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View details. Thus, CTCF and cohesin form a rapidly exchanging 'dynamic complex' rather than a typical stable complex. Since CTCF and cohesin are required for loop domain formation, our results suggest that chromatin loops are dynamic and frequently break and reform throughout the cell cycle. A human cell contains about 2 meters of DNA tightly packed in a compartment called the nucleus.

Within the space inside the nucleus, different parts of the DNA fold into distinct bundles known as domains. These domains are important for organising the genome and are crucial for regulating gene expression, by stimulating specific DNA segments to activate certain genes. Previous research has shown that DNA segments within the same domain frequently interact, whereas DNA segments in different domains rarely do. The domains are often folded into loops that are held together by a ring-shaped protein complex called cohesin, while another protein called CTCF positions cohesin and thereby sets the boundaries between the domains.

Some mutations are known to disrupt these boundaries, which allows certain DNA segments to activate the wrong genes. This can lead to cancer or cause defects when embryos are developing. However, we do not currently understand how these domains are formed or maintained. In particular, it was unclear whether these loop domains are stable or dynamic structures.

Hansen et al. In further experiments, single molecules of cohesin and CTCF were tracked inside cells using super-resolution microscopy. These observations suggest that rather than remaining static, chromatin domains are held together by a dynamic protein complex, with a molecular composition that exchanges over time. This results suggests that DNA loop domains, which were generally assumed to be very stable anchor points, are in fact highly dynamic structures that frequently fall apart and reform.

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The next challenge will be to understand how the dynamic nature of these loop domains contribute to gene regulation. This may, one day, enable us to manipulate the domains to correct faulty folding of DNA in cancer and other diseases.

Mammalian interphase genomes are functionally compartmentalized into topologically associating domains TADs spanning hundreds of kilobases. Moreover, disruption of loop domain boundaries by deletion or silencing of CTCF-binding sites allows abnormal contact between previously separated enhancers and promoters, which can induce aberrant gene activation leading to cancer Flavahan et al.

Yet, despite much progress in characterizing TADs and loop domains, how they are formed and maintained remains unclear. Since CTCF and cohesin causally control domain organization, here we investigated their dynamics and nuclear organization using single-molecule imaging in live cells.

B Sketch of cohesin, with subunits labeled, topologically entrapping DNA. G Co-IP. Halo- and SNAP f -Tags can be covalently conjugated with bright cell-permeable small molecule dyes suitable for single-molecule imaging Figure 1D ; Figure 1—figure supplement 1 ; Grimm et al.

Integrating these results with the recent demonstrations Nora et al. First, we used highly inclined and laminated optical sheet illumination Tokunaga et al. We recorded thousands of binding event trajectories and calculated their survival probability. A double-exponential function, corresponding to specific and non-specific DNA binding Chen et al. The measured RT did not depend on the dye or exposure time Figure 2—figure supplement 1B.

We also note that there is likely an oversampling of binding events at CTCF-binding sites showing the strongest ChIP-Seq enrichment Figure 1E , which tend to be the sites involved in looping Merkenschlager and Nora, A Sketch illustrating HiLo highly inclined and laminated optical sheet illumination Tokunaga et al. Right inset: a log-log survival curve. Error bars show standard deviation between replicates. Each movie lasted 20 min with continuous low-intensity nm excitation and ms camera integration time. Cells were labeled with 1— pM JF Right: sketch of Fucci cell-cycle phase reporter Sakaue-Sawano et al.

This video cannot be played in place because your browser does support HTML5 video. You may still download the video for offline viewing. Related to Figure 2. Laser: nm. Dye: JF One pixel: nm. However, when we used similar transiently over-expressed Halo-CTCF instead of endogenous knock-in cells, we also observed similarly rapid recovery Figure 2—figure supplement 2B , suggesting that over-expression of target proteins can result in artefactual measurements.

This finding underscores the importance of studying endogenously tagged and functional proteins. In addition to its role in holding together chromatin loops, cohesin mediates sister chromatid cohesion from replication in S-phase to mitosis. To control for the cell-cycle, we deployed the Fucci system Sakaue-Sawano et al. The slow mRad21 turnover precluded SMT experiments.

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To investigate this possibility, we analyzed how CTCF and cohesin each explore the nucleus. Tracking fast-diffusing molecules has been a major challenge. To overcome this issue, we took advantage of bright new dyes Grimm et al. To characterize the nuclear search mechanism, we performed kinetic modeling of the measured displacements Figure 3—figure supplement 1B ; Materials and methods; Mazza et al. Nuclear search mechanism parameters. Table 1 lists key parameters for the nuclear search mechanism inferred from model fitting of the displacements in Figure 3 and the residence times in Figure 2.

Kinetic model fits three fitted parameters to raw displacement histograms are shown as black lines. All calculated and fitted parameters are listed in Table 1. Displacement histograms were obtained by merging data from at least 24 cells from at least three replicates. Related to Figure 3. Stroboscopic 1 ms of nm paSMT allows tracking of fast-diffusing molecules. Lasers: and nm. Dye: PA-JF Conversely, a Rad21 mutant Haering et al.

Like this Rad21 mutant, overexpressed wild-type mRadHalo also showed negligible chromatin association Figure 3—figure supplement 1E again underscoring the importance of studying endogenously tagged proteins at physiological concentrations.

Topological association and dissociation of cohesin is regulated by a complex interplay of co-factors such as Nipbl, Sororin and Wapl Skibbens, To resolve these apparently paradoxical findings, we investigated the nuclear organization of CTCF and cohesin simultaneously in the same nucleus. To determine whether individual CTCF and cohesin molecules co-localize, we calculated the pair cross correlation, C r Stone and Veatch, Conversely, CTCF and cohesin were nearly independent at length scales beyond the diffraction limit, emphasizing the importance of super-resolution approaches.

Thus, our two-color dSTORM results provide compelling evidence that a large fraction of CTCF and cohesin molecules indeed co-localize at the single-molecule level inside the nucleus consistent with the LMC model and reveals a clustered nuclear organization. High-intensity co-localization is shown as white. Low-intensity co-localization is not visible. Note, the SNAP dye cp-JF shows slight artefactual labeling of the nuclear envelope, which was removed during image rendering.

D Sketch illustrating the concept of a dynamic loop maintenance complex LMC composed of CTCF and cohesin with frequent CTCF exchange and slow, rare cohesin dissociation, which causes loop deformation and topological re-orientation of chromatin. Chromatin loop domains are widely believed to be very stable structures Andrey et al. While our in vitro biochemical Figure 1G and co-localization Figure 4A—C experiments do demonstrate complex formation between CTCF and cohesin, our SMT experiments paradoxically reveal this complex to be highly transient and dynamic Figures 2 — 3.

Consistent with previous studies, CTCF mainly functions to position cohesin at loop boundaries, whereas cohesin physically holds together the two chromatin strands.