brahma-associated factor (BAF) chromatin remodeling complex subunit Brg1 in the absence of beta-actin. This actin-dependent chromatin reorganization was concomitant with the up-regulation of sets of genes involved in angiogenesis, cytoskeletal organization, andmyofibroblast features in beta-actin KO cells. Some of these genes and phenotypes were gained in a beta-actin dose-dependent manner. Moreover, reintroducing a nuclear localization signal-containing beta-actin in the knockout cells affected nuclear features and gene expression. Our results suggest that, by affecting the genome-wide organization of heterochromatin through the chromatin-binding activity of the BAF complex, beta-actin plays an essential role in the determination of gene expression programs and cellular identity.

  • 21. Xie, Xin
    et al.
    Deliorman, Muhammedin
    Qasaimeh, Mohammad A.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    The relative composition of actin isoforms regulates cell surface biophysical features and cellular behaviors2018In: Biochimica et Biophysica Acta - General Subjects, ISSN 0304-4165, E-ISSN 1872-8006, Vol. 1862, no 5, p. 1079-1090Article in journal (Refereed)
    Abstract [en]

    Background. Cell surface mechanics is able to physically and biomechanically affect cell shape and motility, vesicle trafficking and actin dynamics. The biophysical properties of cell surface are strongly influenced by cytoskeletal elements. In mammals, tissue-specific expression of six actin isoforms is thought to confer differential biomechanical properties. However, the relative contribution of actin isoforms to cell surface properties is not well understood. Here, we sought to investigate whether and how the composition of endogenous actin isoforms directly affects the biomechanical features of cell surface and cellular behavior. Methods: We used fibroblasts isolated from wild type (WT), heterozygous (HET) and from knockout (KO) mouse embryos where both beta-actin alleles are not functional. We applied a combination of genome-wide analysis and biophysical methods such as RNA-seq and atomic force microscopy. Results: We found that endogenous beta-actin levels are essential in controlling cell surface stiffness and pull-off force, which was not compensated by the up-regulation of other actin isoforms. The variations of surface biophysical features and actin contents were associated with distinct cell behaviors in 2D and 3D WT, HET and KO cell cultures. Since beta-actin in WT cells and smooth muscle alpha-actin up-regulated in KO cells showed different organization patterns, our data support the differential localization and organization as a mechanism to regulate the biophysical properties of cell surface by actin isoforms. Conclusions: We propose that variations in actin isoforms composition impact on the biophysical features of cell surface and cause the changes in cell behavior.

  • 22. Xie, Xin
    et al.
    Jankauskas, Robertas
    Mazari, Aslam M. A.
    Drou, Nizar
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    β-actin regulates a heterochromatin landscape essential for optimal induction of neuronal programs during direct reprograming2018In: PLOS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 14, no 12, article id e1007846Article in journal (Refereed)
    Abstract [en]

    During neuronal development, beta-actin serves an important role in growth cone mediated axon guidance. Consistent with this notion, in vivo ablation of the beta-actin gene leads to abnormalities in the nervous system. However, whether beta-actin is involved in the regulation of neuronal gene programs is not known. In this study, we directly reprogramed beta-actin(+/+) WT, beta-actin(+/-) HET and beta-actin(-/-) KO mouse embryonic fibroblast (MEFs) into chemically induced neurons (CiNeurons). Using RNA-seq analysis, we profiled the transcriptome changes among the CiNeurons. We discovered that induction of neuronal gene programs was impaired in KO CiNeurons in comparison to WT ones, whereas HET CiNeurons showed an intermediate levels of induction. ChIP-seq analysis of heterochromatin markers demonstrated that the impaired expression of neuronal gene programs correlated with the elevated H3K9 and H3K27 methylation levels at gene loci in beta-actin deficient MEFs, which is linked to the loss of chromatin association of the BAF complex ATPase subunit Brg1. Together, our study shows that heterochromatin alteration in beta-actin null MEFs impedes the induction of neuronal gene programs during direct reprograming. These findings are in line with the notion that H3K9Me3-based heterochromatin forms a major epigenetic barrier during cell fate change.

  • 23. Xie, Xin
    et al.
    Liu, Pu-Ste
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Analysis of Global Transcriptome Change in Mouse Embryonic Fibroblasts After dsDNA and dsRNA Viral Mimic Stimulation2019In: Frontiers in Immunology, E-ISSN 1664-3224, Vol. 10, article id 836Article in journal (Refereed)
    Abstract [en]

    The activation of innate immunity by viral nucleic acids present in the cytoplasm plays an essential role in controlling viral infection in both immune and non-immune cells. The dsDNA and dsRNA viral mimics can stimulate the cytosolic nucleic acids sensors and activate the antiviral innate immunity. In this study, taking advantage of dsDNA and dsRNA viral mimics, we investigated the global transcriptome changes after the antiviral immunity activation in mouse embryonic fibroblasts. Results from our data identified a positive feedback up-regulation of sensors (e.g., Tlr2, Tlr3, Ddx58, cGAS), transducers (e.g., Traf2, Tbk1) and transcription factors (e.g., Irf7, Jun, Stat1, Stat2) in multiple pathways involved in detecting viral or microbial infections upon viral mimic stimulation. A group of genes involved in DNA damage response and DNA repair such as Parp9, Dtx3l, Rad52 were also up-regulated, implying the involvement of these genes in antiviral immunity. Molecular function analysis further showed that groups of helicase genes (e.g., Dhx58, Helz2), nuclease genes (e.g., Dnase1l3, Rsph10b), methyltransferase genes (e.g., histone methyltransferase Prdm9, Setdb2; RNA methyltransferase Mettl3, Mttl14), and protein ubiquitin-ligase genes (e.g., Trim genes and Rnf genes) were up-regulated upon antiviral immunity activation. In contrast, viral mimic stimulation down-regulated genes involved in a broad range of general biological processes (e.g., cell division, metabolism), cellular components (e.g., mitochondria and ribosome), and molecular functions (e.g., cell-cell adhesion, microtubule binding). In summary, our study provides valuable information about the global transcriptome changes upon antiviral immunity activation. The identification of novel groups of genes up-regulated upon antiviral immunity activation serves as useful resource for mining new antiviral sensors and effectors.

