Hot off the presses! Sep 01 Trends Genet

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Latest Articles Include:

• Editorial Board
  - Trends Genet 25(9):i (2009)
  
• Neutral evolution on mammalian protein surfaces
  Conant GC - Trends Genet 25(9):377-381 (2009)
  Because of their low effective population sizes, natural selection is expected to have reduced effectiveness in organisms such as mammals. By comparing the amino acid substitution rates between mammalian protein surfaces and interiors, it was found that almost a third of the proteins surveyed failed to reject the null hypothesis of neutral substitutions among surface residues. Proteins with such partly neutral evolution nonetheless have no fewer protein interactions than do other proteins. I suggest that natural selection can function to preserve protein interactions without requiring strict conservation of the individual residue contacts that impart those interactions.
• Group I-intron trans-splicing and mRNA editing in the mitochondria of placozoan animals
  Burger G Yan Y Javadi P Lang BF - Trends Genet 25(9):381-386 (2009)
  Placozoa – the simplest known free-living animals – have been considered primitive, early diverging metazoans based on mitochondrial genome structure and phylogeny. Here we reanalyze placozoan mitochondrial DNAs, reported to include a highly unorthodox, fragmented and incomplete cox1 gene. We discover overlooked exons and split group I introns that mediate trans-splicing of the discontinuous placozoan cox1. Furthermore, we find that cox1 expression involves U-to-C editing, reconstituting an otherwise invariant, essential histidine involved in copper binding. These atypical features qualify placozoan mitochondrial gene and genome organization as derived rather than primitive. Whether the Placozoa diverged early or late during metazoan evolution remains unresolved by mitochondrial phylogeny
• Understanding cardiovascular disease through the lens of genome-wide association studies
  Arking DE Chakravarti A - Trends Genet 25(9):387-394 (2009)
  The past few years have seen significant advances in the identification of genetic factors that contribute to complex disease. Progress in cardiovascular diseases (CVD) has been particularly impressive, with genome-wide association studies (GWAS) leading to the identification of 160 loci associated with CVD and its risk factors, many of which implicate new biological pathways. Here we focus on our growing understanding of the genetic contribution to CVD, examining the gene variants that increase the risk of particular CVD events and those underlying traditional CVD risk factors. Although GWAS face several technical challenges, including the potential for both false-positive and false-negative findings, they are starting to provide a unique view of the genetic architecture of a common disease.
• Robustness: mechanisms and consequences
  Masel J Siegal ML - Trends Genet 25(9):395-403 (2009)
  Biological systems are robust to perturbation by mutations and environmental fluctuations. New data are shedding light on the biochemical and network-level mechanisms responsible for robustness. Robustness to mutation might have evolved as an adaptation to reduce the effect of mutations, as a congruent byproduct of adaptive robustness to environmental variation, or as an intrinsic property of biological systems selected for their primary functions. Whatever its mechanism or origin, robustness to mutation results in the accumulation of phenotypically cryptic genetic variation. Partial robustness can lead to pre-adaptation, and thereby might contribute to evolvability. The identification and characterization of phenotypic capacitors – which act as switches of the degree of robustness – are critical to understanding the mechanisms and consequences of robustness.
• More than just orphans: are taxonomically-restricted genes important in evolution?
  Khalturin K Hemmrich G Fraune S Augustin R Bosch TC - Trends Genet 25(9):404-413 (2009)
  Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such 'orphan' or 'taxonomically-restricted' genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes. Here we focus on evidence from Hydra suggesting that taxonomically-restricted genes play a role in the creation of phylum-specific novelties such as cnidocytes, in the generation of morphological diversity, and in the innate defence system. We propose that taxon-specific genes drive morphological specification, enabling organisms to adapt to changing conditions.
• Diversity of Polycomb group complexes in plants: same rules, different players?
  Hennig L Derkacheva M - Trends Genet 25(9):414-423 (2009)
  Polycomb Group (PcG) proteins form an epigenetic memory system that is conserved in plants and animals and controls gene expression during development. Loss of plant PcG proteins leads to loss of organ identity and to cell overproliferation. Our understanding of plant PcG protein function has recently been advanced by the identification of additional proteins required for transcriptional repression by PcG and by the purification of an Arabidopsis PcG protein complex. These data indicate that Polycomb Repressive Complex 2 (PRC2)-like complexes in animals and plants have to associate with Plant Homeo Domain (PHD)-finger proteins for efficient deposition of histone H3 trimethylated at lysine 27 (H3K27me3) and transcriptional repression. Subsequently, H3K27me3 at target genes assist to recruit additional PcG protein complexes – PRC1 in animals and potentially LIKE HETEROCHROMATIN PROTEIN-1 (LHP1) and the RING finger gene product AtRING1 in plants. A picture is emerging i! n which the general mechanisms of PcG protein function are well conserved between animals and plants, but in which individual players have been exchanged during evolution.