It has been postulated that a myriad of long noncoding RNAs (lncRNAs) contribute 
to gene regulation. In fission yeast, glucose starvation triggers lncRNA 
transcription across promoter regions of stress-responsive genes including fbp1 
(fructose-1,6-bisphosphatase1). At the fbp1 promoter, this transcription 
promotes chromatin remodeling and fbp1 mRNA expression. Here, we demonstrate 
that such upstream noncoding transcription facilitates promoter association of 
the stress-responsive transcriptional activator Atf1 at the sites of 
transcription, leading to activation of the downstream stress genes. Genome-wide 
analyses revealed that ∼50 Atf1-binding sites show marked decrease in Atf1 
occupancy when cells are treated with a transcription inhibitor. Most of these 
transcription-enhanced Atf1-binding sites are associated with stress-dependent 
induction of the adjacent mRNAs or lncRNAs, as observed in fbp1 These 
Atf1-binding sites exhibit low Atf1 occupancy and high histone density in 
glucose-rich conditions, and undergo dramatic changes in chromatin status after 
glucose depletion: enhanced Atf1 binding, histone eviction, and histone H3 
acetylation. We also found that upstream transcripts bind to the Groucho-Tup1 
type transcriptional corepressors Tup11 and Tup12, and locally antagonize their 
repressive functions on Atf1 binding. These results reveal a new mechanism in 
which upstream noncoding transcription locally magnifies the specific activation 
of stress-inducible genes via counteraction of corepressors.