Carbon- and nitrogen-quality signaling to translation are mediated by distinct GATA-type transcription factors

The target of rapamycin (Tor) proteins sense nutrients and control transcri ption and translation relevant to cell growth. Treating cells with the immu nosuppressant rapamycin leads to the intracellular formation of an Fpr1p-ra pamycin-Tor ternary complex that in turn leads to translational down-regula tion. A more rapid effect is a rich transcriptional response resembling tha t when cells are shifted from high- to low-quality carbon or nitrogen sourc es. This transcriptional response is partly mediated by the nutrient-sensit ive transcription factors GLN3 and NIL1 (also named GAT1). Here, we show th at these GATA-type transcription factors control transcriptional responses that mediate translation by several means. Four observations highlight upst ream roles of GATA-type transcription factors in translation. In their abse nce, processes caused by rapamycin or poor nutrients are diminished: transl ation repression. eIF4G protein loss, transcriptional down-regulation of pr oteins involved in translation, and RNA polymerase I/III activity repressio n. The Tor proteins preferentially use Gln3p or Nil1p to downregulate trans lation in response to low-quality nitrogen or carbon. respectively. Functio nal consideration of the genes regulated by Gln3p or Nil1p reveals the logi c of this differential regulation. Besides integrating control of transcrip tion and translation, these transcription factors constitute branches downs tream of the multichannel Tor proteins that can be selectively modulated in response to distinct (carbon- and nitrogen-based) nutrient signals from th e environment.