Low concentrations of dimethyl sulphoxide accelerate conjugation and incorporation of glycine and glucosamine intetrahymena

Summary Dimethyl sulphoxide at relatively low comentrations, 0.01 to 1 mM, enhanced the conjugation and cell-to-cell adhesion of complementary strains of matingTetrahymena thermophila. The time required to form stable conjugates was reduced by dimethyl sulphoxide. This chemical stimulated the uptake of glycine and glucosamine from the suspending media. Incorporation of 2-¹⁴C-glycine and 6-³H-D-glucosamine into protein and glycoprotein was enhanced in whole cells, surface membrane and cilia. Incorporation of glucosamine into the microsomal fraction was increased in the dimethyl sulphoxidetreated cells while there was little change in glycine incorporation. There were no detectable changes in glycine and glucosamine incorporation into the nuclear fractions isolated from conjugatingTetrahymena exposed to dimethyl sulphoxide.     

Esterase 6 of Drosophila melanogaster: Kinetics of transfer to females,decay in females and male recovery

Esterase 6 (E.C. 3.1.1.1) is an enzyme in the reproductive system of Drosophila melanogaster and is transferred from males to females at mating. This enzyme is conveyed during the first 3 min of a copulation lasting approximately 20 min and remains active in the female reproductive tract for 1–2 hr after mating. Males require 24–48 hr to recover premating levels of esterase 6 activity. These results suggest that the effect of esterase 6 on the rate of sperm loss in females, which extends to 4 days after mating, is indirect since activity in the female falls rapidly after insemination. It is suggested that esterase 6 may also be a part of a pheromone system which influences female reproductive behaviour.     

Control of Cell Elongation in Nitella by Endogenous Cell Wall pH Gradients: MULTIAXIAL EXTENSIBILITY AND GROWTH STUDIES

The multiaxial stress of turgor pressure was stimulated in vitro by inflating isolated Nitella cell walls with mercury. The initial in vitro extension at pH 6.5, 5 atmospheres pressure, returned the wall approximately to the in vivo stressed length, and did not induce any additional extension during a 15-minute period. Upon release of pressure, a plastic deformation was observed which did not correlate with cell growth rates until the final stages of cell maturation. Since wall plasticity does not correlate with growth rate, a metabolic factor(s) is implicated. Walls at all stages of development exhibited a primary yield stress between 0 and 2 atmospheres, while rapidly growing cells (1-3% per hour) exhibited a secondary yield stress of 4 to 5 atmospheres. The creep rate and plastic deformation of young walls were markedly enhanced by acid buffers (10 millimolar, pH ≤ 5.3).     

Initial stages in the onset of senescence in tobacco leaves

A marked loss of leucine ¹⁴C incorporation occurred in chloroplasts isolated from Nicotiana rustica L. leaves exposed to 24 hours of darkness. This loss is not due to an initial decline in RNA-synthesis potential of the chloroplasts, as was inferred from the extent of UTP incorporation by the isolated chloroplasts. Upon reillumination of the leaves, leucine incorporation by the isolated chloroplasts reverted to its original level within 3 to 4 hours, hence it is doubtful whether the period of 24 hours after detachment should be regarded as the initial phase of leaf senescence.     

Role of Interaction and Nucleoside Diphosphate Kinase B in Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator Function by cAMP-Dependent Protein Kinase A

Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-dependent protein kinase A (PKA) and ATP-regulated chloride channel. Here, we demonstrate that nucleoside diphosphate kinase B (NDPK-B, NM23-H2) forms a functional complex with CFTR. In airway epithelia forskolin/IBMX significantly increases NDPK-B co-localisation with CFTR whereas PKA inhibitors attenuate complex formation. Furthermore, an NDPK-B derived peptide (but not its NDPK-A equivalent) disrupts the NDPK-B/CFTR complex in vitro (19-mers comprising amino acids 36–54 from NDPK-B or NDPK-A). Overlay (Far-Western) and Surface Plasmon Resonance (SPR) analysis both demonstrate that NDPK-B binds CFTR within its first nucleotide binding domain (NBD1, CFTR amino acids 351–727). Analysis of chloride currents reflective of CFTR or outwardly rectifying chloride channels (ORCC, DIDS-sensitive) showed that the 19-mer NDPK-B peptide (but not its NDPK-A equivalent) reduced both chloride conductances. Additionally, the NDPK-B (but not NDPK-A) peptide also attenuated acetylcholine-induced intestinal short circuit currents. In silico analysis of the NBD1/NDPK-B complex reveals an extended interaction surface between the two proteins. This binding zone is also target of the 19-mer NDPK-B peptide, thus confirming its capability to disrupt NDPK-B/CFTR complex. We propose that NDPK-B forms part of the complex that controls chloride currents in epithelia.     

A micro method for simultaneous determination of galactosyltransferase and 5''-nucleotidase activities in cell fractions.

Galactosyltransferase and 5'-nucleotidase were assayed in the same reaction mixture, with ovalbumin as exogenous acceptor of (14-C)galactose and with (3-H)AMP as the substrate for the 5'-nucleotidase assay. The substrates and reaction products of either assay had no significant effect on the activity of the other enzyme.     

Is Working More Costly than Waiting in Monkeys?

We studied how value for instrumental action is discounted by predicted effort and delay. The monkeys were trained to perform instrumental trials that required a bar release when a visual target changed from red-to-green. There were two trial conditions. In delay trials, after the monkeys performed one instrumental trial correctly a reward was delivered 0–7 seconds later. In work trials, the monkeys had to perform 0, 1, or 2 additional instrumental trials to obtain a reward. The lengths of trials in delay matched the time it took to complete work trials. The length of delay or number of trials was indicated by a visual cue presented throughout the trial. Our hypothesis was that the monkeys would all show temporal discounting of reward in the delay trials, and that in the work trials the monkeys’ performance might reflect an additional cost due to working. The error rate increased linearly as remaining cost increased for all 8 monkeys. For 4 monkeys the error rate was significantly larger in work trials than in delay trials (effort sensitive monkeys). For the other 4 monkeys there was no significant difference in error rate (effort insensitive monkeys). Since the error rate has an inverse relation with value for action, these results suggest that value is discounted hyperbolically by effort as well as by delay. Error rates generally increased as the testing sessions progressed and the total reward accumulated (i.e., effect of reward devaluation). The relative impact of delay and effort on error rates was reasonably stable within subjects. Thus, within the monkey population there seems to be a significant dichotomy in the sensitivity governing whether working is more costly than waiting, possibly arising from a constitutional or genetic trait.