In social behavior research, the focus often remains on animal dyads, limiting the understanding of complex interactions. Recent trends favor naturalistic setups, offering unique insights into intricate social behaviors. Social behavior stems from chance, individual preferences, and group dynamics, necessitating high-resolution quantitative measurements and statistical modeling. This study leverages the Eco-HAB system, an automated experimental setup that employs radiofrequency identification tracking to observe naturally formed mouse cohorts in a controlled yet naturalistic setting, and uses statistical inference models to decipher rules governing the collective dynamics of groups of 10–15 individuals. Applying maximum entropy models on the coarse-grained co-localization patterns of mice unveils social rules in mouse hordes, quantifying sociability through pairwise interactions within groups, the impact of individual versus social preferences, and the effects of considering interaction structures among three animals instead of two. Reproducing co-localization patterns of individual mice reveals stability over time, with the statistics of the inferred interaction strength capturing social structure. By separating interactions from individual preferences, the study demonstrates that altering neuronal plasticity in the prelimbic cortex – the brain structure crucial for sociability – does not eliminate signatures of social interactions, but makes the transmission of social information between mice more challenging. The study demonstrates how the joint probability distribution of the mice positions can be used to quantify sociability.

Chromosome structure is complex, and many aspects of chromosome organization are still not understood. Measuring the stiffness of chromosomes offers valuable insight into their structural properties. In this study, we analyzed the stiffness of chromosomes from metaphase I (MI) and metaphase II (MII) oocytes. Our results revealed a tenfold increase in stiffness (Young’s modulus) of MI chromosomes compared to somatic chromosomes. Furthermore, the stiffness of MII chromosomes was found to be lower than that of MI chromosomes. We examined the role of meiosis-specific cohesin complexes in regulating chromosome stiffness. Surprisingly, the stiffness of chromosomes from three meiosis-specific cohesin mutants did not significantly differ from that of wild-type chromosomes, indicating that these cohesins may not be primary determinants of chromosome stiffness. Additionally, our findings revealed an age-related increase of chromosome stiffness for MI oocytes. Since aging is associated with elevated levels of DNA damage, we investigated the impact of etoposide-induced DNA damage on chromosome stiffness and found that it led to a reduction in stiffness in MI oocytes. Overall, our study underscores the dynamic and cyclical nature of chromosome stiffness, modulated by both the cell cycle and age-related factors.