In the past few decades, an individual's experience and body condition have been shown to affect not only its traits, but also those of offspring and subsequent generations, known as transgenerational effects. A recent study in the flour beetle Tribolium castaneum demonstrated that female age and density impacted fecundity and egg-laying preference for a novel resource. I tested the prediction that female age and density impact fitness related traits such as fecundity and the speed of offspring development, potentially influencing subsequent evolution. I used the flour beetle, Tribolium castaneum for experimental evolution in a full factorial design, with populations founded by young or old females sourced from either low or high density populations. Founder context had immediate consequences on fecundity and oviposition resource choice across fifteen generations of evolution, and by generation 15, the four founder treatments had similar fecundity and preference values. Founder context affected the harmonic mean size, however, populations had similar size dynamics. Founder context also influenced the impact of an inadvertent parasitic infection on populations. While the mechanisms underlying parental founder effects remain unclear, clearly founder context needs to be considered while assessing evolutionary outcomes.

Ligand-induced transcription relies on enhancer clusters, but what keeps these regulatory hubs primed for rapid activation? In estrogen-responsive genes, enhancer clusters are swiftly decorated by estrogen receptor-alpha (ER alpha) within minutes of ligand stimulation, far too fast for traditional chromatin remodeling, suggesting they are maintained in a poised state by unknown factors. Yet, this activation is transient; ER alpha-bound clusters lose their strength as ER-alpha dissociates approximately three hours post-stimulation, raising a fundamental question: how do these clusters remain accessible between successive cycles of estrogen signaling? Such as those occurring during the menstrual cycle. Here, we reveal a surprising mechanism: in the absence of ER alpha, at the end of signaling, the androgen receptor (AR) steps in as a placeholder, primarily occupying estrogen response elements (EREs) and, to a lesser extent, AR and FOXA1 binding sites. This placeholder function is mediated by direct DNA binding, as mutations in ARs DNA-binding domain abolish its recruitment. Strikingly, when AR cannot bind, FOXA1 floods these enhancer clusters, dramatically increasing chromatin activity and priming them for even stronger ER alpha binding in the next round of estrogen stimulation. This suggests that AR passively maintains enhancer clusters in an optimal poised state, preventing excessive FOXA1-driven enhancer reprogramming, an event linked to transcriptional rewiring in breast cancer cells. Our findings redefine enhancer regulation, revealing a dynamic interplay between transcription factors that safeguard enhancer clusters between signaling cycles. By demonstrating functional redundancy at these regulatory elements, we challenge the conventional separation between pioneering and transcription factors, shedding new light on how enhancer landscapes are maintained and reshaped over time.