Clays are of paramount importance for soil stability, but also in applications ranging from oil recovery to composites and hydrogels. Generically, clays are divided into two subclasses: macroscopically swelling, ‘active’ clays that have the capacity for taking up large amounts of water to form stable gels, and ‘passive’ or non-swelling clays; the former stabilize soils whereas the latter are known to lead to landslides. However, it has been unclear so far what mechanisms underlie clay swelling. Here, we report the first observation of a temperature-induced transition from a passive to an active, swelling clay. We propose a simple description of the swelling transition; while net attractive interactions are dominant at low temperatures so that the clay particles remain attached to each other in stacks, at higher temperatures it is energetically favourable for the clay to swell due to the entropy that is gained by counterions which are liberated during swelling.

We show experimentally that gaseous CO2 intercalates into the interlayer space of the synthetic smectite clay Na-fluorohectorite at conditions not too far from ambient. The mean interlayer repetition distance of the clay when CO2 is intercalated is found to be 12.5 Å for the conditions -20 °C and 15 bar. The magnitude of the expansion of the interlayer upon intercalation is indistinguishable from that observed in the dehydrated-monohydrated transition for H2O, but the possibility of water intercalation is ruled out by a careful analysis of the experimental conditions and repeating the measurements exposing the clay to nitrogen gas. The dynamics of the process is observed to be dependent on the pressure, with a higher Page 2 of 15 intercalation rate at increased pressure. The rate of CO2 intercalation at the studied conditions is found to be several orders of magnitude slower than the intercalation rate of water or humidity at ambient pressure and temperature.

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Base lesions in DNA can stall the replication machinery or induce mutations if bypassed. Consequently, lesions must be repaired before replication or in a post-replicative process to maintain genomic stability. Base excision repair (BER) is the main pathway for repair of base lesions and is known to be associated with DNA replication, but how BER is organized during replication is unclear. Here we coupled the iPOND (isolation of proteins on nascent DNA) technique with targeted mass-spectrometry analysis, which enabled us to detect all proteins required for BER on nascent DNA and to monitor their spatiotemporal orchestration at replication forks. We demonstrate that XRCC1 and other BER/single-strand break repair (SSBR) proteins are enriched in replisomes in unstressed cells, supporting a cellular capacity of post-replicative BER/SSBR. Importantly, we identify for the first time the DNA glycosylases MYH, UNG2, MPG, NTH1, NEIL1, 2 and 3 on nascent DNA. Our findings suggest that a broad spectrum of DNA base lesions are recognized and repaired by BER in a post-replicative process.