Latest Articles Include:
- From the editors
- Nat Rev Mol Cell Biol 10(7):437 (2009)
- Cell signalling: An activating inhibitor?
- Nat Rev Mol Cell Biol 10(7):439 (2009)
- Seeing red
- Nat Rev Mol Cell Biol 10(7):440 (2009)
- Gene expression: UV-induced coupling
- Nat Rev Mol Cell Biol 10(7):440 (2009)
- Apoptosis: Death by ubiquitylation
- Nat Rev Mol Cell Biol 10(7):441 (2009)
- In brief: Cytoskeleton, Cell division, DNA damage response
- Nat Rev Mol Cell Biol 10(7):441 (2009)
- Membrane trafficking: Lipid sorting and clustering
- Nat Rev Mol Cell Biol 10(7):442 (2009)
- Protein degradation: Assembly from the base
- Nat Rev Mol Cell Biol 10(7):442 (2009)
- In brief: Membrane trafficking, Protein translocation, Development, Cell death
- Nat Rev Mol Cell Biol 10(7):442 (2009)
- Cell signalling: A fertility network
- Nat Rev Mol Cell Biol 10(7):443 (2009)
- Building on the shoulders of giants
- Nat Rev Mol Cell Biol 10(7):444 (2009)
- Gene expression: Complex interactions
- Nat Rev Mol Cell Biol 10(7):444 (2009)
- Collective cell migration in morphogenesis, regeneration and cancer
- Nat Rev Mol Cell Biol 10(7):445-457 (2009)
The collective migration of cells as a cohesive group is a hallmark of the tissue remodelling events that underlie embryonic morphogenesis, wound repair and cancer invasion. In such migration, cells move as sheets, strands, clusters or ducts rather than individually, and use similar actin- and myosin-mediated protrusions and guidance by extrinsic chemotactic and mechanical cues as used by single migratory cells. However, cadherin-based junctions between cells additionally maintain 'supracellular' properties, such as collective polarization, force generation, decision making and, eventually, complex tissue organization. Comparing different types of collective migration at the molecular and cellular level reveals a common mechanistic theme between developmental and cancer research. - Dynamics and diversity in autophagy mechanisms: lessons from yeast
- Nat Rev Mol Cell Biol 10(7):458-467 (2009)
Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy. - Proximal events in Wnt signal transduction
- Nat Rev Mol Cell Biol 10(7):468-477 (2009)
The Wnt family of secreted ligands act through many receptors to stimulate distinct intracellular signalling pathways in embryonic development, in adults and in disease processes. Binding of Wnt to the Frizzled family of receptors and to low density lipoprotein receptor-related protein 5 (LRP5) or LRP6 co-receptors stimulates the intracellular Wnt–beta-catenin signalling pathway, which regulates beta-cateninstability and context-dependent transcription. This signalling pathway controls many processes, such as cell fate determination, cell proliferation and self-renewal of stem and progenitor cells. Intriguingly, the transmembrane receptor Tyr kinases Ror2 and Ryk, as well as Frizzledreceptors that act independently of LRP5 or LRP6, function as receptors for Wnt and activate beta-catenin-independent pathways. This leads to changes in cell movement and polarity and to the antagonism of the beta-catenin pathway. - Boveri revisited: chromosomal instability, aneuploidy and tumorigenesis
- Nat Rev Mol Cell Biol 10(7):478-487 (2009)
The mitotic checkpoint is a major cell cycle control mechanism that guards against chromosome missegregation and the subsequent production of aneuploid daughter cells. Most cancer cells are aneuploid and frequently missegregate chromosomes during mitosis. Indeed, aneuploidy is a common characteristic of tumours, and, for over 100 years, it has been proposed to drive tumour progression. However, recent evidence has revealed that although aneuploidy can increase the potential for cellular transformation, it also acts to antagonize tumorigenesis in certain genetic contexts. A clearer understanding of the tumour suppressive function of aneuploidy might reveal new avenues for anticancer therapy. - Clearing the way for mitosis: is cohesin a target?
- Nat Rev Mol Cell Biol 10(7):489-496 (2009)
In interphase, chromosomes are associated with proteins and RNAs that participate in many processes, such as DNA replication, transcription, recombination and repair of DNA damage. These components (for example, cohesin) might have to be removed during mitosis, as they might become obstacles that inhibit chromosome segregation or reduce its fidelity. Such a clearing mechanism that operates along mitotic chromosomes might require proteins that are implicated in chromosome segregation. I propose that condensin and DNA topoisomerase II (TOP2), as well as separase, help to clear the way for mitosis. - Bio-art: the ethics behind the aesthetics
- Nat Rev Mol Cell Biol 10(7):496-500 (2009)
Bio-art represents a crossover of art and the biological sciences, with living matter, such as genes, cells or animals, as its new media. Such manipulations of life require collaborations with scientists and considerable financial backing. Herein, I consider bio-art that goes 'under the skin' — in which DNA, cells or proteins are used as the media and means — to highlight the ethical implications of reducing life to art.
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