Saturday, September 24, 2011

Hot off the presses! Oct 01 Trends Cell Biol

The Oct 01 issue of the Trends Cell Biol is now up on Pubget (About Trends Cell Biol): 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 Cell Biol 21(10):i (2011)
  • Corrigendum: Long noncoding RNAs and human disease: [Trends in Cell Biology 21 (2011), 354–361]
    - Trends Cell Biol 21(10):561 (2011)
  • Essence of life: essential genes of minimal genomes
    - Trends Cell Biol 21(10):562-568 (2011)
    Essential genes are absolutely required for cell survival. Determination of the universal minimal set of genes needed to sustain life is, therefore, expected to contribute greatly to our understanding of life at its simplest level, with applications in medicine and synthetic biology. The search for the minimal genome has led to the identification of often variable gene sets. We argue here that, based on the outcome of these analyses, it is becoming increasingly evident that some genes, and the functions encoded by them, are absolutely necessary for the survival of any living entity, whereas others can be omitted. We also examine ways of determining the minimal genome and discuss possible practical applications of a minimal cell.
  • Taking a "good" look at free radicals in the aging process
    - Trends Cell Biol 21(10):569-576 (2011)
    The mitochondrial free radical theory of aging (MFRTA) proposes that aging is caused by damage to macromolecules by mitochondrial reactive oxygen species (ROS). This is based on the observed association of the rate of aging and the aged phenotype with the generation of ROS and oxidative damage. However, recent findings, in particular in Caenorhabditis elegans but also in rodents, suggest that ROS generation is not the primary or initial cause of aging. Here, we propose that ROS are tightly associated with aging because they play a role in mediating a stress response to age-dependent damage. This could generate the observed correlation between aging and ROS without implying that ROS damage is the earliest trigger or main cause of aging.
  • Axon regeneration mechanisms: insights from C. elegans
    - Trends Cell Biol 21(10):577-584 (2011)
    Understanding the mechanisms of axon regeneration is of great importance to the development of therapeutic treatments for spinal cord injury or stroke. Axon regeneration has long been studied in diverse vertebrate and invertebrate models, but until recently had not been analyzed in the genetically tractable model organism Caenorhabditis elegans. The small size, simple neuroanatomy, and transparency of C. elegans allows single fluorescently labeled axons to be severed in live animals using laser microsurgery. Many neurons in C. elegans are capable of regenerative regrowth, and can in some cases re-establish functional connections. Large-scale genetic screens have begun to elucidate the genetic basis of axon regrowth.
  • Central nervous system myelin: structure, synthesis and assembly
    - Trends Cell Biol 21(10):585-593 (2011)
    The wrapping of multiple layers of myelin membrane sheets around an axon is of fundamental importance for the function of the nervous system. In the central nervous system (CNS) oligodendrocytes synthesize tremendous amounts of cellular membrane to form multiple myelin internodes of highly stable membranes with a specific set of tightly packed lipids and proteins. In recent years, mouse mutants have allowed great advances in our understanding of the functional and structural role of many of the major components of myelin. The challenge now is to extend this knowledge to unravel the molecular machinery and mechanisms required to synthesize, assemble and wrap myelin multiple times around an axon at the appropriate developmental time. Such insight will be essential in designing new therapeutic strategies to promote remyelination in demyelinating disorders such as multiple sclerosis.
  • Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies
    - Trends Cell Biol 21(10):594-603 (2011)
    Intact synaptic homeostasis is a fundamental prerequisite for a healthy brain. Thus, it is not surprising that altered synaptic morphology and function are involved in the molecular pathogenesis of so-called synaptopathies including autism, schizophrenia (SCZ) and Alzheimer's disease (AD). Intriguingly, various recent studies revealed a crucial role of postsynaptic ProSAP/Shank scaffold proteins in all of the aforementioned disorders. Considering these findings, we follow the hypothesis that ProSAP/Shank proteins are key regulators of synaptic development and plasticity with clear-cut isoform-specific roles. We thus propose a model where ProSAP/Shank proteins are in the center of a postsynaptic signaling pathway that is disrupted in several neuropsychiatric disorders.
  • Regulation of microtubule dynamics by TOG-domain proteins XMAP215/Dis1 and CLASP
    - Trends Cell Biol 21(10):604-614 (2011)
    The molecular mechanisms by which microtubule-associated proteins (MAPs) regulate the dynamic properties of microtubules (MTs) are still poorly understood. We review recent advances in our understanding of two conserved families of MAPs, the XMAP215/Dis1 and CLASP family of proteins. In vivo and in vitro studies show that XMAP215 proteins act as microtubule polymerases at MT plus ends to accelerate MT assembly, and CLASP proteins promote MT rescue and suppress MT catastrophe events. These are structurally related proteins that use conserved TOG domains to recruit tubulin dimers to MTs. We discuss models for how these proteins might use these individual tubulin dimers to regulate dynamic behavior of MT plus ends.
  • Regulating Rap small G-proteins in time and space
    - Trends Cell Biol 21(10):615-623 (2011)
    Signaling by the small G-protein Rap is under tight regulation by its GEFs and GAPs. These are multi-domain proteins that are themselves controlled by distinct upstream pathways, and thus couple different extra- and intracellular cues to Rap. The individual RapGEFs and RapGAPs are, in addition, targeted to specific cellular locations by numerous anchoring mechanisms and, consequently, may control different pools of Rap. Here, we review the various activating signals and targeting mechanisms of these proteins and discuss their contribution to the spatiotemporal regulation and biological functions of the Rap proteins.

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