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AbstractHsst! Histones rock!pp. 5437–5445Histones were a nuisance to molecular biologists in the early days – they were small, very basic, and did not do anything except neutralizing the charge on DNA. Then nucleosomes were discovered. Containing two sets of histones and a discrete chunk of DNA, they gave us structure. And now they give us targets. Transcriptional accessibility to DNA is regulated, in part, through the addition or removal of acetyl groups on histones. The work reported here by Naldi et al. examines the specificity and kinetics of drugs targeted at the histone deacetylases. This is complicated by the existence of three classes of HDACs: class I‐specific, class II‐specific, and non‐specific types of inhibitors. Each has a different pattern of effectiveness judged by hyperacetylation due to blocking of deacetylation. Over certain ranges of concentration, the inhibitors also affect cell progress through the cell cycle at specific transition points. magnified imageRound and round we go: Listeria monocytogenes in cells and outpp. 5484–5496Listeria monocytogenes has been recognized as a food‐borne pathogen for some time but is still not understood in a detailed proteomic fashion. Enter Van de Velde et al., with cultures stirring and centrifuges spinning, 2‐D DIGE gels running and MALDI power pulsing, asking “where?” and “how?” After identifying ∼400 spots out of ∼1600 resolved, some ∼200 answers have become at least partially visible. Of those, 60 were under‐expressed, with functions including stress defense and transport systems reduced. Over‐expressed were synthesis of cell envelope lipids, fatty acids, and glyceraldehyde‐3‐phosphate. A decrease in expression of D‐alanyl‐D‐alanine ligase reduced the thickness of the cell wall and rendered the cell wall more susceptible to ampicillin, an interesting potential opportunity for new drug. magnified imageCheckers anyone? (or draughts)pp. 5562–5566It seems that there is noise and there is noise – and then there is microarray noise. Structural noise, procedural noise, biological noise, and instrumental noise all contribute to the cacophony. To discern a change of 10% in levels of prostate‐specific antigen by conventional means required Anderson et al. to run 37 replicates. The power of the statistics increased dramatically when samples and controls were arrayed as checkers (samples on the red, controls on the black squares). As a result of the assay changes, CVs improved by 68% and required only two replicates for a 40% change and six replicates for a 10% change. It looks like they may deserve a king or two. magnified image