The longevity bottleneck hypothesis states that early mammals spending over 100 million years as small, short-lived animals led to gene loss or inactivation of traits associated with longevity and left a legacy that is observed in the marked ageing phenotype of modern mammals, in particular long-lived species such as humans.

SOX9⁺ epithelial progenitors at distal tips of lung branches undergo cell allocation and differentiation sequentially along the distal-to-proximal axis. The proximal progeny becomes the conducting airways while the distal descendants produce alveolar cells. This model represents our current understanding of how cell number and fate decisions contribute to lung patterning.

Organisms adapt to environmental demands, ensuring their survival and well-being by modifying cellular identities, shaped by chromatin configurations. Here, we propose that environmental signals are sensed by “Integrators”, orchestrating the epigenetic and transcriptional processes governing cellular identity. Adverse environmental factors such as pollution disrupt epigenetic control contributing to disease development.

Epithelia are the first organized structures to appear during animal development and evolution. Although key characteristics are shared among diverse epithelia, the mechanism they form is highly divergent. The challenge for dividing cells in the early embryo to form the primary epithelium has been resolved in unique ways across Metazoa.

DNA methyltransferase 3B (Dnmt3b) knockout conceptuses show embryonic lethality due to impaired placental formation. These placental cells exhibit aberrant DNA methylation and de-repression of germline genes. We propose that germline gene expression disrupts normal placental development through altered transcript regulation, disrupted cell division, and spurious piRNA silencing of endogenous retroviruses.