This paper examines whether it is possible to recognise specific patterns of institutionally regulated downward (towards children) and upward (towards the old) intergenerational obligations with regard to care and financial support, and to identify specific country profiles and clusters of countries in Europe. Based on the three-fold conceptualisation of familialism by default, supported familialism and de-familialisation, and using a complex set of indicators, we describe how countries, by means of policies, allocate intergenerational responsibilities between families and the state, also paying attention to their gender impact. The study includes all 27 EU countries and for the first time offers a comparative overview of a diversified set of policies with regard to both children and the old. It concludes that although specific policy profiles emerge with regard to the two sets of obligations, these do not always coincide. Furthermore, contrary to widespread opinion, supported familialism and de-familialisation are not always contrasting policy approaches. In some countries, they actually represent part of an integrated approach to public support of intergenerational obligations. Moreover, the gender impact of supported familialism may be different and even contrary, depending on the specific instrument. Finally, once the road of oversimplification is excluded, only one statistically sound cluster of countries emerges. It is, however, possible to detect groups of countries that are similar. These only partly overlap with prevalent welfare regime types.

We have identified in the Streptococcus pneumoniae genome sequence a two-component system (TCS13, Blp [bacteriocin-like peptide]) which is closely related to quorum-sensing systems regulating cell density-dependent phenotypes such as the development of genetic competence or the production of antimicrobial peptides in lactic acid bacteria. In this study we present evidence that TCS13 is a peptide-sensing system that controls a regulon including genes encoding Blps. Downstream of the Blp TCS (BlpH R) we identified open reading frames (blpAB) that have the potential to encode an ABC transporter that is homologous to the ComA/B export system for the competence-stimulating peptide ComC. The putative translation product of blpC, a small gene located downstream of blpAB, has a leader peptide with a Gly-Gly motif. This leader peptide is typical of precursors processed by this family of transporters. Microarray-based expression profiling showed that a synthetic oligopeptide corresponding to the processed form of BlpC (BlpC*) induces a distinct set of 16 genes. The changes in the expression profile elicited by synthetic BlpC* depend on BlpH since insertional inactivation of its corresponding gene abolishes differential gene induction. Comparison of the promoter regions of the blp genes disclosed a conserved sequence element formed by two imperfect direct repeats upstream of extended ؊10 promoter elements. We propose that BlpH is the sensor for BlpC* and the conserved sequence element is a recognition sequence for the BlpR response regulator.Signaling mechanisms controlling multicellular behavior of bacteria have attracted much attention in current research. In gram-negative bacteria, homoserine-lactone-based communication systems are prominent. Research in this area led to the term "quorum sensing" for phenomena that are controlled by cell density (12). In gram-positive bacteria, quorum sensing is accomplished by signaling systems that depend on the secretion and sensing of small peptides (11,19). At least two different mechanisms for sensing the presence of pheromone-like peptides are known (21). The first involves import of the peptide and interaction with an intracellular factor (22); the second involves binding to the extracellular portion of a membranebound histidine kinase. This leads to the autophosphorylation of the kinase and subsequent activation, e.g., phosphorylation of a cognate response regulator that mediates changes in gene expression. Quorum-sensing systems regulate a plethora of cellular functions. In Staphylococcus aureus, the AgrC-AgrAsystem is involved in the density-dependent regulation of virulence (18). In Lactobacillus strains, the production of bacteriocins is dependent on peptide-regulated two-component systems (TCS) (4, 10). In Streptococcus pneumoniae, the development of genetic competence (the natural ability to take up DNA) has been shown to be regulated by the comC-DE system (29).The com system of S. pneumoniae was the first quorumsensing system for which a biological function was defined. ...

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SummaryBiofilms are communities of surface-attached, matrixembedded microbial cells that can resist antimicrobial chemotherapy and contribute to persistent infections. Using an Escherichia coli biofilm model we found that exposure of bacteria to subinhibitory concentrations of ribosome-targeting antibiotics leads to strong biofilm induction. We present evidence that this effect is elicited by the ribosome in response to translational stress. Biofilm induction involves upregulation of the polysaccharide adhesin poly-b-1,6-N-acetyl-glucosamine (poly-GlcNAc) and two components of the poly-GlcNAc biosynthesis machinery, PgaA and PgaD. Poly-GlcNAc control depends on the bacterial signalling molecules guanosine-bis 3Ј, 5Ј(diphosphate) (ppGpp) and bis-(3Ј-5Ј)-cyclic di-GMP (c-di-GMP). Treatment with translation inhibitors causes a ppGpp hydrolase (SpoT)-mediated reduction of ppGpp levels, resulting in specific derepression of PgaA. Maximal induction of PgaD and poly-GlcNAc synthesis requires the production of c-di-GMP by the dedicated diguanylate cyclase YdeH. Our results identify a novel regulatory mechanism that relies on ppGpp signalling to relay information about ribosomal performance to the Pga machinery, thereby inducing adhesin production and biofilm formation. Based on the important synergistic roles of ppGpp and c-di-GMP in this process, we suggest that interference with bacterial second messenger signalling might represent an effective means for biofilm control during chronic infections.

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