  • 24. Xie, Xin
    et al.
    Mahmood, S. Raza
    Gjorgjieva, Tamara
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Emerging roles of cytoskeletal proteins in regulating gene expression and genome organization during differentiation2020In: Nucleus, ISSN 1949-1034, E-ISSN 1949-1042, Vol. 11, no 1, p. 53-65Article, review/survey (Refereed)
    Abstract [en]

    In the eukaryotic cell nucleus, cytoskeletal proteins are emerging as essential players in nuclear function. In particular, actin regulates chromatin as part of ATP-dependent chromatin remodeling complexes, it modulates transcription and it is incorporated into nascent ribonucleoprotein complexes, accompanying them from the site of transcription to polyribosomes. The nuclear actin pool is undistinguishable from the cytoplasmic one in terms of its ability to undergo polymerization and it has also been implicated in the dynamics of chromatin, regulating heterochromatin segregation at the nuclear lamina and maintaining heterochromatin levels in the nuclear interiors. One of the next frontiers is, therefore, to determine a possible involvement of nuclear actin in the functional architecture of the cell nucleus by regulating the hierarchical organization of chromatin and, thus, genome organization. Here, we discuss the repertoire of these potential actin functions and how they are likely to play a role in the context of cellular differentiation.

  • 25. Xie, Xin
    et al.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    An actin-based nucleoskeleton involved in gene regulation and genome organization2018In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 506, no 2, p. 378-386Article in journal (Refereed)
    Abstract [en]

    In eukaryotic cells gene regulation is dependent on global genome organization. This is achieved, in response to favorable environmental conditions, through spatial redistribution of chromatin and changes in global epigenetic levels. This eventually drives movement of gene-rich chromatin loops and formation of DNA loops, consolidating neighborhoods of gene expression and silencing. One of the challenges for future work is to examine how these neighborhoods are formed and whether they host genes involved in the same cellular functions for sustained expression or silencing over time. In the present review, we summarize evidence that actin and actin-associated proteins regulate gene activity. Furthermore we discuss how these specific nuclear tasks in which actin is engaged are important to organize and consolidate the mammalian genome, ensuring gene activation and repression of gene programs important to establish cellular identity. We propose that these mechanisms are essential to control cellular development and differentiation.

  • 26. Xie, Xin
    et al.
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    Elevated transforming growth factor signaling activation in -actin-knockout mouse embryonic fibroblasts enhances myofibroblast features2018In: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 233, no 11, p. 8884-8895Article in journal (Refereed)
    Abstract [en]

    Signaling by the transforming growth factor- (TGF-) is an essential pathway regulating a variety of cellular events. TGF- is produced as a latent protein complex and is required to be activated before activating the receptor. The mechanical force at thecell surface is believed to be a mechanism for latent TGF- activation. Using -actin null mouse embryonic fibroblasts as a model, in which actin cytoskeleton and cell-surface biophysical features are dramatically altered, we reveal increased TGF-1 activation and the upregulation of TGF- target genes. In -actin null cells, we show evidence that the enhanced TGF- signaling relies on the active utilization of latent TGF-1 in the cell culture medium. TGF- signaling activation contributes to the elevated reactive oxygen speciesproduction, which is likely mediated by the upregulation of Nox4. The previously observed myofibroblast phenotype of -actin null cells is inhibited by TGF- signaling inhibition, while the expression of actin cytoskeleton genes and angiogenic phenotype are not affected. Together, our study shows a scenario that the alteration of the actin cytoskeleton and the consequent changes in cellular biophysical features lead to changes in cell signaling process such as TGF- activation, which in turn contributes to the enhanced myofibroblast phenotype.

  • 27. Xie, Xin
    et al.
    Venit, Tomas
    Drou, Nizar
    Percipalle, Piergiorgio
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
    In Mitochondria beta-Actin Regulates mtDNA Transcription and Is Required for Mitochondrial Quality Control2018In: iScience, E-ISSN 2589-0042 , Vol. 3, p. 226-237Article in journal (Refereed)
    Abstract [en]

    In eukaryotic cells, actin regulates both cytoplasmic and nuclear functions. However, whether actin-based structures are present in the mitochondria and are involved in mitochondrial functions has not been investigated. Here, using wild-type beta-actin +/+ and knockout (KO) b-actin -/- mouse embryonic fibroblasts we show evidence for the defect in maintaining mitochondrial membrane potential (MMP) in beta-actin-null cells. MMP defects were associated with impaired mitochondrial DNA (mtDNA) transcription and nuclear oxidative phosphorylation (OXPHOS) gene expression. Using super-resolution microscopy we provided direct evidence on the presence of beta-actin-containing structures inside mitochondria. Large aggregates of TFAM-stained nucleoids were observed in bulb-shaped mitochondria in KO cells, suggesting defects in mitochondrial nucleoid segregation without beta-actin. The observation that mitochondria-targeted beta-actin rescued mtDNA transcription and MMP suggests an indispensable functional role of a mitochondrial beta-actin pool necessary for mitochondrial quality control.

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