Yeast HMO1 may regulate cell growth through both cytoplasmic and nuclear functions

HMO1 is a Saccharomyces cerevisiae HMGB protein which is required for normal growth. What causes the growth deficiency in hmo1‐ Δ yeast strains is not known. HMO1 has been reported to participate in RNA polymerase I transcription and to interact with the cytoplasmic protein FKBP12. When hmo1‐ Δ strains are transformed with plasmid bearing full length HMO1 (Wt) or an HMO1 truncation lacking the nuclear localization signal (HMO1‐boxAB) under control of a strong promoter (Gal or ADH promoter), only HMO1‐boxAB recovers the growth deficiency, while expression of Wt does not. When transformed with plasmid in which the HMO1 gene is under control of its own promoter, expression of both Wt and HMO1‐boxAB recover the growth deficiency. HMO1 promoter—LacZ fusion has greater activity in hmo1‐ Δ mutant than in wild type cells. These results show that HMO1 downregulates its own expression through binding its promoter. Since FKBP12 is the only reported cytoplasmic protein which interacts with HMO1 physically and genetically, as FKBP12‐rapamycin complex inhibits TOR1 signaling in yeast growth regulation, and since HMO1‐boxAB can restore the growth phenotype, we are exploring the possibility that HMO1 also serves a cytoplasmic function, possibly in the TOR1 signaling pathway.