The body-size dependence of mutual interference.
Ontology highlight
ABSTRACT:
SUBMITTER: DeLong JP
PROVIDER: S-EPMC4090548 | biostudies-literature | 2014 Jun
REPOSITORIES: biostudies-literature
Publications
The parameters that drive population dynamics typically show a relationship with body size. By contrast, there is no theoretical or empirical support for a body-size dependence of mutual interference, which links foraging rates to consumer density. Here, I develop a model to predict that interference may be positively or negatively related to body size depending on how resource body size scales with consumer body size. Over a wide range of body sizes, however, the model predicts that interferenc ...[more]
Similar Datasets
Project description:Interference competition occurs when access to an available resource is negatively affected by interactions with other individuals, where mutual interference involves individuals of the same species. The interactive phenomena among individuals may be size-dependent, since body size is a major factor that may alter prey consumption rates and ultimately the dynamics and structure of food webs.A study was initiated in order to evaluate the effect of mutual interference in the prey-specific attack rates and handling times of same size class predators, incorporating variation in consumer size. For this purpose, laboratory functional response experiments were conducted using same age predators, that is, newly hatched (first instar) or mature (fifth instar) nymphs of the polyphagous mirid predator Macrolophus pygmaeus preying on Ephestia kuehniella (Lepidoptera: Pyralidae) eggs.The experiments involved four predator density treatments, that is, one, two, three, or four predators of same age, that is, either first- or fifth-instar nymphs, which were exposed to several prey densities. The Crowley-Martin model, which allows for interference competition between foraging predators, was used to fit the data.The results showed that mutual interference between predator's nymphs may occur that affect their foraging efficiency. The values of the attack rate coefficient were dependent on the predator density and for the first-instar nymphs were significantly lower at the highest predator density than the lower predator densities, whereas for the fifth-instar nymphs in all density treatments were significantly lower to that of the individual foragers' ones.These results indicate that mutual interference is more intense for larger predators and is more obvious at low prey densities where the competition level is higher. The wider use of predator-dependent functional response models will help toward a mechanistic understanding of intraspecific interactions and its consequences on the stability and structure of food webs.
| S-EPMC7863380 | biostudies-literature
Project description:The average body size of brachiopods from a single habitat type increased gradually by more than two orders of magnitude during their initial Cambrian-Devonian radiation. This increase occurred nearly in parallel across all major brachiopod clades (classes and orders) and is consistent with Cope's rule: the tendency for size to increase over geological time. The increase is not observed within small, constituent clades (represented here by families), which underwent random, unbiased size changes. This scale-dependence is caused by the preferential origination of new families possessing initially larger body sizes. However, this increased family body size does not confer advantages in terms of greater geological duration or genus richness over families possessing smaller body sizes. We suggest that the combination of size-biased origination of families and parallel size increases among major, more inclusive brachiopod clades from a single habitat type is best explained by long-term, secular environmental changes during the Paleozoic that provided opportunities for body size increases associated with major morphological evolution.
| S-EPMC2291137 | biostudies-literature
Project description:During infection with adenovirus, massive changes in the transcription of virus genes are observed, suggesting that the expression of cellular genes may also be modulated. To characterize the levels of cellular RNA species in infected cells, cDNA arrays were screened 24 h after infection of HeLa cells with wild-type adenovirus type 5, strain dl309. Despite complete transduction of the cells, fewer than 20 cellular genes (out of 4,600 analyzed and 1,200 found detectable and expressed above background) were altered more than threefold in their corresponding RNA levels compared to mock-infected cells. In particular, the expression of the myc oncogene was reduced at the mRNA level. This reduction was dependent on the replication of virus DNA and partially dependent on the presence of the adenovirus gene products E1B-55 kDa and E4orf6, but not E4orf3. On the other hand, MYC protein had an increased half-life in infected cells, resulting in roughly constant steady-state protein levels. The adenovirus E1A gene product is necessary and sufficient to stabilize MYC. Overexpressed MYC inhibited adenovirus replication and the proper formation of the virus replication centers. We conclude that adenovirus infection leads to the stabilization of MYC, perhaps as a side effect of E1A activities. On the other hand, myc mRNA levels are negatively regulated during adenovirus infection, and this may avoid the detrimental effect of excessive MYC on adenovirus replication.
