Rooting portions of a young pseudosporochnalean from the catskill delta complex of New York

Premise of research. Pseudosporochnales (Cladoxylopsida) were conspicuous elements of the Earth’s earliest forests. Recent evidence has done much to clarify basic aspects of the pseudosporochnalean architecture, but important questions remain about the developmental processes responsible for growth from juvenile individuals to trees of sometimes considerable size. Methodology. Presented here is combined compression/permineralization evidence of a young member of the group from a late Devonian (early Frasnian) locality also containing Eospermatopteris (Wattieza), currently the largest reconstructed pseudosporochnalean tree. Standard pyrite preparations were made and analyzed with reflected light. Pivotal results. The anatomically preserved portion of the trunk with an expanded base lacking a central vascular column shows abundant evidence of appendages with apparent rooting function supplied by traces comprised of primary and often secondary xylem. Traces arise within parenchyma near the trunk center and follow lax courses with multiple divisions outward and downward to the surface, finally enveloping the plant base for some distance. In the upper portion of the specimen, likely near the transition between the base bearing rooting appendages and the aerial shoot, the traces form a vascular plexus toward the periphery of the stem, with the bulk of vascular tissues comprising secondary xylem. Similar but differently oriented vascularization also occurs near the base. Conclusions. Here we hypothesize a unique form of “bipolar” development in this specimen, and potentially all pseudosporochnaleans, by means of a trunk base bearing an appendicular system of positively geotropic rooting appendages. In addition, we hypothesize that diffuse meristematic activity of the base plus the vascular plexus may have a previously unrecognized role in the development of pseudosporochnaleans from the small specimen observed here to large body size. We also suggest that this tissue offers an explanation for the enigmatic genus Xenocladia known from tissue fragments of large size found in coeval marine sediments of New York State. Given current incomplete understanding of development within the Pseudosprochnales, considering the rooting system as sui generis confers the advantage of adequate description of this organ, without necessarily specifying correspondence or homology with other groups

Overexpression of SIRT1 Protects Pancreatic β-Cells Against Cytokine Toxicity by Suppressing the Nuclear Factor-κB Signaling Pathway

OBJECTIVE—SIRT1, a class III histone/protein deacetylase, is known to interfere with the nuclear factor-κB (NF-κB) signaling pathway and thereby has an anti-inflammatory function. Because of the central role of NF-κB in cytokine-mediated pancreatic β-cell damage, we postulated that SIRT1 might work in pancreatic β-cell damage models

A Complete Pathway Model for Lipid A Biosynthesis in Escherichia coli.

Lipid A is a highly conserved component of lipopolysaccharide (LPS), itself a major component of the outer membrane of Gram-negative bacteria. Lipid A is essential to cells and elicits a strong immune response from humans and other animals. We developed a quantitative model of the nine enzyme-catalyzed steps of Escherichia coli lipid A biosynthesis, drawing parameters from the experimental literature. This model accounts for biosynthesis regulation, which occurs through regulated degradation of the LpxC and WaaA (also called KdtA) enzymes. The LpxC degradation signal appears to arise from the lipid A disaccharide concentration, which we deduced from prior results, model results, and new LpxK overexpression results. The model agrees reasonably well with many experimental findings, including the lipid A production rate, the behaviors of mutants with defective LpxA enzymes, correlations between LpxC half-lives and cell generation times, and the effects of LpxK overexpression on LpxC concentrations. Its predictions also differ from some experimental results, which suggest modifications to the current understanding of the lipid A pathway, such as the possibility that LpxD can replace LpxA and that there may be metabolic channeling between LpxH and LpxB. The model shows that WaaA regulation may serve to regulate the lipid A production rate when the 3-deoxy-D-manno-oct-2-ulosonic acid (KDO) concentration is low and/or to control the number of KDO residues that get attached to lipid A. Computation of flux control coefficients showed that LpxC is the rate-limiting enzyme if pathway regulation is ignored, but that LpxK is the rate-limiting enzyme if pathway regulation is present, as it is in real cells. Control also shifts to other enzymes if the pathway substrate concentrations are not in excess. Based on these results, we suggest that LpxK may be a much better drug target than LpxC, which has been pursued most often