Akademik Veri Yönetim Sistemi
Biochemical Genetics, 2026 (SCI-Expanded, Scopus)
The Target of Rapamycin (TOR) signaling pathway is a central regulator of cell growth, metabolism, and aging across eukaryotes. In Saccharomyces cerevisiae, TOR1 deletion extends lifespan, yet the underlying transcriptional architecture remains incompletely characterized. RNA-seq analysis was performed on wild-type and tor1Δ mutant cells during exponential growth in glucose-rich conditions to identify key longevity-associated gene expression changes. Differential expression analysis revealed 3091 genes altered by TOR1 deletion, including 736 annotated as lifespan-related in the Saccharomyces Genome Database. TOR1 deletion triggered broad transcriptional reprogramming, including suppression of ribosome biogenesis and translation machinery, alongside induction of pathways supporting energy conservation, reserve carbohydrate metabolism, and stress resistance. These expression changes reflect a shift toward a metabolically reprogrammed state characterized by enhanced mitochondrial function and cellular redox balance. Promoter motif analysis implicated nutrient- and stress-responsive transcription factors such as Adr1 with its paralog YGR067C, Hap4, Mig1, and Msn4 in regulating these changes. Notably, HXK1 was among the most highly upregulated genes suggesting a potential regulatory role beyond its catalytic function, possibly contributing to transcriptional reprogramming under TOR1-deficient conditions. These findings demonstrate that TOR1 deletion coordinates a survival-oriented transcriptional program through lifespan-associated regulatory circuits. This study supports TORC1 as a central hub linking nutrient sensing to lifespan-related transcriptional networks. These findings provide novel insights into the transcriptional basis of yeast longevity and suggest that targeting TOR-regulated metabolic nodes may represent a promising strategy for modulating aging.