| S-EPMC161938 | biostudies-literature
Project description:BackgroundInterference competition occurs when access to resources is negatively affected by the presence of other individuals. Within a species or population, this is known as mutual interference, and it is often modelled with a scaling exponent, m, on the number of predators. Originally, mutual interference was thought to vary along a continuum from prey dependence (no interference; m = 0) to ratio dependence (m = -1), but a debate in the 1990's and early 2000's focused on whether prey or ratio dependence was the better simplification. Some have argued more recently that mutual interference is likely to be mostly intermediate (that is, between prey and ratio dependence), but this possibility has not been evaluated empirically.ResultsWe gathered estimates of mutual interference from the literature, analyzed additional data, and created the largest compilation of unbiased estimates of mutual interference yet produced. In this data set, both the alternatives of prey dependence and ratio dependence were observed, but only one data set was consistent with prey dependence. There was a tendency toward ratio dependence reflected by a median m of -0.7 and a mean m of -0.8.ConclusionsOverall, the data support the hypothesis that interference is mostly intermediate in magnitude. The data also indicate that interference competition is common, at least in the systems studied to date. Significant questions remain regarding how different factors influence interference, and whether interference can be viewed as a characteristic of a particular population or whether it generally shifts from low to high levels as populations increase in density.
| S-EPMC3024213 | biostudies-literature
Project description:Conditional expression of the glucokinase regulatory protein in insulinoma cells, under control of the reverse tetracycline-dependent transactivator, was used to investigate whether expression of this protein de novo would alter the intracellular distribution of glucokinase. The regulatory protein, which was undetectable in the basal state, could be induced by doxycycline to levels comparable to those of liver and was detected mostly in the nucleus. Concomitantly, glucokinase accumulated in the nucleus. Human embryonic kidney cells were transiently transfected to express glucokinase and the regulatory protein, either separately or together. Each protein localized predominantly to the cytoplasm when expressed alone. On co-expression, however, both proteins localized virtually entirely to the nucleus. The enzymic activity of glucokinase was not required for promoting nuclear import of the two proteins, as shown with a glucose-phosphorylation-deficient mutant. Finally, in embryonic kidney cells expressing the regulatory protein alone, treatment with leptomycin B resulted in a partial redistribution of the protein from the cytoplasm to the nucleus, suggesting that this protein can shuttle between the two compartments.
| S-EPMC1221056 | biostudies-other
Project description:Mutual interference involves direct interactions between individuals of the same species that may alter their foraging success. Larvae of aphidophagous coccinellids typically stay within a patch during their lifetime, displaying remarkable aggregation to their prey. Thus, as larvae are exposed to each other, frequent encounters may affect their foraging success. A study was initiated in order to determine the effect of mutual interference in the coccinellids' feeding rate. One to four 4th larval instars of the fourteen-spotted ladybird beetle Propylea quatuordecimpunctata were exposed for 6 hours into plastic containers with different densities of the black bean aphid, Aphis fabae, on potted Vicia faba plants. The data were used to fit a purely prey-dependent Holling type II model and its alternatives which account for interference competition and have thus far been underutilized, i.e. the Beddington-DeAngelis, the Crowley-Martin and a modified Hassell-Varley model. The Crowley-Martin mechanistic model appeared to be slightly better among the competing models. The results showed that although the feeding rate became approximately independent of predator density at high prey density, some predator dependence in the coccinellid's functional response was observed at the low prey-high predator density combination. It appears that at low prey densities, digestion breaks are negligible so that the predators do waste time interfering with each other, whereas at high prey densities time loss during digestion breaks may fully accommodate the cost of interference, so that the time cost may be negligible.
| S-EPMC4710538 | biostudies-literature
Project description:The spatial and temporal coordination of chromosome segregation with cytokinesis is essential to ensure that each daughter cell receives the correct complement of chromosomal and cytoplasmic material. In yeast, mitotic exit and cytokinesis are coordinated by signaling cascades whose terminal components include a nuclear Dbf2-related family kinase and a noncatalytic subunit, Mps one binding (Mob) 1. There are five human Mob1 isoforms, all of which display redundant localization patterns at the spindle poles and kinetochores in early mitosis, and the spindle midzone during cytokinesis. Mob1 shares similar localization patterns to Polo-like kinase (Plk1) and the chromosomal passenger complex (CPC), and although depletion of Plk1 resulted in a loss of Mob1 from the spindle poles, Mob1 recruitment to kinetochores was unaffected. Conversely, disruption of CPC signaling resulted in a loss of Mob1 from kinetochores without disrupting recruitment to the spindle poles. In Mob1-depleted cells, the relocalization of the CPC and mitotic kinesin-like protein (MKLP) 2 to the spindle midzone was delayed during early anaphase, and as a consequence, the midzone recruitment of MKLP1 also was affected. Together, these results suggest that Mob1 and the other mammalian orthologues of the mitotic exit network regulate mitotic progression by facilitating the timely mobilization of the CPC to the spindle midzone.
