Predation and fragmentation portrayed in the statistical structure of prey time series

<p>Abstract</p> <p>Background</p> <p>Statistical autoregressive analyses of direct and delayed density dependence are widespread in ecological research. The models suggest that changes in ecological factors affecting density dependence, like predation and landscape heterogeneity are directly portrayed in the first and second order autoregressive parameters, and the models are therefore used to decipher complex biological patterns. However, independent tests of model predictions are complicated by the inherent variability of natural populations, where differences in landscape structure, climate or species composition prevent controlled repeated analyses. To circumvent this problem, we applied second-order autoregressive time series analyses to data generated by a realistic agent-based computer model. The model simulated life history decisions of individual field voles under controlled variations in predator pressure and landscape fragmentation. Analyses were made on three levels: comparisons between predated and non-predated populations, between populations exposed to different types of predators and between populations experiencing different degrees of habitat fragmentation.</p> <p>Results</p> <p>The results are unambiguous: Changes in landscape fragmentation and the numerical response of predators are clearly portrayed in the statistical time series structure as predicted by the autoregressive model. Populations without predators displayed significantly stronger negative direct density dependence than did those exposed to predators, where direct density dependence was only moderately negative. The effects of predation versus no predation had an even stronger effect on the delayed density dependence of the simulated prey populations. In non-predated prey populations, the coefficients of delayed density dependence were distinctly positive, whereas they were negative in predated populations. Similarly, increasing the degree of fragmentation of optimal habitat available to the prey was accompanied with a shift in the delayed density dependence, from strongly negative to gradually becoming less negative.</p> <p>Conclusion</p> <p>We conclude that statistical second-order autoregressive time series analyses are capable of deciphering interactions within and across trophic levels and their effect on direct and delayed density dependence.</p

Constellation Shaping for WDM systems using 256QAM/1024QAM with Probabilistic Optimization

In this paper, probabilistic shaping is numerically and experimentally investigated for increasing the transmission reach of wavelength division multiplexed (WDM) optical communication system employing quadrature amplitude modulation (QAM). An optimized probability mass function (PMF) of the QAM symbols is first found from a modified Blahut-Arimoto algorithm for the optical channel. A turbo coded bit interleaved coded modulation system is then applied, which relies on many-to-one labeling to achieve the desired PMF, thereby achieving shaping gain. Pilot symbols at rate at most 2% are used for synchronization and equalization, making it possible to receive input constellations as large as 1024QAM. The system is evaluated experimentally on a 10 GBaud, 5 channels WDM setup. The maximum system reach is increased w.r.t. standard 1024QAM by 20% at input data rate of 4.65 bits/symbol and up to 75% at 5.46 bits/symbol. It is shown that rate adaptation does not require changing of the modulation format. The performance of the proposed 1024QAM shaped system is validated on all 5 channels of the WDM signal for selected distances and rates. Finally, it was shown via EXIT charts and BER analysis that iterative demapping, while generally beneficial to the system, is not a requirement for achieving the shaping gain.Comment: 10 pages, 12 figures, Journal of Lightwave Technology, 201

The molecular basis of TnrA control by glutamine synthetase in bacillus subtilis

© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.TnrA is amaster regulator of nitrogen assimilation in Bacillus subtilis. This study focuses on the mechanism of how glutamine synthetase (GS) inhibits TnrA function in response to key metabolites ATP, AMP, glutamine, and glutamate. We suggest a model of two mutually exclusive GS conformations governing the interaction with TnrA. Inthe ATP-bound state (A-state), GS is catalytically active but unable to interact with TnrA. This conformation was stabilized by phosphorylated L-methionine sulfoximine (MSX), fixing the enzymein the transition state. When occupied by glutamine (or its analogue MSX), GS resides in a conformation that has high affinity for TnrA (Q-state). The A-and Q-state are mutually exclusive, and in agreement, ATP and glutamine bind to GS in a competitive manner. At elevated concentrations of glutamine, ATP is no longer able to bind GS and to bring it into the A-state. AMP efficiently competes with ATP and prevents formation of the A-state, thereby favoring GS-TnrA interaction. Surface plasmon resonance analysis shows that TnrA bound to a positively regulated promoter fragment binds GS in the Q-state, whereas it rapidly dissociates from a negatively regulated promoter fragment. These data imply that GS controls TnrA activity at positively controlled promoters by shielding the transcription factor in the DNA-bound state. Accordingtosize exclusion and multiangle light scattering analysis, the dodecameric GS can bind three TnrA dimers. The highly interdependent ligand binding properties of GS reveal this enzyme as a sophisticated sensor of the nitrogen and energy state of the cell to control the activity of DNA-bound TnrA

