Abstract
It has been proposed that interactions between mammalian chromosomes, or transchromosomal interactions (also known as kissing chromosomes), regulate gene expression and cell fate determination. Here we aimed to identify novel transchromosomal interactions in immune cells by high-resolution genome-wide chromosome conformation capture. Although we readily identified stable interactions in cis, and also between centromeres and telomeres on different chromosomes, surprisingly we identified no gene regulatory transchromosomal interactions in either mouse or human cells, including previously described interactions. We suggest that advances in the chromosome conformation capture technique and the unbiased nature of this approach allow more reliable capture of interactions between chromosomes than previous methods. Overall our findings suggest that stable transchromosomal interactions that regulate gene expression are not present in mammalian immune cells and that lineage identity is governed by cis, not trans chromosomal interactions.
Highlights
IntroductionRecent technological advances have allowed characterisation of the elaborate three-dimensional structures that form from this DNA [1]
Each chromosome contains just one DNA molecule
We readily identified stable interactions within chromosomes and between centromeres and telomeres on different chromosomes, surprisingly we identified no gene regulatory transchromosomal interactions in either mouse or human cells, including those previously described
Summary
Recent technological advances have allowed characterisation of the elaborate three-dimensional structures that form from this DNA [1] These structures include topologically associated domains, which partition the chromosome, and elegant DNA loops that link gene promoters to distant enhancers. In addition to these intrachromosomal structures formed within the same DNA molecule, there are transchromosomal interactions formed between different chromosomes. In T cells, a regulatory region on mouse chromosome 11 (the T helper 2 locus control region; LCR) was suggested to interact with loci encoding the cytokine interferon gamma (Ifng) on chromosome 10 [10] and interleukin 17 (IL-17) on chromosome 1 [11] Perturbation of these interactions was associated with altered expression of Ifng and IL-17, respectively. In mouse B cell progenitors, the interaction between the immunoglobulin heavy chain (Igh) locus on chromosome 12 and the immunoglobulin light chain (Igk) locus on chromosome 6 was important for the rearrangement of the heavy chain locus [12]
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