Hot off the presses! Aug 01 Trends Genet

The Aug 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 25(8):i (2009)
  
• Are transposable elements simply silenced or are they under house arrest?
  - Trends Genet 25(8):333-334 (2009)
  Despite their role as key players in evolution, it is commonly thought that transposable elements are selected against and silenced. However, their importance in chromosomal biology and, therefore, cell division suggests that their presence in many eukaryote genomes is the result of their having been selected as major components of heterochromatin.
• What controls nucleosome positions?
  - Trends Genet 25(8):335-343 (2009)
  The DNA of eukaryotic genomes is wrapped in nucleosomes, which strongly distort and occlude the DNA from access to most DNA-binding proteins. An understanding of the mechanisms that control nucleosome positioning along the DNA is thus essential to understanding the binding and action of proteins that carry out essential genetic functions. New genome-wide data on in vivo and in vitro nucleosome positioning greatly advance our understanding of several factors that can influence nucleosome positioning, including DNA sequence preferences, DNA methylation, histone variants and post-translational modifications, higher order chromatin structure, and the actions of transcription factors, chromatin remodelers and other DNA-binding proteins. We discuss how these factors function and ways in which they might be integrated into a unified framework that accounts for both the preservation of nucleosome positioning and the dynamic nucleosome repositioning that occur across biological! conditions, cell types, developmental processes and disease.
• Developmental genome rearrangements in ciliates: a natural genomic subtraction mediated by non-coding transcripts
  - Trends Genet 25(8):344-350 (2009)
  Several classes of non-protein-coding RNAs have recently been identified as epigenetic regulators of developmental genome rearrangements in ciliates, providing an interesting insight into the role of genome-wide transcription. In these unicellular eukaryotes, extensive rearrangements of the germline genome occur during the development of a new somatic macronucleus from the germline micronucleus. Rearrangement patterns are not dictated by the germline sequence, but reproduce the pre-existing rearrangements of the maternal somatic genome, implying a homology-dependent global comparison of germline and somatic genomes. We review recent evidence showing that this is achieved by a natural genomic subtraction, computed by pairing interactions between meiosis-specific, germline scnRNAs (small RNAs that resemble metazoan piRNAs) and longer non-coding transcripts from the somatic genome. We focus on current models for the RNA-based mechanisms enabling the cell to recognize the ! germline sequences to be eliminated from the somatic genome and to maintain an epigenetic memory of rearrangement patterns across sexual generations.
• What's in a name? Y chromosomes, surnames and the genetic genealogy revolution
  - Trends Genet 25(8):351-360 (2009)
  Heritable surnames are highly diverse cultural markers of coancestry in human populations. A patrilineal surname is inherited in the same way as the non-recombining region of the Y chromosome and there should, therefore, be a correlation between the two. Studies of Y haplotypes within surnames, mostly of the British Isles, reveal high levels of coancestry among surname cohorts and the influence of confounding factors, including multiple founders for names, non-paternities and genetic drift. Combining molecular genetics and surname analysis illuminates population structure and history, has potential applications in forensic studies and, in the form of 'genetic genealogy', is an area of rapidly growing interest for the public.
• Genetics of complex neurological disease: challenges and opportunities for modeling epilepsy in mice and rats
  - Trends Genet 25(8):361-367 (2009)
  Currently, 20 genetic variants are known to cause Mendelian forms of human epilepsy, leaving a vast heritability undefined. Rodent models for genetically complex epilepsy have been studied for many years, but only recently have strong candidate genes emerged, including Cacna1 g in the GAERS rat model of absence epilepsy and Kcnj10 in the low seizure threshold of DBA/2 mice. In parallel, a growing number of mouse mutations studied on multiple strain backgrounds reveal the impact of genetic modifiers on seizure severity, incidence or form – perhaps mimicking the complexity seen in humans. The field of experimental genetics in rodents is poised to study discrete epilepsy mutations on a diverse choice of strain backgrounds to develop better models and identify modifiers. But, it must find the right balance between embracing the strain diversity available, with the ability to detect and characterize genetic effects. Using alternative strain backgrounds when studying epile! psy mutations will enhance the modeling of epilepsy as a complex genetic disease.
• Understanding synergy in genetic interactions
  - Trends Genet 25(8):368-376 (2009)
  Synergy occurs when the contribution of two mutations to the phenotype of a double mutant exceeds the expectations from the additive effects of the individual mutations. The molecular characterization of genes involved in synergistic interactions has revealed that synergy mainly results from mutations in functionally related genes. Recent research in Arabidopsis thaliana has advanced our understanding of the scenarios resulting in synergistic phenotypes. Those involving homologous loci usually result from various levels of functional redundancy. Some of these loci fail to complement each other or become dose-dependent in certain multiple mutant combinations, suggesting that the effects of haploinsufficiency and redundancy can combine. Synergy involving non-homologous genes probably reflects the topology of the regulatory or metabolic networks and can arise when pathways that converge at a node are disrupted. The Hub genes provide a remarkable example, these genes have ! an extraordinary number of connections and mutations that interact with many unrelated pathways.