Volume 616

  • No. 7958 27 April 2023

    Loop feedback

    In eukaryotes, the protein complex cohesin plays a key role in folding genomic DNA by extruding the DNA into loops. An important element in this process is the DNA-binding protein CTCF, which has been proposed to regulate loop formation. In this week’s issue, Jan-Michael Peters, Cees Dekker and their colleagues shed light on the mechanism behind CTCF’s action. The researchers visualized interactions between single molecules of CTCF (shown in pink on the cover) and cohesin (blue) in vitro, finding that CTCF is sufficient to block loop extrusion by cohesin. They also found that not only does CTCF halt loop extrusion in an orientation-dependent manner, but it also sometimes causes the loops to shrink or changes the direction in which they grow. Crucially, this regulatory role of CTCF’s loop-extrusion blocking activity is itself controlled by the tension of the DNA to which the CTCF and cohesin are bound.

  • No. 7957 20 April 2023

    Crash course

    Although currently there is no known threat to Earth from asteroids, strategies to protect the planet from a collision are being explored. On 26 September 2022, NASA and the Johns Hopkins Applied Physics Laboratory successfully tested one such approach: the Double Asteroid Redirection Test (DART) spacecraft was deliberately crashed into Dimorphos, a moon orbiting the small asteroid Didymos, resulting in a change in the moon’s orbit. In this week’s issue, five papers explore the test and the effects of the collision. One paper reconstructs the impact; a second looks at the change to Dimorphos’s orbit caused by the impact. A third paper reports observations from the Hubble Space Telescope of the material ejected during the collision. A fourth paper uses modelling to characterize the transfer of momentum that resulted from the impact. And the final paper reports on citizen science observations before, during and after the collision.

  • No. 7956 13 April 2023

    Acquired taste

    Octopuses use chemotactile receptors (CRs) in the suckers on their arms to ‘taste by touch’ as they explore their sea-floor environment. These proteins evolved from neurotransmitter receptors to allow octopuses to detect poorly soluble natural products on contact. In this week’s issue, two papers by Nicholas Bellono, Ryan Hibbs and their colleagues use cephalopod CRs to probe the structural basis of sensory-receptor evolution. In the first, the researchers describe the adaptations in octopus protein structures that underlie the change in receptor function from neurotransmission to detecting environmental stimuli. In the second paper, the team uses this information to explore how tuning sensory receptors drives new behaviour in various cephalopods, including octopus, squid and cuttlefish. Taken together, the studies offer a basis for understanding how subtle structural adaptations can drive novel traits and behaviours that are suited to specific ecological contexts.

  • No. 7955 6 April 2023

    Tumour promotion

    In 1947, Isaac Berenblum proposed that the development of cancer was a two-stage process: the first step introduces mutations into healthy cells, the second then promotes tumour growth through tissue inflammation. In this week’s issue, Charles Swanton and his colleagues investigate the role of particulate matter in prompting the development of non-small-cell lung cancers and find that cancer initiation in response to pollution conforms to Berenblum’s model. The researchers investigated especially fine particles called PM2.5, which are smaller than 2.5 micrometres and are typically found in smoke and vehicle emissions. Looking at nearly 33,000 people from four countries, they found a clear link between prolonged exposure to PM2.5 and the development of lung cancers observed in people who had never smoked. In further studies in mice, the team found that PM2.5 seems to trigger an influx of immune cells and the release of the signalling molecule interleukin-1β in lung cells, which exacerbates inflammation and helps drive tumour progression in cells in normal tissue with specific cancer-driver mutations. Taken together, the results suggest that PM2.5 could act as a tumour promoter and could aggravate existing cancerous mutations present in normal tissue.