TOR inactivation triggers heterochromatin formation in rDNA during glucose starvation

In response to environmental cues, such as nutrient starvation, living organisms modulate gene expression through mechanisms involving histone modifications. Specifically, nutrient depletion inactivates the TOR (target of rapamycin) pathway, leading to reduced expression of ribosomal genes. While these regulatory mechanisms are well elucidated in budding yeast Saccharomyces cerevisiae, their conservation across diverse organisms remains unclear. In this study, we demonstrate that fission yeast Schizosaccharomyces pombe cells repress ribosomal gene transcription through a different mechanism. TORC1, which accumulates in the rDNA region, dissociates upon starvation, resulting in enhanced methylation of H3K9 and heterochromatin formation, facilitated by dissociation of the stress-responsive transcription factor Atf1 and accumulation of the histone chaperone FACT. We propose that this mechanism might be adapted in mammals that possess Suv39H1 and HP1, which are absent in budding yeast. [Display omitted] •TORC1 accumulates in fission yeast rDNA•Heterochromatin forms in rDNA when TORC1 is inactivated by starvation•TORC1 inactivation promotes Atf1 dissociation, resulting in rDNA heterochromatin•The mechanism uncovered in this study is divergent from that in budding yeast Hirai et al. reveal that heterochromatin forms in fission yeast rDNA when the TOR (target of rapamycin) pathway is inactivated during starvation. While the mechanism suppressing rDNA transcription is well studied in budding yeast, the discovered mechanism is likely conserved in higher eukaryotes, such as humans, sharing common heterochromatinization processes with fission yeast.