Everyday, Scientist Live turns its eyes to the Web around it and highlights news and research across the Internet. Today we look take an extended look at the Open Access debate.
OPEN ACCESS
2008 has been a good year for access to research. Effective New Year's Day, both the Canadian Institutes of Health Research and the Howard Hughes Medical Institute require publicly accessible archiving of papers published by their grantees. Also in January, the European Research Council announced its European Union-wide open-access mandate.
In February, the Harvard Faculty of Arts and Sciences voted to give the University a worldwide license to exercise copyright in each faculty member's scholarly articles for the purpose of making these articles freely available; Harvard Law School committed to mandatory free access in May. In March, the European University Association endorsed open-access repositories, and in April the United States National Institutes of Health Public Access Policy took effect, bringing America's leading sponsor of biomedical research into the impressive circle of agencies that require archiving of papers resulting from the research they fund.
Judging by the ever-increasing number of submissions to PLoS journals, authors appear to be voting with their manuscripts for open access to research.
- The PLoS Medicine Editors (2008) Next Stop, Don't Block the Doors: Opening Up Access to Clinical Trials Results. PLoS Med 5(7): e160 doi:10.1371/journal.pmed.0050160
BIOLOGY
Leaf size depends on cell number and size. However, leaves are not simply the sum of cell size and number; rather, they are under the control of an unknown, organ-wide integration system. The existence of such a system is strongly suggested by two mysterious phenomena: compensation and high-ploidy syndrome. Compensation is characterized by cell enlargement triggered by a significant decrease in cellular proliferation, while plants with high-ploidy syndrome have more than eight sets of homologous chromosomes (8C), resulting in an increase in cell volume, but smaller leaves. Determining the mechanisms underlying these phenomena will provide important insight into the mechanism of multicellular organogenesis.
- Tsukaya H (2008) Controlling Size in Multicellular Organs: Focus on the Leaf. PLoS Biol 6(7): e174 doi:10.1371/journal.pbio.0060174
MICROBIOLOGY
Bacteria are small unicellular organisms who could well enjoy a bohemian life-moving independently wherever and whenever they want to and existing with no regard for conventional rules of behavior. In spite of this apparent freedom, most bacteria abandon their footloose lifestyle as soon as they come into contact with a surface. Irrespective of whether the surface is of biotic or abiotic origin, they clinch to it, forgoing independence in favor of settling down. Similar to animals that gather in flocks and people who live in societies, surface-attached microbes can form networks as multicellular communities called biofilms. Bacterial biofilms are heterogeneous structures of increasing complexity that consist of differently specialized cells enclosed in a self-produced polymeric matrix associated with the surface.
Depending on the setting and the composition of biofilms, they may have either beneficial or detrimental effects on our environment and health. One of the most serious concerns about biofilms is their high antibiotic tolerance, which makes the treatment of infections difficult and contributes to the spread of antibiotic resistance among pathogenic bacteria. A high antibiotic tolerance in biofilm bacteria can partly be explained by a surface-induced change in gene expression, but how does this happen? What are the first critical steps towards an orderly life on a surface and how are these controlled?
These questions have puzzled scientists for a considerable amount of time, and still do. Attempts to solve these questions can be roughly divided into two major approaches: one focusing on physicochemical aspects of cell-surface interactions, the other aiming at elucidating the expression of adhesion-specific genes. When bacteria approach a surface they encounter an energy barrier, and a balance of repulsive and attractive forces determines whether adhesion occurs. Several theoretical models originally developed for colloidal particles have been used to describe this process, including the Derjaguin-Landau-Verwey-Overbeek (DLVO) theory, the thermodynamic approach, and an extended DLVO theory. However, the predictions made for cell-surface interactions in terms of electrostatic interaction forces or interfacial energy have only limited success, because they do not take into account the heterogeneity of bacterial cell surfaces. Bacterial cells not only have a variety of cell surface structures, they also sense and respond to changes in their environment by immediately adjusting their gene expression, which results in dynamic cell surface alterations.
Among surface-induced cellular changes, an altered expression of cell envelope components is of particular interest because it directly affects the mode of intimate cell-surface contact. To understand the genetic basis of the decisions bacteria make upon surface contact, many studies have focused either on the characterization of adhesion factors or on the isolation of biofilm-deficient mutants. During the past decade, a huge interest in biofilm research has resulted in amazing insights into how various cell surface structures affect the rate and extent of attachment, e.g.,, how biofilms grow and develop in coordinated steps, e.g., how the extracellular matrix is produced, e.g., and how bacteria inside biofilms communicate via signal molecules, e.g..
However, the very first steps that actually cause bacteria to stick to a surface and that are required to trigger reprogramming of gene expression are still not well understood. To a large extent, this lack of knowledge is due to a lack of appropriate methodology.
- Otto K (2008) Considering the First Steps toward a Stable and Orderly Way of Bacterial Life. PLoS Biol 6(7): e180 doi:10.1371/journal.pbio.0060180
