Marie Rogne

• Nguyen, Xuan Thang; Martiensen, Emily Louise Beecher; Abdelhalim, Mohamed; Tran, Trung; Ledsaak, Marit & Rogne, Marie [Show all 8 contributors for this article] (2026). Proteome-wide multi-omics profiling of osteosarcoma transcription factor networks. bioRxiv (preprint article). doi: 10.64898/2026.03.29.714917. Full text in Research Archive Show summary

  Osteosarcoma (OS) is an aggressive bone cancer that most commonly affects children and young adults. OS exhibits a high degree of genomic complexity, as well as cellular plasticity, and dynamic transcriptional regulation is suggested to contribute to treatment resistance and metastasis. Cell lines are well characterized as models to advance our knowledge on OS biology. HOS and U2OS cells have increased invasiveness and higher migratory ability compared with MG63. In this study, we employed a tandem array of consensus transcription factor response elements (catTFREs) proteomic approach to characterize transcription factor (TF) regulatory networks related to OS aggressiveness. We mapped 7,594 proteins and enriched 352 transcription factors and coregulators. When we integrated proteomics with cell line specific gene expression and chromatin accessibility we classified the proteins into different OS cell line dependent sub-clusters and identified TFs and coregulators common for all cell lines and specific for individual cell lines. We demonstrate that RUNX2, MYBL2 and HMGA2 are specifically enriched in HOS and U2OS and may be linked to the cell aggressiveness. ETV5, JUNB, NFIX and ZEB1 were among TFs specific to MG63. Our analysis provides a more comprehensive understanding of the transcriptional drivers that shape OS regulatory landscapes and may have future therapeutic implications.

• Sharma, Ankush; Akshay, Akshay; Rogne, Marie & Eskeland, Ragnhild (2021). ShinyArchR.UiO: user-friendly,integrative and open-source tool for visualization of single-cell ATAC-seq data using ArchR. Bioinformatics. ISSN 1367-4803. 38(3), p. 834–836. doi: 10.1093/bioinformatics/btab680. Full text in Research Archive Show summary

  Motivation: Mapping of chromatin accessibility landscapes in single-cells and the integration with gene expression enables a better understanding of gene regulatory mechanisms defining cell identities and cell-fate determination in development and disease. Generally, raw data generated from single-cell Assay for Transposase-Accessible Chromatin sequencing (scATAC-seq) are deposited in repositories that are generally inaccessible due to lack of in-depth knowledge of computational programming. Results: We have developed ShinyArchR.UiO, an R-based shiny app, that facilitates scATAC-seq data accessibility and visualisation in a user-friendly, interactive, and open-source web interface. ShinyArchR.UiO is an application that can streamline collaborative efforts for interpretation of massive chromatin accessibility datasets and allow for open access data sharing for wider audiences.

• Caglayan, Safak; Hashim, Adnan; Cieslar-Pobuda, Artur; Jensen, Vidar; Behringer, Sidney & Talug, Burcu [Show all 16 contributors for this article] (2020). Optic Atrophy 1 Controls Human Neuronal Development by Preventing Aberrant Nuclear DNA Methylation. iScience. 23(6). doi: 10.1016/j.isci.2020.101154. Full text in Research Archive Show summary

  Optic atrophy 1 (OPA1), a GTPase at the inner mitochondrial membrane involved in regulating mitochondrial fusion, stability, and energy output, is known to be crucial for neural development: Opa1 heterozygous mice show abnormal brain development, and inactivating mutations in OPA1 are linked to human neurological disorders. Here, we used genetically modified human embryonic and patient-derived induced pluripotent stem cells and reveal that OPA1 haploinsufficiency leads to aberrant nuclear DNA methylation and significantly alters the transcriptional circuitry in neural progenitor cells (NPCs). For instance, expression of the forkhead box G1 transcription factor, which is needed for GABAergic neuronal development, is repressed in OPA1+/− NPCs. Supporting this finding, OPA1+/− NPCs cannot give rise to GABAergic interneurons, whereas formation of glutamatergic neurons is not affected. Taken together, our data reveal that OPA1 controls nuclear DNA methylation and expression of key transcription factors needed for proper neural cell specification.