| S-EPMC2814784 | biostudies-literature
Project description:The mechanism of body growth in mammals is poorly understood. Here, we report the regulatory networks involved in body growth through analyzing transcriptomes of pituitary and epiphyseal tissues of Debao ponies and Mongolian horses at juvenile and adult stages. We found that GHR was expressed little in long bones though GH was highly expressed in Debao ponies compared with Mongolian horses. Moreover, m-RAS and ATF3, involved in the GHR pathway, were found to be significantly downregulated in juvenile ponies, which slowed the proliferation of bone osteocytes. However, WNT2 and PLCβ2 were obviously upregulated in juvenile Debao ponies, which led to premature mineralization of bone extracellular matrix. Furthermore, we found that the WNT/Ca2+ pathway may be responsible for the regulation of body growth. We then demonstrated that GHR was lacking in long bones of Debao ponies using RT-qPCR and Western blot. Treatment with WNT antagonist 1 decreased expression of the WNT pathway (P≤0.05) in vitro. The transduction of ATDC5 cells with GHR-RNAi lentivirus decreased expression of the GHR pathway (P≤0.05). Additionally, detection of plasma hormone concentrations showed that the ponies had higher levels of IGF-1 as juveniles and GH in adulthood than Mongolian horses, indicating that the hormone regulation in Debao ponies differs from that in Mongolian horses. Our work provides an insight into the genetic regulation for dwarf growth in mammals and a reference for therapeutic strategy for dwarfism
2021-01-27 | GSE146145 | GEO
Project description:Molecular dynamics simulations were performed for the prediction of the finite-size effects of Maxwell-Stefan diffusion coefficients of molecular mixtures and a wide variety of binary Lennard-Jones systems. A strong dependency of computed diffusivities on the system size was observed. Computed diffusivities were found to increase with the number of molecules. We propose a correction for the extrapolation of Maxwell-Stefan diffusion coefficients to the thermodynamic limit, based on the study by Yeh and Hummer ( J. Phys. Chem. B , 2004 , 108 , 15873 - 15879 ). The proposed correction is a function of the viscosity of the system, the size of the simulation box, and the thermodynamic factor, which is a measure for the nonideality of the mixture. Verification is carried out for more than 200 distinct binary Lennard-Jones systems, as well as 9 binary systems of methanol, water, ethanol, acetone, methylamine, and carbon tetrachloride. Significant deviations between finite-size Maxwell-Stefan diffusivities and the corresponding diffusivities at the thermodynamic limit were found for mixtures close to demixing. In these cases, the finite-size correction can be even larger than the simulated (finite-size) Maxwell-Stefan diffusivity. Our results show that considering these finite-size effects is crucial and that the suggested correction allows for reliable computations.
| S-EPMC5943679 | biostudies-literature
Project description:Carcinogenesis is one of the leading health concerns afflicting presumably every single animal species, including humans. Currently, cancer research expands considerably beyond medicine, becoming a focus in other branches of natural science. Accumulating evidence suggests that a proportional scale of tumor deaths involves domestic and wild animals and poses economical or conservation threats to many species. Therefore, understanding the genetic and physiological mechanisms of cancer initiation and its progression is essential for our future action and contingent prevention. From this perspective, I used an evolutionary-based approach to re-evaluate the baseline for debate around Peto's paradox. First, I review the background of information on which current understanding of Peto's paradox and evolutionary concept of carcinogenesis have been founded. The weak points and limitations of theoretical modeling or indirect reasoning in studies based on intraspecific, comparative studies of carcinogenesis are highlighted. This is then followed by detail discussion of an effect of the body mass in cancer research and the importance of cell size in consideration of body architecture; also, I note to the ambiguity around cell size invariance hypothesis and hard data for variability of cell size across species are provided. Finally, I point to the new research area that is driving concepts to identify exact molecular mechanisms promoting the process of tumorigenesis, which in turn may provide a proximate explanation of Peto's paradox. The novelty of the approach proposed therein lies in intraspecies testing of the effect of differentiation of cell size/number on the probability of carcinogenesis while controlling for the confounding effect of body mass/size.
| S-EPMC9746147 | biostudies-literature