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Role of nutrient-sensing during the evolutionary adaptation to DNA replication stress
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Resumo(s)
"A central question in evolutionary cell biology is how essential cellular processes can be rewired while maintaining their function. Compensatory evolution, in which
spontaneous mutations restore fitness after genetic or environmental perturbations, provides a powerful framework for studying this plasticity. Under stable, nutrient-rich conditions, compensatory evolution often follows parallel trajectories, with independent
populations converging on similar genetic solutions. However, cells in natural or disease
contexts rarely experience such uniformity. Fluctuating nutrient levels and metabolic
states continuously reshape selective pressures, yet how these factors influence the
robustness and predictability of evolutionary adaptation to stress remains largely
unknown. This thesis investigates compensatory evolution in response to DNA
replication stress induced by the deletion of the replication fork-associated factor CTF4
in Saccharomyces cerevisiae. Previous work showed that adaptation to constitutive replication
stress follows highly predictable trajectories under constant conditions.(...)"
Descrição
Palavras-chave
Evolutionary adaptation Replication stress Environment Nutrient-sensing Target of rapamycin (TOR) complex Saccharomyces cerevisiae