• Rogne, Marie; Chu, Dinh Toi; Küntziger, Thomas M.; Mylonakou, Maria-Niki; Collas, Philippe & Tasken, Kjetil (2018). OPA1-anchored PKA phosphorylates perilipin 1 on S522 and S497 in adipocytes differentiated from human adipose stem cells. Molecular Biology of the Cell. ISSN 1059-1524. 29(12), p. 1487–1501. doi: 10.1091/mbc.E17-09-0538. Full text in Research Archive Show summary

  Optic atrophy 1 (OPA1) is the A-kinase anchoring protein targeting the pool of protein kinase A (PKA) responsible for perilipin 1 phosphorylation, a gatekeeper for lipolysis. However, the involvement of OPA1-bound PKA in the downstream regulation of lipolysis is unknown. Here we show up-regulation and relocation of OPA1 from mitochondria to lipid droplets during adipocytic differentiation of human adipose stem cells. We employed various biochemical and immunological approaches to demonstrate that OPA1-bound PKA phosphorylates perilipin 1 at S522 and S497 on lipolytic stimulation. We show that the first 30 amino acids of OPA1 are essential for its lipid droplet localization as is OMA1-dependent processing. Finally, our results indicate that presence of OPA1 is necessary for lipolytic phosphorylation of downstream targets. Our results show for the first time, to our knowledge, how OPA1 mediates adrenergic control of lipolysis in human adipocytes by regulating phosphorylation of perilipin 1.

• Rogne, Marie; Svärd, Oksana; Madsen-Østerbye, Julia-Kristina Jensen; Hashim, Adnan; Tjønnfjord, Geir Erland & Staerk, Judith (2018). Cytokinesis arrest and multiple centrosomes in B cell chronic lymphocytic leukaemia. Journal of Cellular and Molecular Medicine. ISSN 1582-1838. 22(5), p. 2846–2855. doi: 10.1111/jcmm.13579. Full text in Research Archive Show summary

  Cytokinesis failure leads to the emergence of tetraploid cells and multiple centrosomes. Chronic lymphocytic leukaemia (CLL) is the most common haematological malignancy in adults and is characterized by clonal B cell expansion. Here, we show that a significant number of peripheral blood CLL cells are arrested in cytokinesis and that this event occurred after nuclear envelope reformation and before cytoplasmic abscission. mRNA expression data showed that several genes known to be crucial for cell cycle regulation, checkpoint and centromere function, such as ING4, ING5, CDKN1A and CDK4, were significantly dysregulated in CLL samples. Our results demonstrate that CLL cells exhibit difficulties in completing mitosis, which is different from but may, at least in part, explain the previously reported accumulation of CLL cells in G0/1.

• Fuglerud, Bettina Maria; Ledsaak, Marit; Rogne, Marie; Eskeland, Ragnhild & Gabrielsen, Odd Stokke (2018). The pioneer factor activity of c-Myb involves recruitment of p300 and induction of histone acetylation followed by acetylation-induced chromatin dissociation. Epigenetics & Chromatin. 11(1). doi: 10.1186/s13072-018-0208-y. Full text in Research Archive Show summary

