DNA methylation regulates phenotype-dependent transcriptional activity in Candida albicans

DNA methylation is a common epigenetic signaling mechanism associated with silencing of repeated DNA and transcriptional regulation in eukaryotes. Here we report that DNA methylation in the human fungal pathogen Candida albicans is primarily localized within structural genes and modulates transcript...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 108; no. 29; pp. 11965 - 11970
Main Authors Mishra, Prashant K, Baum, Mary, Carbon, John
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 19.07.2011
National Acad Sciences
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Summary:DNA methylation is a common epigenetic signaling mechanism associated with silencing of repeated DNA and transcriptional regulation in eukaryotes. Here we report that DNA methylation in the human fungal pathogen Candida albicans is primarily localized within structural genes and modulates transcriptional activity. Major repeat sequences and multigene families are largely free of DNA methylation. Among the genes subject to DNA methylation are those associated with dimorphic transition between yeast and hyphal forms, switching between white and opaque cells, and iron metabolism. Transcriptionally repressed methylated loci showed increased frequency of C-to-T transitions during asexual growth, an evolutionarily stable pattern of repression associated mutation that could bring about genetic alterations under changing environmental or host conditions. Dynamic differential DNA methylation of structural genes may be one factor contributing to morphological plasticity that is cued by nutrition and host interaction.
Bibliography:http://dx.doi.org/10.1073/pnas.1109631108
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Contributed by John Carbon, June 14, 2011 (sent for review January 24, 2011)
1Present address: National Cancer Institute, Bethesda, MD 20889.
Author contributions: P.K.M., M.B., and J.C. designed research; P.K.M. performed research; P.K.M., M.B., and J.C. analyzed data; and P.K.M., M.B., and J.C. wrote the paper.
ISSN:0027-8424
1091-6490
1091-6490
DOI:10.1073/pnas.1109631108