Cieneguiticeras, a new genus of Tithonian oppeliids (Ammonoidea, Late Jurassic)

The new genus Cieneguiticeras, assigned to the family Oppeliidae, is described on the basis of Andean lower-middle Tithonian ammonites from Arroyo Cieneguita, west-central part of the Neuquén-Mendoza Basin, Argentina. The macroconchs are closely homoeomorphic with Neochetoceras Spath and the microconchs have a ‘glochiceratid’-type morphology. The stratigraphic range of Cieneguiticeras nov. gen. includes the lower and middle Tithonian by means of a succession of two or three species which are interpreted as members of a phyletic lineage. Ammonites from the Tithonian of Cuba, Mexico and France are more or less confidently included in this new genus.     

ANKRD13C acts as a molecular chaperone for G protein-coupled receptors

Although the mechanisms that regulate folding and maturation of newly synthesized G protein-coupled receptors are crucial for their function, they remain poorly characterized. By yeast two-hybrid screening, we have isolated ANKRD13C, a protein of unknown function, as an interacting partner for the DP receptor for prostaglandin D(2). In the present study we report the characterization of this novel protein as a regulator of DP biogenesis and trafficking in the biosynthetic pathway. Co-localization by confocal microscopy with an endoplasmic reticulum (ER) marker, subcellular fractionation experiments, and demonstration of the interaction between ANKRD13C and the cytoplasmic C terminus of DP suggest that ANKRD13C is a protein associated with the cytosolic side of ER membranes. Co-expression of ANKRD13C with DP initially increased receptor protein levels, whereas siRNA-mediated knockdown of endogenous ANKRD13C decreased them. Pulse-chase experiments indicated that ANKRD13C can promote the biogenesis of DP by inhibiting the degradation of newly synthesized receptors. However, a prolonged interaction between ANKRD13C and DP resulted in ER retention of misfolded/unassembled forms of the receptor and to their proteasome-mediated degradation. ANKRD13C also regulated the expression of other GPCRs tested (CRTH2, thromboxane A(2) (TPα), and β2-adrenergic receptor), whereas it did not affect the expression of green fluorescent protein, GRK2 (G protein-coupled receptor kinase 2), and VSVG (vesicular stomatitis virus glycoprotein), showing specificity toward G protein-coupled receptors. Altogether, these results suggest that ANKRD13C acts as a molecular chaperone for G protein-coupled receptors, regulating their biogenesis and exit from the ER.     

Synergy between transcription and mRNA processing events

Processing of eukaryotic pre-mRNAs is an important step for the translation of proteins. These processing events include the addition of a cap structure at the 5' terminus of the pre-mRNA, the splicing out of introns and the acquisition of a polyadenosine tail at the 3' terminus of the pre-mRNA. It has now become apparent that the RNA processing events can significantly influence each other. RNA polymerase II appears as a key player in these processes, cooperating with numerous processing factors that are involved in capping, splicing, and polyadenylation. More specifically, the carboxyterminal domain of the large subunit of the enzyme plays a critical role in coordination of the processing events. The number of interactions between the various RNA processing events identified so far reflects the complexity of these reactions. As more studies focus on these interactions, additional links and cellular partners will undoubtedly be discovered.     

Are ABA,ethylene or their interaction involved in the response of leaf growth to soil water deficit? An analysis using naturally occurring variation or genetic transformation of ABA production in maize

The role of abscisic acid (ABA) and its possible interaction with ethylene in mediating leaf elongation response to soil water deficit are a matter of controversy. To address this question, we used a set of maize genotypes with various levels of ABA either due to natural variability or to genetic transformation targeted on NCED/VP14, a key enzyme of ABA synthesis. The transgenic lines yielded less strong phenotypes than available mutants, making it possible to use them under normal growing conditions. We focused on leaf elongation during night periods in order to avoid the confounding effect of ABA on leaf water status. Our results suggest that over a wide range, internal ABA level (measured in both leaf extracts or xylem sap) has no clear effect on leaf elongation response to soil water deficit, except in the case of an antisense line presenting the strongest reduction in ABA accumulation that showed a slight maintenance of leaf elongation during water deficit. Leaf ethylene production rate was variable and not related to water deficit except in the ABA-deficient transgenic lines where it was increased by water deficit on average but not systematically. Moreover, variability in ethylene production rate was not linked to variability in elongation rate. Our results thus suggest that neither ABA nor ethylene seems to play a major role in the control of leaf elongation response to soil water deficit.     

