Genetic basis for daptomycin resistance in enterococci
Palmer KL, Daniel A, Hardy C, Silverman J, Gilmore MS. Harvard Medical School (HMS).
The emergence of multidrug-resistant enterococci is a public health concern. The authors evolved daptomycin-resistant strains of the multidrug-resistant E. faecalis strain V583. Based on the availability of a fully closed genome sequence for V583, the authors used whole-genome resequencing to identify mutations that became fixed over short time scales (about two weeks) upon serial passage in the presence of daptomycin. Seven candidate daptomycin resistance genes and three different mutational paths to daptomycin resistance in E. faecalis were identified. Results demonstrate a mechanism of enterococcal daptomycin resistance genetically distinct from that occurring in staphylococci. Antimicrobial Agents Chemotherapy. 2011 Jul; 55(7):3345-56.

Genome-wide regulation of 5hmC, 5mC, and gene expression by Tet1 hydroxylase in mouse embryonic stem cells
Xu Y, Wu F, Tan L, Kong L, Xiong L, Deng J, Barbera AJ, Zheng L, Zhang H, Huang S, Min J, Nicholson T, Chen T, Xu G, Shi Y, Zhang K, Shi YG. Brigham and Women’s Hospital, HMS.
DNA methylation at the 5 position of cytosine (5mC) in the mammalian genome is a key epigenetic event. The ten-eleven translocation (Tet) family of 5mC-hydroxylases, which convert 5mC to 5-hydroxymethylcytosine (5hmC), offers a way for dynamic regulation of DNA methylation. The authors report that Tet1 binds to unmodified C or 5mC- or 5hmC-modified CpG-rich DNA through its CXXC domain. Genome-wide mapping of Tet1 and 5hmC reveals mechanisms by which Tet1 controls 5hmC and 5mC levels in mouse embryonic stem cells (mESCs). The authors also uncover a comprehensive gene network influenced by Tet1. Molecular Cell. 2011 May 20; 42(4):451-64.

HIV-1 adaptation to NK-cell-mediated immune pressure
Alter G, Heckerman D, Schneidewind A, Fadda L, Kadie CM, Carlson JM, Oniangue-Ndza C, Martin M, Li B, Khakoo SI, Carrington M, Allen TM. Ragon Institute at MGH, MIT and Harvard; Massachusetts General Hospital; HMS.
Recent studies suggest that natural killer (NK) cells can contribute to the control of HIV-1 infection through recognition of virally infected cells by killer immunoglobulin-like receptors (KIRs). The authors describe KIR-associated amino-acid polymorphisms in the HIV-1 sequence on a population level. They show that these polymorphisms can enhance the binding of inhibitory KIRs to HIV-1-infected CD4(+) T cells and reduce the antiviral activity of KIR-positive NK cells. These data demonstrate that HIV-1 can evade NK-cell-mediated immune pressure by selecting for sequence polymorphisms. NK cells might therefore have an underappreciated role in viral evolution. Nature. 2011 Aug 3; 476(7358):96-100.