Hot off the presses! May 01 Nat Rev Mol Cell Biol

The May 01 issue of the Nat Rev Mol Cell Biol is now up on Pubget (About Nat Rev Mol 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:

• From the editors
  - Nat Rev Mol Cell Biol 10(5):299 (2009)
  
• DNA damage response: Higher-order BRCA1 complexity
  - Nat Rev Mol Cell Biol 10(5):301 (2009)
  
• Small RNAs: MicroRNAs get a boost
  - Nat Rev Mol Cell Biol 10(5):302 (2009)
  
• Autophagy: Breaking and exiting
  - Nat Rev Mol Cell Biol 10(5):302 (2009)
  
• Membrane trafficking: Earliest endosomes
  - Nat Rev Mol Cell Biol 10(5):302 (2009)
  
• In brief: Autophagy, Prions, RNA decay, Cell division
  - Nat Rev Mol Cell Biol 10(5):303 (2009)
  
• Cytoskeleton: JMY: actin up in cell motility
  - Nat Rev Mol Cell Biol 10(5):304 (2009)
  
• Epigenetics: A silent inheritance
  - Nat Rev Mol Cell Biol 10(5):304 (2009)
  
• DNA damage response: Change of guard at the checkpoint
  - Nat Rev Mol Cell Biol 10(5):305 (2009)
  
• A new ubiquitin chain, a new signal
  - Nat Rev Mol Cell Biol 10(5):306 (2009)
  
• Technology: Structure provides clues
  - Nat Rev Mol Cell Biol 10(5):306 (2009)
  
• Molecular mechanisms of mTOR-mediated translational control
  - Nat Rev Mol Cell Biol 10(5):307-318 (2009)
  The process of translation requires substantial cellular resources. Cells have therefore evolved complex mechanisms to control overall protein synthesis as well as the translation of specific mRNAs that are crucial for cell growth and proliferation. At the heart of this process is the mammalian target of rapamycin (mTOR) signalling pathway, which senses and responds to nutrient availability, energy sufficiency, stress, hormones and mitogens to modulate protein synthesis. Here, we highlight recent findings on the regulators and effectors of mTOR and discuss specific cases that serve as paradigms for the different modes of mTOR regulation and its control of translation.
• Ubiquitin-like protein activation by E1 enzymes: the apex for downstream signalling pathways
  - Nat Rev Mol Cell Biol 10(5):319-331 (2009)
  Attachment of ubiquitin or ubiquitin-like proteins (known as UBLs) to their targets through multienzyme cascades is a central mechanism to modulate protein functions. This process is initiated by a family of mechanistically and structurally related E1 (or activating) enzymes. These activate UBLs through carboxy-terminal adenylation and thiol transfer, and coordinate the use of UBLs in specific downstream pathways by charging cognate E2 (or conjugating) enzymes, which then interact with the downstream ubiquitylation machinery to coordinate the modification of the target. A broad understanding of how E1 enzymes activate UBLs and how they selectively coordinate UBLs with downstream function has come from enzymatic, structural and genetic studies.
• The trip of the tip: understanding the growth cone machinery
  - Nat Rev Mol Cell Biol 10(5):332-343 (2009)
  The central component in the road trip of axon guidance is the growth cone, a dynamic structure that is located at the tip of the growing axon. During its journey, the growth cone comprises both 'vehicle' and 'navigator'. Whereas the 'vehicle' maintains growth cone movement and contains the cytoskeletal structural elements of its framework, a motor to move forward and a mechanism to provide traction on the 'road', the 'navigator' aspect guides this system with spatial bias to translate environmental signals into directional movement. The understanding of the functions and regulation of the vehicle and navigator provides new insights into the cell biology of growth cone guidance.
• Ion channels versus ion pumps: the principal difference, in principle
  - Nat Rev Mol Cell Biol 10(5):344-352 (2009)
  The incessant traffic of ions across cell membranes is controlled by two kinds of border guards: ion channels and ion pumps. Open channels let selected ions diffuse rapidly down electrical and concentration gradients, whereas ion pumps labour tirelessly to maintain the gradients by consuming energy to slowly move ions thermodynamically uphill. Because of the diametrically opposed tasks and the divergent speeds of channels and pumps, they have traditionally been viewed as completely different entities, as alike as chalk and cheese. But new structural and mechanistic information about both of these classes of molecular machines challenges this comfortable separation and forces its re-evaluation.
• Bringing up the rear: defining the roles of the uropod
  - Nat Rev Mol Cell Biol 10(5):353-359 (2009)
  Renewed interest in cell shape has been prompted by a recent flood of evidence that indicates that cell polarity is essential for the biology of motile cells. The uropod, a protrusion at the rear of amoeboid motile cells such as leukocytes, exemplifies the importance of morphology in cell motility. Remodelling of cell shape by uropod-interfering agents disturbs cell migration. But even though the mechanisms by which uropods regulate cell migration are beginning to emerge, their functional significance remains enigmatic.
• The evolving understanding of COPI vesicle formation
  - Nat Rev Mol Cell Biol 10(5):360-364 (2009)
  The coat protein I (COPI) complex is considered to be one of the best-characterized coat complexes. Studies on how it functions in vesicle formation have provided seminal contributions to the general paradigm in vesicular transport that the ADP-ribosylation factor (ARF) small GTPases are key regulators of coat complexes. Here, we discuss emerging evidence that suggests the need to revise some long-held views on how COPI vesicle formation is achieved.
• Corrigendum: Polo-like kinases: conservation and divergence in their functions and regulation
  - Nat Rev Mol Cell Biol 10(5):364 (2009)
  Nature Reviews Molecular Cell Biology 10, 265–675 | doi:10.1038/nrm2653 The authors would like to amend the text of the article on page 267 and in the legend of figure 1 owing to potentially misleading information. On page 267, right column, the sentence beginning on the fourth line from the bottom should read as follows: "Additionally, PLK1 promotes the centrosomal association of sSGO1, a splice variant of shugoshin 1 (SGO1, also known as SGOL1 in humans; see below) that mediates centriole cohesion46." In the figure 1 legend, part b should read as follows: "Plks function in centriole and centrosome biogenesis in animal cells. PLK4 has a conserved role in driving centriole duplication in S phase, and PLK2 also functions in this process. PLK1 (in humans) and Polo (in Drosophila melanogaster) promote centrosome maturation and function in the G2 and M phases by acting on several targets."