605 research outputs found
A statistical comparison of the AMIE derived and DMSPâSSIES observed highâlatitude ionospheric electric field
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95462/1/jgra18089.pd
Cryptic Population Dynamics: Rapid Evolution Masks Trophic Interactions
Trophic relationships, such as those between predator and prey or between pathogen and host, are key interactions linking species in ecological food webs. The structure of these links and their strengths have major consequences for the dynamics and stability of food webs. The existence and strength of particular trophic links has often been assessed using observational data on changes in species abundance through time. Here we show that very strong links can be completely missed by these kinds of analyses when changes in population abundance are accompanied by contemporaneous rapid evolution in the prey or host species. Experimental observations, in rotifer-alga and phage-bacteria chemostats, show that the predator or pathogen can exhibit large-amplitude cycles while the abundance of the prey or host remains essentially constant. We know that the species are tightly linked in these experimental microcosms, but without this knowledge, we would infer from observed patterns in abundance that the species are weakly or not at all linked. Mathematical modeling shows that this kind of cryptic dynamics occurs when there is rapid prey or host evolution for traits conferring defense against attack, and the cost of defense (in terms of tradeoffs with other fitness components) is low. Several predictions of the theory that we developed to explain the rotifer-alga experiments are confirmed in the phage-bacteria experiments, where bacterial evolution could be tracked. Modeling suggests that rapid evolution may also confound experimental approaches to measuring interaction strength, but it identifies certain experimental designs as being more robust against potential confounding by rapid evolution
Cryptic Population Dynamics: Rapid Evolution Masks Trophic Interactions
Trophic relationships, such as those between predator and prey or between pathogen and host, are key interactions linking species in ecological food webs. The structure of these links and their strengths have major consequences for the dynamics and stability of food webs. The existence and strength of particular trophic links has often been assessed using observational data on changes in species abundance through time. Here we show that very strong links can be completely missed by these kinds of analyses when changes in population abundance are accompanied by contemporaneous rapid evolution in the prey or host species. Experimental observations, in rotifer-alga and phage-bacteria chemostats, show that the predator or pathogen can exhibit large-amplitude cycles while the abundance of the prey or host remains essentially constant. We know that the species are tightly linked in these experimental microcosms, but without this knowledge, we would infer from observed patterns in abundance that the species are weakly or not at all linked. Mathematical modeling shows that this kind of cryptic dynamics occurs when there is rapid prey or host evolution for traits conferring defense against attack, and the cost of defense (in terms of tradeoffs with other fitness components) is low. Several predictions of the theory that we developed to explain the rotifer-alga experiments are confirmed in the phage-bacteria experiments, where bacterial evolution could be tracked. Modeling suggests that rapid evolution may also confound experimental approaches to measuring interaction strength, but it identifies certain experimental designs as being more robust against potential confounding by rapid evolution
Effects of rapid prey evolution on predator-prey cycles
We study the qualitative properties of population cycles in a predator-prey
system where genetic variability allows contemporary rapid evolution of the
prey. Previous numerical studies have found that prey evolution in response to
changing predation risk can have major quantitative and qualitative effects on
predator-prey cycles, including: (i) large increases in cycle period, (ii)
changes in phase relations (so that predator and prey are cycling exactly out
of phase, rather than the classical quarter-period phase lag), and (iii)
"cryptic" cycles in which total prey density remains nearly constant while
predator density and prey traits cycle. Here we focus on a chemostat model
motivated by our experimental system [Fussmann et al. 2000,Yoshida et al. 2003]
with algae (prey) and rotifers (predators), in which the prey exhibit rapid
evolution in their level of defense against predation. We show that the effects
of rapid prey evolution are robust and general, and furthermore that they occur
in a specific but biologically relevant region of parameter space: when traits
that greatly reduce predation risk are relatively cheap (in terms of reductions
in other fitness components), when there is coexistence between the two prey
types and the predator, and when the interaction between predators and
undefended prey alone would produce cycles. Because defense has been shown to
be inexpensive, even cost-free, in a number of systems [Andersson and Levin
1999, Gagneux et al. 2006,Yoshida et al. 2004], our discoveries may well be
reproduced in other model systems, and in nature. Finally, some of our key
results are extended to a general model in which functional forms for the
predation rate and prey birth rate are not specified.Comment: 35 pages, 8 figure
Temporal evolution of the transpolar potential after a sharp enhancement in solar wind dynamic pressure
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95384/1/grl23891.pd
The Ubiquitin Ligase Siah2 is a Female-Specific Regulator of Circadian Rhythms and Metabolism
Circadian clocks enable organisms to predict and align their behaviors and physiologies to constant daily day-night environmental cycle. Because the ubiquitin ligase Siah2 has been identified as a potential regulator of circadian clock function in cultured cells, we have used SIAH2-deficient mice to examine its function in vivo. Our experiments demonstrate a striking and unexpected sexually dimorphic effect of SIAH2-deficiency on the regulation of rhythmically expressed genes in the liver. The absence of SIAH2 in females, but not in males, altered the expression of core circadian clock genes and drastically remodeled the rhythmic transcriptome in the liver by increasing the number of day-time expressed genes, and flipping the rhythmic expression from nighttime expressed genes to the daytime. These effects are not readily explained by effects on known sexually dimorphic pathways in females. Moreover, loss of SIAH2 in females, not males, preferentially altered the expression of transcription factors and genes involved in regulating lipid and lipoprotein metabolism. Consequently, SIAH2-deficient females, but not males, displayed disrupted daily lipid and lipoprotein patterns, increased adiposity and impaired metabolic homeostasis. Overall, these data suggest that SIAH2 may be a key component of a female-specific circadian transcriptional output circuit that directs the circadian timing of gene expression to regulate physiological rhythms, at least in the liver. In turn, our findings imply that sex-specific transcriptional mechanisms may closely interact with the circadian clock to tailor overt rhythms for sex-specific needs
Estimation of changes in the force of infection for intestinal and urogenital schistosomiasis in countries with Schistosomiasis Control Initiative-assisted programmes
The last decade has seen an expansion of national schistosomiasis control programmes in Africa based on large-scale preventative chemotherapy. In many areas this has resulted in considerable reductions in infection and morbidity levels in treated individuals. In this paper, we quantify changes in the force of infection (FOI), defined here as the per (human) host parasite establishment rate, to ascertain the impact on transmission of some of these programmes under the umbrella of the Schistosomiasis Control Initiative (SCI)
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