Mutational Analysis of the Cyanobacterial Nitrogen Regulator PipX

PipX provides a functional link between the cyanobacterial global transcriptional regulator NtcA and the signal transduction protein PII, a protein found in all three domains of life as integrators of signals of the nitrogen and carbon balance. PipX, which is toxic in the absence of PII, can form alternative complexes with NtcA and PII and these interactions are respectively stimulated and inhibited by 2-oxoglutarate, providing a mechanism by which PII can modulate expression at the NtcA regulon. Structural information on PipX-NtcA complexes suggests that PipX coactivates NtcA controlled genes by stabilizing the active conformation of NtcA bound to 2-oxoglutarate and by possibly helping recruit RNA polymerase. To get insights into PipX functions, we perform here a mutational analysis of pipX informed by the structures of PipX-PII and PipX-NtcA complexes and evaluate the impact of point mutations on toxicity and gene expression. Two amino acid substitutions (Y32A and E4A) were of particular interest, since they increased PipX toxicity and activated NtcA dependent genes in vivo at lower 2-oxoglutarate levels than wild type PipX. While both mutations impaired complex formation with PII, only Y32A had a negative impact on PipX-NtcA interactions

Inter-annual growth of Arctic charr (Salvelinus alpinus, L.) in relation to climate variation

BACKGROUND: Major changes in climate have been observed in the Arctic and climate models predict further amplification of the enhanced greenhouse effect at high-latitudes leading to increased warming. We propose that warming in the Arctic may affect the annual growth conditions of the cold adapted Arctic charr and that such effects can already be detected retrospectrally using otolith data. RESULTS: Inter-annual growth of the circumpolar Arctic charr (Salvelinus alpinus, L.) was analysed in relation to climatic changes observed in the Arctic during the last two decades. Arctic charr were sampled from six locations at Qeqertarsuaq in West Greenland, where climate data have been recorded since 1990. Two fish populations met the criteria of homogeny and, consequently, only these were used in further analyses. The results demonstrate a complex coupling between annual growth rates and fluctuations in annual mean temperatures and precipitation. Significant changes in temporal patterns of growth were observed between cohorts of 1990 and 2004. CONCLUSION: Differences in pattern of growth appear to be a consequence of climatic changes over the last two decades and we thereby conclude that climatic affects short term and inter-annual growth as well as influencing long term shifts in age-specific growth patterns in population of Arctic charr

Interaction of the general transcription factor TnrA with the PII-like protein GlnK and glutamine synthetase in Bacillus subtilis

TnrA is a master transcription factor regulating nitrogen metabolism in Bacillus subtilis under conditions of nitrogen limitation. When the preferred nitrogen source is in excess, feedback-inhibited glutamine synthetase (GS) has been shown to bind TnrA and disable its activity. In cells grown with an energetically unfavorable nitrogen source such as nitrate, TnrA is fully membrane-bound via a complex of AmtB and GlnK, which are the transmembrane ammonium transporter and its cognate regulator, respectively, originally termed NrgA and NrgB. The complete removal of nitrate from the medium leads to rapid degradation of TnrA in wild-type cells. In contrast, in AmtB-deficient or GlnK-deficient strains, TnrA is neither membrane-bound nor degraded in response to nitrate depletion. Here, we show that TnrA forms either a stable soluble complex with GlnK in the absence of AmtB, or constitutively binds to GS in the absence of GlnK. In vitro, the TnrA C-terminus is responsible for interactions with either GS or GlnK, and this region appears also to mediate proteolysis, suggesting that binding of GlnK or GS protects TnrA from degradation. Surface plasmon resonance detection assays have demonstrated that GS binds to TnrA not only in its feedback-inhibited form, but also in its non-feedback-inhibited form, although less efficiently. TnrA binding to GlnK or GS responds differentially to adenylate nucleotide levels, with ATP weakening interactions with both partners. Structured digital abstract to by () to by () to by () to by () with by () to by () with by () with by () with by () to by () to by () The present paper reveals a novel mechanism for regulating the stability of the general nitrogen-stress transcription factor TnrA in Bacillus subtilis. TnrA remains resistant to intracellular proteolysis as long as it is complexed to either GlnK or glutamine synthetase (GS). Interaction with both proteins occurs via the C-terminus of TnrA, which is also recognized by the proteolytic activity © 2011 The Authors Journal compilation

Inactivation of the general transcription factor TnrA in Bacillus subtilis by proteolysis

Under conditions of nitrogen limitation, the general transcription factor TnrA in Bacillus subtilis activates the expression of genes involved in assimilation of various nitrogen sources. Previously, TnrA activity has been shown to be controlled by protein-protein interaction with glutamine synthetase, the key enzyme of ammonia assimilation. Furthermore, depending on ATP and 2-oxoglutarate levels, TnrA can bind to the GlnK-AmtB complex. Here, we report that upon transfer of nitrate-grown cells to combined nitrogen-depleted medium, TnrA is rapidly eliminated from the cells by proteolysis. As long as TnrA is membrane-bound through GlnK-AmtB interaction it seems to be protected from degradation. Upon removal of nitrogen sources, the localization of TnrA becomes cytosolic and degradation occurs. The proteolytic activity against TnrA was detected in the cytosolic fraction but not in the membrane, and its presence does not depend on the nitrogen regime of cell growth. The proteolytic degradation of TnrA as a response to complete nitrogen starvation might represent a novel mechanism of TnrA control in B. subtilis. © 2008 SGM