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

The Aug 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(8):501 (2009)
  
• Chromosome biology: OCT4 learns to count
  - Nat Rev Mol Cell Biol 10(8):502 (2009)
  
• Cell signalling: Time for work?
  - Nat Rev Mol Cell Biol 10(8):503 (2009)
  
• Entering a new era with Ero
  - Nat Rev Mol Cell Biol 10(8):503 (2009)
  
• mRNA transport: EGL picks up its cargo
  - Nat Rev Mol Cell Biol 10(8):504 (2009)
  
• Cell signalling: Telomerase gets Wnt talking
  - Nat Rev Mol Cell Biol 10(8):504 (2009)
  
• Post-translational modification: The DUB interaction landscape
  - Nat Rev Mol Cell Biol 10(8):505 (2009)
  
• Cancer biology: WAVEing goodbye to invasion
  - Nat Rev Mol Cell Biol 10(8):506 (2009)
  
• Lipid metabolism: An 'IDOL' regulator of blood cholesterol levels
  - Nat Rev Mol Cell Biol 10(8):506 (2009)
  
• Technology Watch: HITS-CLIP hits target, RNA–protein liaisons
  - Nat Rev Mol Cell Biol 10(8):506 (2009)
  
• Gene expression atlas
  - Nat Rev Mol Cell Biol 10(8):506 (2009)
  
• In brief: Stem cells, Cytoskeleton, Chromatin, Cell polarity
  - Nat Rev Mol Cell Biol 10(8):507 (2009)
  
• Follow the mRNA: a new model for Bicoid gradient formation
  - Nat Rev Mol Cell Biol 10(8):509-512 (2009)
  Morphogens are molecules that specify cell fate in a concentration-dependent manner. A classic example is the Bicoid (BCD) protein, for which the prevailing model is that translation of bcd mRNA occurs from a point source at the anterior pole of the Drosophila melanogaster embryo followed by diffusion to produce a protein gradient. This model has been challenged by experiments showing that the diffusion rate of BCD is too slow to establish the protein gradient. The work described in a recent paper has solved this conundrum by demonstrating that a bcd mRNA gradient prefigures the BCD protein gradient.
• Rab GTPases as coordinators of vesicle traffic
  - Nat Rev Mol Cell Biol 10(8):513-525 (2009)
  Membrane trafficking between organelles by vesiculotubular carriers is fundamental to the existence of eukaryotic cells. Central in ensuring that cargoes are delivered to their correct destinations are the Rab GTPases, a large family of small GTPases that control membrane identity and vesicle budding, uncoating, motility and fusion through the recruitment of effector proteins, such as sorting adaptors, tethering factors, kinases, phosphatases and motors. Crosstalk between multiple Rab GTPases through shared effectors, or through effectors that recruit selective Rab activators, ensures the spatiotemporal regulation of vesicle traffic. Functional impairments of Rab pathways are associated with diseases, such as immunodeficiencies, cancer and neurological disorders.
• Epigenetic dynamics of stem cells and cell lineage commitment: digging Waddington's canal
  - Nat Rev Mol Cell Biol 10(8):526-537 (2009)
  Cells of the early mammalian embryo, including pluripotent embryonic stem (ES) cells and primordial germ cells (PGCs), are epigenetically dynamic and heterogeneous. During early development, this heterogeneity of epigenetic states is associated with stochastic expression of lineage-determining transcription factors that establish an intimate crosstalk with epigenetic modifiers. Lineage-specific epigenetic modification of crucial transcription factor loci (for example, methylation of the Elf5 promoter) leads to the restriction of transcriptional circuits and the fixation of lineage fate. The intersection of major epigenetic reprogramming and programming events in the early embryo creates plasticity followed by commitment to the principal cell lineages of the early conceptus.
• Random versus directionally persistent cell migration
  - Nat Rev Mol Cell Biol 10(8):538-549 (2009)
  Directional migration is an important component of cell motility. Although the basic mechanisms of random cell movement are well characterized, no single model explains the complex regulation of directional migration. Multiple factors operate at each step of cell migration to stabilize lamellipodia and maintain directional migration. Factors such as the topography of the extracellular matrix, the cellular polarity machinery, receptor signalling, integrin trafficking, integrin co-receptors and actomyosin contraction converge on regulation of the Rho family of GTPases and the control of lamellipodial protrusions to promote directional migration.
• Breaking the chains: structure and function of the deubiquitinases
  - Nat Rev Mol Cell Biol 10(8):550-563 (2009)
  Ubiquitylation is a reversible protein modification that is implicated in many cellular functions. Recently, much progress has been made in the characterization of a superfamily of isopeptidases that remove ubiquitin: the deubiquitinases (DUBs; also known as deubiquitylating or deubiquitinating enzymes). Far from being uniform in structure and function, these enzymes display a myriad of distinct mechanistic features. The small number (<100) of DUBs might at first suggest a low degree of selectivity; however, DUBs are subject to multiple layers of regulation that modulate both their activity and their specificity. Due to their wide-ranging involvement in key regulatory processes, these enzymes might provide new therapeutic targets.
• An additional role for SUMO in ubiquitin-mediated proteolysis
  - Nat Rev Mol Cell Biol 10(8):564-568 (2009)
  Although the post-translational modification of proteins with small ubiquitin-like modifier (SUMO) has a role in many biological processes, it was thought that SUMO, unlike ubiquitin, does not target proteins for degradation. However, these views need to be revised, as recent findings in yeast and human cells indicate that SUMO can act as a signal for the recruitment of E3 ubiquitin ligases, which leads to the ubiquitylation and degradation of the modified protein.
• Growth, fluctuation and switching at microtubule plus ends
  - Nat Rev Mol Cell Biol 10(8):569-574 (2009)
  Recent experiments suggest that microtubules do not grow steadily but instead elongate at a rate that varies in time. We argue that this variation might arise from fluctuations in the length of a dynamic GTP–tubulin cap at the microtubule end. We propose that these fluctuations can lead to a switch in the dynamics of a microtubule end between growth and shrinkage, and provide insight into how the sensitivity of this switch can be changed by microtubule polymerases, such as XMAP215, and tensile forces, through the stabilization of initial contacts in the cap.