Phosphoinositide 3-kinase activity controls the chemoattractant-mediated activation and adaptation of adenylyl cyclase

The binding of chemoattractants to cognate G protein-coupled receptors activates a variety of signaling cascades that provide spatial and temporal cues required for chemotaxis. When subjected to uniform stimulation, these responses are transient, showing an initial peak of activation followed by a period of adaptation, in which activity subsides even in the presence of stimulus. A tightly regulated balance between receptor-mediated stimulatory and inhibitory pathways controls the kinetics of activation and subsequent adaptation. In Dictyostelium, the adenylyl cyclase expressed during aggregation (ACA), which synthesizes the chemoattractant cAMP, is essential to relay the signal to neighboring cells. Here, we report that cells lacking phosphoinositide 3-kinase (PI3K) activity are deficient in signal relay. In LY294002-treated cells, this defect is because of a loss of ACA activation. In contrast, in cells lacking PI3K1 and PI3K2, the signal relay defect is because of a loss of ACA adaptation. We propose that the residual low level of 3-phosphoinositides in pi3k(1-/2-) cells is sufficient to generate the initial peak of ACA activity, yet is insufficient to sustain the inhibitory phase required for its adaptation. Thus, PI3K activity is poised to regulate both ACA activation and adaptation, thereby providing a link to ensure the proper balance of counteracting signals required to maintain optimal chemoresponsiveness.     

Predatory Bacteria as Natural Modulators of Vibrio parahaemolyticus and Vibrio vulnificus in Seawater and Oysters

This study shows that naturally occurring Vibrio predatory bacteria (VPB) exert a major role in controlling pathogenic vibrios in seawater and shellfish. The growth and persistence of Vibrio parahaemolyticus and Vibrio vulnificus were assessed in natural seawater and in the Eastern oyster, Crassostrea virginica. The pathogens examined were V. vulnificus strain VV1003, V. parahaemolyticus O1:KUT (KUT stands for K untypeable), and V. parahaemolyticus O3:K6 and corresponding O3:K6 mutants deficient in the toxRS virulence regulatory gene or the rpoS alternative stress response sigma factor gene. Vibrios were selected for streptomycin resistance, which facilitated their enumeration. In natural seawater, oysters bioconcentrated each Vibrio strain for 24 h at 22°C; however, counts rapidly declined to near negligible levels by 72 h. In natural seawater with or without oysters, vibrios decreased more than 3 log units to near negligible levels within 72 h. Neither toxRS nor rpoS had a significant effect on Vibrio levels. In autoclaved seawater, V. parahaemolyticus O3:K6 counts increased 1,000-fold over 72 h. Failure of the vibrios to persist in natural seawater and oysters led to screening of the water samples for VPB on lawns of V. parahaemolyticus O3:K6 host cells. Many VPB, including Bdellovibrio and like organisms (BALOs; Bdellovibrio bacteriovorus and Bacteriovorax stolpii) and Micavibrio aeruginosavorus-like predators, were detected by plaque assay and electron microscopic analysis of plaque-purified isolates from Atlantic, Gulf Coast, and Hawaiian seawater. When V. parahaemolyticus O3:K6 was added to natural seawater containing trace amounts of VPB, Vibrio counts diminished 3 log units to nondetectable levels, while VPB increased 3 log units within 48 h. We propose a new paradigm that VPB are important modulators of pathogenic vibrios in seawater and oysters.     

Association between history and physical examination factors and change in lumbar multifidus muscle thickness after spinal manipulation in patients with low back pain

Understanding the clinical characteristics of patients with low back pain (LBP) who display improved lumbar multifidus (LM) muscle function after spinal manipulative therapy (SMT) may provide insight into a potentially synergistic interaction between SMT and exercise. Therefore, the purpose of this study was to identify the baseline historical and physical examination factors associated with increased contracted LM muscle thickness one week after SMT. Eighty-one participants with LBP underwent a baseline physical examination and ultrasound imaging assessment of the LM muscle during submaximal contraction before and one week after SMT. The relationship between baseline examination variables and 1-week change in contracted LM thickness was assessed using correlation analysis and hierarchical multiple linear regression. Four variables best predicted the magnitude of increases in contracted LM muscle thickness after SMT. When combined, these variables suggest that patients with LBP, (1) that are fairly acute, (2) have at least a moderately good prognosis without focal and irritable symptoms, and (3) exhibit signs of spinal instability, may be the best candidates for a combined SMT and lumbar stabilization exercise (LSE) treatment approach.     

Steady-state increase of cAMP-response element binding protein, Rac, and PAK signaling in presenilin-deficient neurons

Mutations in the genes encoding presenilins (PS1 and PS2) account for the majority of cases of early-onset Alzheimer's disease. PS1 and PS2 form the catalytic center of γ-secretase, an enzyme responsible for intramembraneous proteolysis of several type I transmembrane proteins. Many γ-secretase substrates are coupled to intracellular signaling events such as cAMP-response element binding protein and Rac1/p21-activated kinase pathways, which are associated with synaptic function. Here, we have examined the activation of these pathways in neurons lacking PS1 expression or γ-secretase activity. We found evidence for heightened steady-state activation of cAMP-response element binding protein, Rac1, and p21-activated kinase signaling in PS-deficient neurons. Our study highlights the importance of PS-dependent proteolytic cleavage of γ-secretase substrates in regulating neuronal signal transduction.