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Yeast High Mobility Group Protein HMO1 Negatively Regulates Its Own Expression
Author(s) -
Xiao Lijuan,
Grove Anne
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.495.14
Subject(s) - biology , high mobility group , microbiology and biotechnology , gene , transcription (linguistics) , transfection , gene knockdown , gene expression , cancer research , genetics , linguistics , philosophy
The Saccharomyces cerevisiae high mobility group protein HMO1 is composed of two DNA binding domains, box A and box B, and a lysine‐rich C‐terminal tail. HMO1 plays various crucial functions in chromosomal dynamics processes, and it has been proposed to coordinate rRNA and ribosomal protein (RP) gene transcription. Strains bearing hmo1 mutant alleles are viable, but have growth defects. For recovery of the growth phenotype, we found that excess HMO1 is deleterious to cell growth, while expression of truncated HMO1 lacking the C‐terminal tail can recover the growth phenotype, suggesting that expression of HMO1 is strictly regulated. A β‐galactosidase reporter construct driven by the Hmo1 promoter was created, and the β‐galactosidase activity assay showed that HMO1 negatively regulates its own expression, and that the C‐terminal tail is unnecessary for this regulation. The hmo1Δ strain is less sensitive to rapamycin, which inhibits the Target of Rapamycin (TOR) kinase. The β‐galactosidase activity assay showed that rapamycin represses HMO1 gene expression, but only when HMO1 is present, which is very similar to what was reported for RP gene expression, where the TOR‐dependent repression of RP genes is alleviated in the absence of HMO1. We therefore propose that HMO1 mediates a similar regulation of its own expression and that of RP genes in response to TOR signaling.