| description |
In eukaryotic cells, ribosome production requires the activity of all three RNA polymerases along with enormous amounts of energy and resources. Therefore, it is strictly and coordinately regulated in response to certain environmental conditions. Fpr1 forms a complex with rapamycin, an immunosuppressive agent, and this binary complex inhibits TORC1, a central player of coordinated production of ribosomes. Despite the crucial role of Fpr1 in drug efficacy, its involvement in ribosomal biogenesis under physiological conditions remains unclear. Previous studies revealed that mutation of FPR1 causes synthetic lethality with mutation of HMO1, a well-known transcriptional regulator of ribosomal component genes. Our recent study revealed that deletion of HMO1 and FPR1 decreased transcription of RPL25, which encodes one of essential ribosomal proteins (RPs), thereby causing such a synthetic growth defect. Here, we found that Fpr1 specifically binds to promoters of RPGs including RPL25 in a Rap1-dependent manner, further promoting Fhl1/Ifh1-binding to some specific RPG promoters. Based on these results, we concluded that Fpr1 is a transcriptional regulator of RPGs. |