  Background The concept of pioneer transcription factors is emerging as an essential part of the epigenetic regulation, taking place during cell development and differentiation. However, the precise molecular mechanism underlying pioneer factor activity remains poorly understood. We recently reported that the transcription factor c-Myb acts as a pioneer factor in haematopoiesis, and a point mutation in its DNA binding domain, D152V, is able to abrogate this function. Results Here, we show that specific histone modifications, including H3K27ac, prevent binding of c-Myb to histone tails, representing a novel effect of histone modifications, namely restricting binding of a pioneer factor to chromatin. Furthermore, we have taken advantage of the pioneer-defect D152V mutant to investigate mechanisms of c-Myb’s pioneer factor activity. We show that c-Myb-dependent transcriptional activation of a gene in inaccessible chromatin relies on c-Myb binding to histones, as well as on c-Myb interacting with the histone acetyltransferase p300. ChIP assays show that both wild type and the D152V mutant of c-Myb bind to a selected target gene at its promoter and enhancer, but only wild-type c-Myb causes opening and activation of the locus. Enhancement of histone acetylation restores activation of the same gene in the absence of c-Myb, suggesting that facilitating histone acetylation is a crucial part of the pioneer factor function of c-Myb. Conclusions We suggest a pioneer factor model in which c-Myb binds to regions of closed chromatin and then recruits histone acetyltransferases. By binding to histones, c-Myb facilitates histone acetylation, acting as a cofactor for p300 at c-Myb bound sites. The resulting H3K27ac leads to chromatin opening and detachment of c-Myb from the acetylated chromatin. We propose that the latter phenomenon, acetylation-induced chromatin dissociation, represents a mechanism for controlling the dynamics of pioneer factor binding to chromatin.

• Rogne, Marie & Tasken, Kjetil (2014). Compartmentalization of cAMP signaling in adipogenesis, lipogenesis and lipolysis. Hormone and Metabolic Research. ISSN 0018-5043. 46(12), p. 833–840. doi: 10.1055/s-0034-1389955. Full text in Research Archive
• Rogne, Marie & Tasken, Kjetil (2013). Cell signalling analyses in the functional genomics era. New Biotechnology. ISSN 1871-6784. 30(3), p. 333–338. doi: 10.1016/j.nbt.2013.01.003. Full text in Research Archive
• Aksaas, Anne Kristin; Larsen, Anja C V; Rogne, Marie; Rosendal, Ken Roger; Kvissel, Anne Katrine & Skålhegg, Bjørn Steen (2011). G-patch domain and KOW motifs-containing protein, GPKOW; a nuclear RNA-binding protein regulated by protein kinase A. Journal of Molecular Signaling. 6, p. 1–14. doi: 10.1186/1750-2187-6-10. Full text in Research Archive
• Rogne, Marie; Stokka, Anne Jorunn; Tasken, Kjetil; Collas, Philippe & Kuntziger, Thomas Michel (2009). Mutually exclusive binding of PP1 and RNA to AKAP149 affects the mitochondrial network. Human Molecular Genetics. ISSN 0964-6906. 18(5), p. 978–987. doi: 10.1093/hmg/ddn425. Full text in Research Archive
• Kuntziger, Thomas Michel; Rogne, Marie; Folstad, Rikke Lise & Collas, Philippe (2006). Association of PP1 with its regulatory subunit AKAP149 is regulated by serine phosphorylation flanking the RVXF motif of AKAP149. Biochemistry. ISSN 0006-2960. 45(18), p. 5868–5877. Full text in Research Archive
• Rogne, Marie; Landsverk, Bjarnason Helga; Eynde, A.V.; Beullens, Monique; Bollen, M. & Collas, Philippe [Show all 7 contributors for this article] (2006). The KH-Tudor domain of A-Kinase anchoring protein 149 mediates RNA-dependent self-association. Biochemistry. ISSN 0006-2960. 45(50), p. 14980–14989. Full text in Research Archive
• Landsverk, Bjarnason Helga; Rogne, Marie; Bollen, M.; Kuntziger, Thomas Michel & Collas, Philippe (2005). PNUTS enhances in vitro chromosome decondensation in a PP1-dependent manner. Biochemical Journal. ISSN 0264-6021. 15, p. 709–17. Full text in Research Archive

View all works in NVA

• Caglayan, Safak; Rogne, Marie & Staerk, Judith (2016). Genome scale analysis of crosstalk between the nuclear lamina and the DNA epigenome. Full text in Research Archive
• Jacobsen, Bente Marie Berntsen; Rogne, Marie & Collas, Philippe (2006). Expression of Lamin A/C, a Marker of Differentiation, in Mesenchymal Stem Cells from Human Adipose Tissue. Full text in Research Archive

View all works in NVA