Tuesday, September 13, 2011

Hot off the presses! Oct 01 Trends Genet

The Oct 01 issue of the Trends Genet is now up on Pubget (About Trends Genet): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

  • Editorial Board
    - Trends Genet 27(10):i (2011)
  • Speed-bumps ahead for the genetics of later-life diseases
    - Trends Genet 27(10):387-388 (2011)
  • Histone modification: cause or cog?
    - Trends Genet 27(10):389-396 (2011)
    Histone modifications are key components of chromatin packaging but whether they constitute a 'code' has been contested. We believe that the central issue is causality: are histone modifications responsible for differences between chromatin states, or are differences in modifications mostly consequences of dynamic processes, such as transcription and nucleosome remodeling? We find that inferences of causality are often based on correlation and that patterns of some key histone modifications are more easily explained as consequences of nucleosome disruption in the presence of histone modifying enzymes. We suggest that the 35-year-old DNA accessibility paradigm provides a mechanistically sound basis for understanding the role of nucleosomes in gene regulation and epigenetic inheritance. Based on this view, histone modifications and variants contribute to diversification of a chromatin landscape shaped by dynamic processes that are driven primarily by transcription an! d nucleosome remodeling.
  • The molecular origins of evolutionary innovations
    - Trends Genet 27(10):397-410 (2011)
    The history of life is a history of evolutionary innovations, qualitatively new phenotypic traits that endow their bearers with new, often game-changing abilities. We know many individual examples of innovations and their natural history, but we know little about the fundamental principles of phenotypic variability that permit new phenotypes to arise. Most phenotypic innovations result from changes in three classes of systems: metabolic networks, regulatory circuits, and macromolecules. I here highlight two important features that these classes of systems share. The first is the ubiquity of vast genotype networks – connected sets of genotypes with the same phenotype. The second is the great phenotypic diversity of small neighborhoods around different genotypes in genotype space. I here explain that both features are essential for the phenotypic variability that can bring forth qualitatively new phenotypes. Both features emerge from a common cause, the robustness of p! henotypes to perturbations, whose origins are linked to life in changing environments.
  • New and old ways to control meiotic recombination
    - Trends Genet 27(10):411-421 (2011)
    The unique segregation of homologs, rather than sister chromatids, at the first meiotic division requires the formation of crossovers (COs) between homologs by meiotic recombination in most species. Crossovers do not form at random along chromosomes. Rather, their formation is carefully controlled, both at the stage of formation of DNA double-strand breaks (DSBs) that can initiate COs and during the repair of these DSBs. Here, we review control of DSB formation and two recently recognized controls of DSB repair: CO homeostasis and CO invariance. Crossover homeostasis maintains a constant number of COs per cell when the total number of DSBs in a cell is experimentally or stochastically reduced. Crossover invariance maintains a constant CO density (COs per kb of DNA) across much of the genome despite strong DSB hotspots in some intervals. These recently uncovered phenomena show that CO control is even more complex than previously suspected.
  • RNA in pieces
    - Trends Genet 27(10):422-432 (2011)
    Eukaryotic genomes accommodate numerous types of information within diverse DNA and RNA sequence elements. At many loci, these elements overlap and the same sequence is read multiple times during the production, processing, localization, function and turnover of a single transcript. Moreover, two or more transcripts from the same locus might use a common sequence in different ways, to perform distinct biological roles. Recent results show that many transcripts also undergo post-transcriptional cleavage to release specific fragments, which can then function independently. This phenomenon appears remarkably widespread, with even well-documented transcript classes such as messenger RNAs yielding fragments. RNA fragmentation significantly expands the already extraordinary spectrum of transcripts present within eukaryotic cells, and also calls into question how the 'gene' should be defined.
  • Noncoding RNAs and enhancers: complications of a long-distance relationship
    - Trends Genet 27(10):433-439 (2011)
    Spatial and temporal regulation of gene expression is achieved through instructions provided by the distal transcriptional regulatory elements known as enhancers. How enhancers transmit such information to their targets has been the subject of intense investigation. Recent advances in high throughput analysis of the mammalian transcriptome have revealed a surprising result indicating that a large number of enhancers are transcribed to noncoding RNAs. Although long noncoding RNAs were initially shown to confer epigenetic transcriptional repression, recent studies have uncovered a role for a class of such transcripts in gene-specific activation, often from distal genomic regions. In this review, we discuss recent findings on the role of long noncoding RNAs in transcriptional regulation, with an emphasis on new developments on the functional links between long noncoding RNAs and enhancers.

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