A novel downstream regulatory element cooperates with the silencing machinery to repress EPA1 expression in Candida glabrata.

Autor: Gallegos-García V; IPICYT, División de Biología Molecular, Instituto Potosino de Investigación Científica y Tecnológica, San Luis Potosí, San Luis Potosí, 78216, México., Pan SJ, Juárez-Cepeda J, Ramírez-Zavaleta CY, Martin-del-Campo MB, Martínez-Jiménez V, Castaño I, Cormack B, De Las Peñas A
Jazyk: angličtina
Zdroj: Genetics [Genetics] 2012 Apr; Vol. 190 (4), pp. 1285-97. Date of Electronic Publication: 2012 Jan 10.
DOI: 10.1534/genetics.111.138099
Abstrakt: Candida glabrata, an opportunistic fungal pathogen, adheres to mammalian epithelial cells; adherence is mediated primarily by the Epa1 adhesin. EPA1 is a member of a large gene family of ≈ 23 paralogues, which encode putative adhesins. In this study, we address how EPA1 transcription is regulated. Our data show that EPA1 expression is subject to two distinct negative regulatory mechanisms. EPA1 transcription is repressed by subtelomeric silencing: the Sir complex (Sir2-Sir4), Rap1, Rif1, yKu70, and yKu80 are required for full repression. Activation of EPA1 occurs immediately after dilution of stationary phase (SP) cells into fresh media; however, transcription is rapidly repressed again, limiting expression to lag phase, just as the cells exit stationary phase. This repression following lag phase requires a cis-acting regulatory negative element (NE) located in the EPA1 3'-intergenic region and is independent of telomere proximity. Bioinformatic analysis shows that there are 10 copies of the NE-like sequence in the C. glabrata genome associated with other EPA genes as well as non-EPA genes.
Databáze: MEDLINE