Reviews & Analysis

Proteins that move and manipulate DNA share certain properties that are crucial for the preservation of the genetic material. Such proteins are often large and multimeric, they require energy to enforce the reaction directionality, they move stochastically and their activity changes DNA topology.

Plant-pathogenic bacteria use several virulence strategies to infect their hosts. Recent developments have dissected the sophisticated molecular mechanisms that are used by bacterial pathogens to interfere with pathogen-recognition receptor-mediated defences and to manipulate important plant processes to promote pathogenesis.

Recent studies have challenged the view that transcription is predominantly regulated at the level of RNA polymerase II recruitment to promoters. Transcription is also regulated at the level of elongation by factors that act directly upon RNA polymerase II or that manipulate the chromatin environment.

The use of mouse models has provided a wealth of data regarding the molecular mechanisms that control cardiac hypertrophy, ventricular remodelling and heart failure. Many of the signalling components involved are potential therapeutic targets for treating various forms of heart disease.

A subset of intracellular transmembrane proteins such as acid-hydrolase receptors, as well as extracellular toxins such as Shiga toxin, undergoes retrograde transport from endosomes to thetrans-Golgi network. Recent studies have begun to provide insights into the molecular machinery involved.

The extensive biochemical and molecular characterization of telomerase holoenzymes has provided new insights into the regulation and function of this specialized polymerase in different model organisms. New approaches are now required to investigate telomerases in physiological context.

The transfer of poly(ADP-ribose) (PAR) to proteins is mediated by the growing family of PAR polymerases. This post-translational modification regulates many important cellular processes, including maintenance of genome integrity, gene expression and cell division, and is emerging as an important epigenetic mark.

Proteins are controlled by post-translational modifications that can be recognized by specific protein-interaction domains. These domains read the state of the proteome and therefore couple post-translational modifications to cellular organization. But how domodification-dependent interactionssynergize to regulate cell behaviour?

The ERBB network is one of the most studied areas in signal transduction, and it exemplifies the pathogenic power of aberrant signalling. Systems-level modelling and an understanding of the network's circuitry, robustness and controls will enable the development of novel cancer therapies.

The exosome complex of 3′→5′ exoribonucleases degrades many types of RNA in the nucleus and the cytoplasm that are targeted by the cell's RNA-surveillance machinery. It is also responsible for the precise trimming of the 3′ ends of nuclear RNA precursors during RNA maturation.

Recent advances have shed light on the interactions that occur between pathogens and endocytic pathway components. With the aim of generating suitable replication niches, microorganisms use existing cellular pathways and have developed selective and manipulative behaviour to avoid lysosome-mediated killing.

Different chromatin remodellers affect the nucleosome structure in different ways. However, a model that is based on the fact that all remodellers have a catalytic ATPase subunit that resembles known DNA-translocating motor proteins indicates that remodellers function as directional DNA translocases.

Cystic fibrosis transmembrane conductance regulator (CFTR), a Cl⁻-ion channel, assembles into dynamic macromolecular complexes. Understanding how these complexes regulate the intracellular trafficking and activity of CFTR provides a unique insight into the aetiology of cystic fibrosis and other diseases.

Polymerizing actin seems to provide the force for deforming and moving membranes at different steps of the endocytic pathway. Live-cell imaging is shedding light on the order and timing of the molecular events and mechanisms of actin function during endocytosis.

The nonsense-mediated mRNA decay (NMD) pathway ensures that mRNAs that harbour premature termination, or nonsense, codons are targeted for rapid degradation. New insights into the process of NMD have provided unexpected glimpses of the complexity of translation termination.

Post-translational modifications define the functional and structural plasticity of proteins in archaea, prokaryotes and eukaryotes. Combining state-of-the-art technologies in molecular cell biology, protein mass spectrometry and bioinformatics, it is now feasible to study the role of distinct protein post-translational modifications.

ADP-ribosylation factor (ARF) proteins regulate membrane trafficking and actin remodelling along the secretory and endocytic pathways. However, recent evidence has revealed that the function of ARF proteins can influence cellular processes such as phagocytosis, cell division and tumour-cell invasion.

Recent studies have highlighted the crucial role of ubiquitin and ubiquitin-like modifications in the regulation of translesion DNA synthesis and various DNA-repair processes such as homologous recombination, nucleotide-excision repair and base-excision repair.

Vascular endothelial growth factors (VEGFs) regulate vascular development during embryogenesis and angiogenesis in the adult. The recently developed cancer treatments that target VEGF receptor activation highlight the clinical relevance of inhibiting VEGF pathways that are exaggerated in pathological angiogenesis.

Structural maintenance of chromosomes (SMC) proteins are highly conserved ATPases that function in chromosome organization and dynamics. Their unique architecture provides insight into how these protein machines tether, fold and manipulate the genome in an ATP-dependent manner.