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Bacterial infections and antibiotic resistance are an increasing concern for the world. Here the authors report a class of cationic antimicrobial polymers that cluster local facial amphiphilicity from repeating units to enhance interactions with bacterial membranes without requiring a high unfavorable entropic loss.

Lee, Barone et al. engineered a mutant form of LSD1, Y391K, which renders the nucleosome demethylase activity of LSD1 insensitive to Lys14 acetylation of histone H3, providing a useful tool to illuminate the functional consequences of disconnecting histone modification crosstalk.

Antibodies are a primary tool to assess histone post-translational modifications. However, different antibodies and batches might vary in their ability to recognize those modifications, depending on the kind of assay used. Now a systematic analysis of different antibodies and an open database containing the validation results are presented.

The MSL complex is involved in upregulation of genes on the Drosophila melanogaster male X chromosome during dosage compensation. Using mutagenesis, the MSL3 chromodomain is now shown to interact with methylated histone H3K36 and is implicated in the spreading of the dosage-compensation complex from its initial binding sites, defining a process of spreading by activation complexes analogous to that defined for silencing complexes.

Male Drosophila X chromosomes are highly transcribed to achieve dosage parity with females. This process is mediated by the MSL complex, though binding has been detected at only a subset of X chromosomal loci. MSL-dependent histone H4K16 acetylation is now found across the male X, suggesting widespread, but transient, MSL function.

As part of the modENCODE initiative, which aims to characterize functional DNA elements in D. melanogaster and C. elegans, this study presents a genome-wide chromatin landscape of the fruitfly, based on 18 histone modifications. Nine prevalent chromatin states are described. Integrating these analyses with other data types reveals individual characteristics of different genomic elements. The work provides a resource of unprecedented scale for future experimental investigations.

The MSL complex acts on chromatin to and is required for X-chromosome dosage compensation. Chromatin-interacting protein MS (ChIP-MS) is now used to identify proteins and histone modifications interacting with the MSL complex, leading to the identification of CG4747. Functional analysis indicates that this protein is involved in targeting MSL to H3K36me3-containing chromatin.

Different organisms use a variety of mechanisms to compensate for X chromosome dosage imbalance between the sexes. In Drosophila, the MSL complex increases transcription on the single X chromosome of males and is thought to regulate transcription elongation, although mechanistic details have been unclear. Here, a global run-on sequencing technique is used to reveal that the MSL complex seems to enhance transcription by facilitating the progression of RNA polymerase II across the bodies of active X linked genes. In this way, MSL can impose dosage compensation on diverse genes with a wide range of transcription levels along the X chromosome.

A large collection of new modENCODE and ENCODE genome-wide chromatin data sets from cell lines and developmental stages in worm, fly and human are analysed; this reveals many conserved features of chromatin organization among the three organisms, as well as notable differences in the composition and locations of repressive chromatin.

Differences in the sex-chromosome karyotype of many animal species create imbalances between X-chromosome and autosomal gene products that require compensation. Genome-wide analyses have been instrumental in driving recent progress in understanding the transcriptional regulatory mechanisms underlying dosage compensation. This Review focuses on emerging models for dosage compensation in mammals, flies and nematodes.