Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning

Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning: "Nadya Kondrashov, Aya Pusic, Craig R. Stumpf, Kunihiko Shimizu, Andrew C. Hsieh, Shifeng Xue, Junko Ishijima, Toshihiko Shiroishi, Maria Barna. Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation. Here we identify mutations of the Ribosomal Protein L38 (...."

An Epigenetic Signature for Monoallelic Olfactory Receptor Expression

An Epigenetic Signature for Monoallelic Olfactory Receptor Expression: "Angeliki Magklara, Angela Yen, Bradley M. Colquitt, E. Josephine Clowney, William Allen, Eirene Markenscoff-Papadimitriou, Zoe A. Evans, Pouya Kheradpour, George Mountoufaris, Catriona Carey, Gilad Barnea, Manolis Kellis, Stavros Lomvardas. Constitutive heterochromatin is traditionally viewed as the static form of heterochromatin that silences pericentromeric and telomeric repeats in a cell cycle- and differentiation-independent mann...."

High conservation of transcription factor binding and evidence for combinatorial regulation across six Drosophila species

High conservation of transcription factor binding and evidence for combinatorial regulation across six Drosophila species: "

High conservation of transcription factor binding and evidence for combinatorial regulation across six Drosophila species

Nature Genetics 43, 414 (2011).
doi:10.1038/ng.808

Authors: Qiye He, Anaïs F Bardet, Brianne Patton, Jennifer Purvis, Jeff Johnston, Ariel Paulson, Madelaine Gogol, Alexander Stark & Julia Zeitlinger

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Growth and development

Growth and development: "

Growth and development

Nature Communications 2, 295 (2011). doi:10.1038/ncomms1322

With a year of publications under its belt, Nature Communications has established itself as an accommodating venue for the natural sciences.

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Formation of stress-specific p53 binding patterns is influenced by chromatin but not by modulation of p53 binding affinity to response elements

Formation of stress-specific p53 binding patterns is influenced by chromatin but not by modulation of p53 binding affinity to response elements: "

The p53 protein is crucial for adapting programs of gene expression in response to stress. Recently, we revealed that this occurs partly through the formation of stress-specific p53 binding patterns. However, the mechanisms that generate these binding patterns remain largely unknown. It is not established whether the selective binding of p53 is achieved through modulation of its binding affinity to certain response elements (REs) or via a chromatin-dependent mechanism. To shed light on this issue, we used a microsphere assay for protein–DNA binding to measure p53 binding patterns on naked DNA. In parallel, we measured p53 binding patterns within chromatin using chromatin immunoprecipitation and DNase I coupled to ligation-mediated polymerase chain reaction footprinting. Through this experimental approach, we revealed that UVB and Nutlin-3 doses, which lead to different cellular outcomes, induce similar p53 binding patterns on naked DNA. Conversely, the same treatments lead to stress-specific p53 binding patterns on chromatin. We show further that altering chromatin remodeling using an histone acetyltransferase inhibitor reduces p53 binding to REs. Altogether, our results reveal that the formation of p53 binding patterns is not due to the modulation of sequence-specific p53 binding affinity. Rather, we propose that chromatin and chromatin remodeling are required in this process.
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Selective interactions of boundaries with upstream region of Abd-B promoter in Drosophila bithorax complex and role of dCTCF in this process

Selective interactions of boundaries with upstream region of Abd-B promoter in Drosophila bithorax complex and role of dCTCF in this process: "

Expression of the genes Ubx, abd-A, and Abd-B of the bithorax complex depends on its cis-regulatory region, which is divided into discrete functional domains (iab). Boundary/insulator elements, named Mcp, Fab-6, Fab-7 and Fab-8 (PTS/F8), have been identified at the borders of the iab domains. Recently, binding sites for a Drosophila homolog of the vertebrate insulator protein CTCF have been identified in Mcp, Fab-6 and Fab-8 and also in several regions that correspond to predicted boundaries, Fab-3 and Fab-4 in particular. Taking into account the inability of the yeast GAL4 activator to stimulate the white promoter when the activator and the promoter are separated by a 5-kb yellow gene, we have tested functional interactions between the boundaries. The results show that all dCTCF-containing boundaries interact with each other. However, inactivation of dCTCF binding sites in Mcp, Fab-6 and PTS/F8 only partially reduces their ability to interact, suggesting the presence of additional protein(s) supporting distant interactions between the boundaries. Interestingly, only Fab-6, Fab-7 (which contains no dCTCF binding sites) and PTS/F8 interact with the upstream region of the Abd-B promoter. Thus, the boundaries might be involved in supporting the specific interactions between iab enhancers and promoters of the bithorax complex.

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Genome-wide analysis reveals novel molecular features of mouse recombination hotspots

Genome-wide analysis reveals novel molecular features of mouse recombination hotspots: "

Genome-wide analysis reveals novel molecular features of mouse recombination hotspots

Nature 472, 7343 (2011). doi:10.1038/nature09869

Authors: Fatima Smagulova, Ivan V. Gregoretti, Kevin Brick, Pavel Khil, R. Daniel Camerini-Otero & Galina V. Petukhova

Meiotic recombination predominantly occurs at discrete genomic loci called recombination hotspots, but the features defining these areas are still largely unknown (reviewed in refs 1–5). To allow a comprehensive analysis of hotspot-associated DNA and chromatin characteristics, we developed a direct molecular approach for mapping meiotic DNA double-strand breaks that initiate recombination. Here we present the genome-wide distribution of recombination initiation sites in the mouse genome. Hotspot centres are mapped with approximately 200-nucleotide precision, which allows analysis of the fine structural details of the preferred recombination sites. We determine that hotspots share a centrally distributed consensus motif, possess a nucleotide skew that changes polarity at the centres of hotspots and have an intrinsic preference to be occupied by a nucleosome. Furthermore, we find that the vast majority of recombination initiation sites in mouse males are associated with testis-specific trimethylation of lysine 4 on histone H3 that is distinct from histone H3 lysine 4 trimethylation marks associated with transcription. The recombination map presented here has been derived from a homogeneous mouse population with a defined genetic background and therefore lends itself to extensive future experimental exploration. We note that the mapping technique developed here does not depend on the availability of genetic markers and hence can be easily adapted to other species with complex genomes. Our findings uncover several fundamental features of mammalian recombination hotspots and underline the power of the new recombination map for future studies of genetic recombination, genome stability and evolution.

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