Scale Factor Self-Dual Cosmological Models

We implement a conformal time scale factor duality for Friedmann-Robertson-Walker cosmological models, which is consistent with the weak energy condition. The requirement for self-duality determines the equations of state for a broad class of barotropic fluids. We study the example of a universe filled with two interacting fluids, presenting an accelerated and a decelerated period, with manifest UV/IR duality. The associated self-dual scalar field interaction turns out to coincide with the "radiation-like" modified Chaplygin gas models. We present an equivalent realization of them as gauged K\"ahler sigma models (minimally coupled to gravity) with very specific and interrelated K\"ahler- and super-potentials. Their applications in the description of hilltop inflation and also as quintessence models for the late universe are discussed.Comment: v3, improved and extended version to be published in JHEP; new results added to sect.2; 4 figures; 17pg

New Massive Gravity Domain Walls

The properties of the asymptotic $AdS_3$ space-times representing flat domain walls (DW's) solutions of the New Massive 3D Gravity with scalar matter are studied. Our analysis is based on $I^{st}$ order BPS-like equations involving an appropriate superpotential. The Brown-York boundary stress-tensor is used for the calculation of DW's tensions as well as of the $CFT_2$'s central charges. The holographic renormalization group flows and the phase transitions in specific deformed $CFT_2$ dual to 3D massive gravity model with quadratic superpotential are discussed.Comment: 12 pages,v2-misprints corrected,comments concerning BPS eqs. for NMG model in d>3 added in Sect.

Cell Size and the Initiation of DNA Replication in Bacteria

In eukaryotes, DNA replication is coupled to the cell cycle through the actions of cyclin-dependent kinases and associated factors. In bacteria, the prevailing view, based primarily from work in Escherichia coli, is that growth-dependent accumulation of the highly conserved initiator, DnaA, triggers initiation. However, the timing of initiation is unchanged in Bacillus subtilis mutants that are ∼30% smaller than wild-type cells, indicating that achievement of a particular cell size is not obligatory for initiation. Prompted by this finding, we re-examined the link between cell size and initiation in both E. coli and B. subtilis. Although changes in DNA replication have been shown to alter both E. coli and B. subtilis cell size, the converse (the effect of cell size on DNA replication) has not been explored. Here, we report that the mechanisms responsible for coordinating DNA replication with cell size vary between these two model organisms. In contrast to B. subtilis, small E. coli mutants delayed replication initiation until they achieved the size at which wild-type cells initiate. Modest increases in DnaA alleviated the delay, supporting the view that growth-dependent accumulation of DnaA is the trigger for replication initiation in E. coli. Significantly, although small E. coli and B. subtilis cells both maintained wild-type concentration of DnaA, only the E. coli mutants failed to initiate on time. Thus, rather than the concentration, the total amount of DnaA appears to be more important for initiation timing in E. coli. The difference in behavior of the two bacteria appears to lie in the mechanisms that control the activity of DnaA

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field