Nanoprocessability of a one-dimensional oxalato-bridged cobalt(II) complex with 1,2,4-triazole

The polymer {[Co(ox)(Htr)₂] · 2H₂O}_n (ox = oxalate dianion; Htr = 1,2,4-triazole) (1) has been synthesized and characterized by FT-IR spectroscopy, thermal analysis, variable-temperature magnetic measurements and X-ray diffraction methods. The physical analysis allows us to propose a one-dimensional structure in which [Co(Htr)₂]²⁺ units are bridged by bis-bidentate oxalato ligands. Magnetic measurements at variable temperature show an overall antiferromagnetic behavior of the compound. Isolated chains of this polymer have been obtained by sonication of 1 in water and deposition on mica or on mica treated with poly-l-lysine. Circular molecules and nano-fibres have been isolated on Highly Oriented Pyrolitic Graphite (HOPG) by casting deposition of sonicated solutions of 1 in ethanol. The direct reaction on HOPG surface between Co^II, H₂ox and Htr has proved a useful route to isolate one-dimensional systems on surfaces. The development of new strategies to characterize these types of polymers on surfaces opens the possibility to perform nano-scale studies on their properties and their potential use as nano-materials.     

Creation of an allosteric phosphofructokinase starting with a nonallosteric enzyme. The case of dictyostelium discoideum phosphofructokinase.

An allosteric phosphofructokinase (PFK) was created by sequence manipulation of the nonallosteric enzyme from the slime mold Dictyostelium discoideum (DdPFK). Most amino acid residues proposed as important for catalytic and allosteric sites are conserved in DdPFK except for a few of them, and their reversion did not modify its kinetic behavior. However, deletions at the unique C-terminal extension of this PFK produced a markedly allosteric enzyme. Thus, a mutant lacking the last 26 C-terminal residues exhibited hysteresis in the time course, intense cooperativity (n(H) = 3.8), and a 200-fold decrease in the apparent affinity for fructose 6-phosphate (S(0.5) = 4500 microm), strong activation by fructose 2,6-bisphosphate (K(act) = 0.1 microm) and fructose 1,6-bisphosphate (K(act) = 40 microm), dependence on enzyme concentration, proton inhibition, and subunit association-dissociation in response to fructose 6-phosphate versus the nonhysteretic and hyperbolic wild-type enzyme (n(H) = 1.0; K(m) = 22 microm) that remained as a stable tetramer. Systematic deletions and point mutations at the C-tail region of DdPFK identified the last C-terminal residue, Leu(834), as critical to produce a nonallosteric enzyme. All allosteric mutants were practically insensitive to MgATP inhibition, suggesting that this effect does not involve the same allosteric transition as that responsible for fructose 6-phosphate cooperativity and fructose bisphosphate activation.     

Chromothripsis: Breakage-fusion-bridge over and over again

The acquisition of massive but localized chromosome translocations, a phenomenon termed chromothripsis, has received widespread attention since its discovery over a year ago. Until recently, chromothripsis was believed to originate from a single catastrophic event, but the molecular mechanisms leading to this event are yet to be uncovered. Because a thorough interpretation of the data are missing, the phenomenon itself has wrongly acquired the status of a mechanism used to justify many kinds of complex rearrangements. Although the assumption that all translocations in chromothripsis originate from a single event has met with criticism, satisfactory explanations for the intense but localized nature of this phenomenon are still missing. Here, we show why the data used to describe massive catastrophic rearrangements are incompatible with a model comprising a single event only and propose a molecular mechanism in which a combination of known cellular pathways accounts for chromothripsis. Instead of a single traumatic event, the protection of undamaged chromosomes by telomeres can limit repetitive breakage-fusion-bridge events to a single chromosome arm. Ultimately, common properties of chromosomal instability, such as aneuploidy and centromere fission, might establish the complex genetic pattern observed in this genomic state.