Repression of the yeast HO gene by the MAT 2 and MATa1 homeodomain proteins

ABSTRACT The two mating types of the yeast Saccharomyces cerevisiae can be interconverted in both homothallic and heterothallic strains. Previous work indicates that all yeast cells contain the information to be both a and α and that the HO gene (in homothallic strains) promotes a change in mating type by causing a change at the mating type locus itself. In both heterothallic and homothallic strains, a defective α mating type locus can be converted to a functional a locus and subsequently to a functional α locus. In contrast, action of the HO gene does not restore mating ability to a strain defective in another gene for mating which is not at the mating type locus. These observations indicate that a yeast cell contains an additional copy (or copies) of α information, and lead to the "cassette" model for mating type interconversion. In this model, HM a and hmα loci are blocs of unexpressed α regulatory information, and HMα and hm a loci are blocs of unexpressed a regulatory information. These blocs are silent because they lack an essential site for expression, and become active upon insertion of this information (or a copy of the information) into the mating type locus by action of the HO gene.

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Identification of Homeodomain Proteins, PBX1 and PREP1, Involved in the Transcription of Murine Leukemia Virus

Molecular and Cellular Biology ◽

10.1128/mcb.23.3.831-841.2003 ◽

2003 ◽

Vol 23 (3) ◽

pp. 831-841 ◽

Cited By ~ 24

Author(s):

Sheng-Hao Chao ◽

John R. Walker ◽

Sumit K. Chanda ◽

Nathanael S. Gray ◽

Jeremy S. Caldwell

Keyword(s):

Murine Leukemia Virus ◽

Kinase Inhibitors ◽

Leukemia Virus ◽

Moloney Murine Leukemia Virus ◽

Viral Transcription ◽

Long Terminal Repeats ◽

Homeodomain Proteins ◽

Cellular Genes ◽

Simplex Virus ◽

Murine Leukemia

ABSTRACT Cyclin-dependent kinase inhibitors (CDKIs) have been shown to block human immunodeficiency virus and herpes simplex virus. It is hypothesized that CDKIs block viral replication by inhibiting transcription of specific cellular genes. Here we find that three CDKIs, flavopiridol, purvalanol A, and methoxy-roscovitine, block Moloney murine leukemia virus (MLV) transcription events. Using gene expression microarray technology to examine the inhibitory effects of CDKIs, we observed a cellular gene, the pre-B-cell leukemia transcription factor 1 (Pbx1) gene, down-regulated by CDKI treatment. The PBX consensus element (PCE), TGATTGAC, is conserved in the long terminal repeats of several murine retroviruses, including Moloney MLV. Mutations in the PCE completely inhibited viral transcription whereas overexpression of PBX1 and a PBX1-associated protein, PREP1, enhanced viral transcription. The interaction between the PCE and PBX1-PREP1 proteins was confirmed by gel shift experiments. Blocking PBX1 protein synthesis resulted in a significant decrease in viral transcription. Collectively, our results represent the first work demonstrating that the homeodomain proteins PBX1 and PREP1 are cellular factors involved in Moloney MLV transcription regulation.

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