Rolf Ohlsson Group

The eukaryotic cell nucleus holds keys to many secrets of life. For example, the DNA blueprint is condensed >100.000-fold from its linear shape to the very limited physical confines of the nuclear structure. Despite this tight packaging, the higher order chromatin structure must somehow allow regulated access to selected parts of the genome to enable specific transcription profiles during developmental windows. There must also be a substantial measure of precision in these processes, as chromatin features must be faithfully copied to re-enact conformations pivotal for the memory of a cell lineage, and to enable progressive restrictions in cell fates during development. These processes are aided by the organization of the nucleus into multiple, highly specialized functional compartments.

The epigenetic reprogramming process governs the fate of the developing mammalian zygote by regulating the early allocation of the three germ layers and many other later pivotal processes during the lifetime of the individual. Unfortunately, genetic mutations can target the reprogramming process, or, as generally presumed, can be rendered unstable due to abnormal environmental cues, such as inflammation or viral infection. The result is epigenetic instability, a condition not only initiating cancer, but also enabling the selection of meta-stable epigenetic marks sustaining abnormal proliferation at ectopic sites during the malignant process.

It is becoming increasingly clear that the epigenome influences the expressivity of the genome in 3 dimensions within the nuclear architecture (Göndör and Ohlsson, Nature review genetics, 2009). The group has developed novel technologies to explore this issue using super high throughput sequencing analysis (Zhao et al, nature genetics 2006; Göndör, Rougier and Ohlsson, nature protocols, 2008). This approach allows the assessment of factors establishing long-range interaction between chromatin fibres within the same chromosome or between chromosomes (Mariano and Ohlsson, patent pending). These technologies will be applied to explore the epigenetic progenitor origin of human cancer stating that all human cancers involve epigenetic lesions in stem/progenitor cells (Feinberg, Ohlsson, Henikoff, Nature review genetics, 2006). In addition, the group is exploring reprogramming of chromosomal networks in human embryonic stem cells and iPS cells in relationship with other epigenetic features, such as replication timing, replication origins and epigenetic marks of the primary chromatin fibres. The overall aim of these projects is to break new ground in our understanding of the 3rd dimension of the epigenome and how it relates to both pediatric and adult cancers. It can also explain quantitative traits and genome-wide association screens of human diseases from novel perspectives.

Project Leaders

Satish Srinivas Kitambi

Terumi Kohwi-Shigematsu


Group members

Professor, senior

Rolf Ohlsson


Yoshinori KohwiAssociated
Terumi Kohwi-ShigematsuAssociated



The visualization of large organized chromatin domains enriched in the H3K9me2 mark within a single chromosome in a single cell.
Chen X, Yammine S, Shi C, Tark-Dame M, Göndör A, Ohlsson R
Epigenetics 2014 Nov;9(11):1439-45

Chromatin in situ proximity (ChrISP): single-cell analysis of chromatin proximities at a high resolution.
Chen X, Shi C, Yammine S, Göndör A, Rönnlund D, Fernandez-Woodbridge A, et al
BioTechniques 2014 ;56(3):117-8, 120-4

A bright monomeric green fluorescent protein derived from Branchiostoma lanceolatum.
Shaner N, Lambert G, Chammas A, Ni Y, Cranfill P, Baird M, et al
Nat. Methods 2013 May;10(5):407-9

CTCF-binding sites within the H19 ICR differentially regulate local chromatin structures and cis-acting functions.
Guibert S, Zhao Z, Sjölinder M, Göndör A, Fernandez A, Pant V, et al
Epigenetics 2012 Apr;7(4):361-9

Window into the complexities of chromosome interactomes.
Göndör A, Woodbridge A, Shi C, Aurell E, Imreh M, Ohlsson R
Cold Spring Harb. Symp. Quant. Biol. 2010 ;75():493-500

Gene expression: The coherent Mediator.
Ohlsson R
Nature 2010 Sep;467(7314):406-7

Transforming growth factor beta promotes complexes between Smad proteins and the CCCTC-binding factor on the H19 imprinting control region chromatin.
Bergström R, Savary K, Morén A, Guibert S, Heldin C, Ohlsson R, et al
J. Biol. Chem. 2010 Jun;285(26):19727-37

Chromosomal networks as mediators of epigenetic states: the maternal genome connection.
Sumida N, Ohlsson R
Epigenetics 2010 May;5(4):297-300

CTCF shapes chromatin by multiple mechanisms: the impact of 20 years of CTCF research on understanding the workings of chromatin.
Ohlsson R, Bartkuhn M, Renkawitz R
Chromosoma 2010 Aug;119(4):351-60

Does CTCF mediate between nuclear organization and gene expression?
Ohlsson R, Lobanenkov V, Klenova E
Bioessays 2010 Jan;32(1):37-50

Mutational analysis of the poly(ADP-ribosyl)ation sites of the transcription factor CTCF provides an insight into the mechanism of its regulation by poly(ADP-ribosyl)ation.
Farrar D, Rai S, Chernukhin I, Jagodic M, Ito Y, Yammine S, et al
Mol. Cell. Biol. 2010 Mar;30(5):1199-216

Does CTCF mediate between nuclear organization and gene expression?
Ohlsson R, Lobanenkov V, Klenova E
Bioessays 2010 Jan;32(1):37-50

Nonallelic transvection of multiple imprinted loci is organized by the H19 imprinting control region during germline development.
Sandhu K, Shi C, Sjölinder M, Zhao Z, Göndör A, Liu L, et al
Genes Dev. 2009 Nov;23(22):2598-603

Chromosome crosstalk in three dimensions.
Göndör A, Ohlsson R
Nature 2009 Sep;461(7261):212-7

Replication timing and epigenetic reprogramming of gene expression: a two-way relationship?
Göndör A, Ohlsson R
Nat. Rev. Genet. 2009 04;10(4):269-76

CpG methylation of the IFNG gene as a mechanism to induce immunosuppression [correction of immunosupression] in tumor-infiltrating lymphocytes.
Janson P, Marits P, Thörn M, Ohlsson R, Winqvist O
J. Immunol. 2008 Aug;181(4):2878-86

Chromatin insulators and cohesins.
Göndör A, Ohlsson R
EMBO Rep. 2008 Apr;9(4):327-9

All Publications In PubMed

Link to all publications in PubMed

Tumour Biology