The interspecific mass–density relationship and plant geometry

We present an a priori theoretical framework for the interspecific allometric relationship between stand mass and plant population density. Our model predicts a slope of −\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}\frac{1}{3}\end{equation*}\end{document} between the logarithm of stand mass and the logarithm of stand density, thus conflicting with a previously assumed slope of −½. Our model rests on a heuristic separation of resource-limited living mass and structural mass in the plant body. We point out that because of similar resource requirements among plants of different sizes, a nonzero plant mass–density slope is primarily defined by structural mass. Specifically, the slope is a result of (i) the physical size-dependent relationship between stem width and height, (ii) foliage-dependent demands of conductance, and (iii) the cumulative nature of structural mass. The data support our model, both when the potential sampling bias of taxonomic relatedness is accounted for and when it is not. Independent contrasts analyses show that observed relationships among variables are not significantly different from the assumptions made to build the model or from its a priori predictions. We note that the dependence of the plant mass–density slope on the functions of structural mass provides a cause for the difference from the zero slope found in the animal population mass–density relationship; for the most part, animals do not have a comparable cumulative tissue type.

Factors controlling the competition among rotational and vibrational energy transfer channels in glyoxal

The state-to-state transfer of rotational and vibrational energy has been studied for S1 glyoxal (CHOCHO) in collisions with D2, N2, CO and C2H4 using crossed molecular beams. A laser is used to pump glyoxal seeded in He to its S1 zero point level with zero angular momentum about its top axis (K′ = 0). The inelastic scattering to each of at least 26 S1 glyoxal rotational and rovibrational levels is monitored by dispersed S1–S0 fluorescence. Various collision partners are chosen to investigate the relative influences of reduced mass and the collision pair interaction potential on the competition among the energy transfer channels. When the data are combined with that obtained previously from other collision partners whose masses range from 2 to 84 amu, it is seen that the channel competition is controlled primarily by the kinematics of the collisional interaction. Variations in the intermolecular potential play strictly a secondary role.

Signaling of need, sibling competition, and the cost of honesty

Young birds and mammals frequently solicit food by means of extravagant and apparently costly begging displays. Much attention has been devoted to the idea that these displays are honest signals of need, and that their apparent cost serves to maintain their honesty. Recent analyses, however, have shown that the cost needed to maintain a fully informative, honest signal may often be so great that both offspring (signaler) and parent (receiver) would do better to refrain from communication. This apparently calls into question the relevance of the costly signaling hypothesis. Here, I show that this argument overlooks the impact of sibling competition. When multiple signalers must compete for the attention of a receiver (as is commonly the case in parent–offspring interactions), I show that (all other things being equal) individual equilibrium signal costs will typically be lower. The greater the number of competitors, the smaller the mean cost, though the maximum level of signal intensity employed by very needy signalers may actually increase with the number of competitors. At the same time, costs become increasingly sensitive to relatedness among signalers as opposed to relatedness between signalers and receivers. As a result of these trends, signaling proves profitable for signalers under a much wider range of conditions when there is competition (though it is still likely to be unprofitable for receivers).

A model of ocular dominance column development by competition for trophic factor

Recent experimental evidence has shown that application of certain neurotrophic factors (NTs) to the developing primary visual cortex prevents the development of ocular dominance (OD) columns. One interpretation of this result is that afferents from the lateral geniculate nucleus compete for postsynaptic trophic factor in an activity-dependent manner. Application of excess trophic factor eliminates this competition, thereby preventing OD column formation. We present a model of OD column development, incorporating Hebbian synaptic modification and activity-driven competition for NT, which accounts for both normal OD column development as well as the prevention of that development when competition is removed. In the “control” situation, when available NT is below a critical amount, OD columns form normally. These columns form without weight normalization procedures and in the presence of positive inter-eye correlations. In the “experimental” case, OD column development is prevented in a local neighborhood in which excess NT has been added. Our model proposes a biologically plausible mechanism for competition between neural populations that is motivated by several pieces of experimental data, thereby accounting for both normal and experimentally perturbed conditions.

Models of immune memory: On the role of cross-reactive stimulation, competition, and homeostasis in maintaining immune memory

There has been much debate on the contribution of processes such as the persistence of antigens, cross-reactive stimulation, homeostasis, competition between different lineages of lymphocytes, and the rate of cell turnover on the duration of immune memory and the maintenance of the immune repertoire. We use simple mathematical models to investigate the contributions of these various processes to the longevity of immune memory (defined as the rate of decline of the population of antigen-specific memory cells). The models we develop incorporate a large repertoire of immune cells, each lineage having distinct antigenic specificities, and describe the dynamics of the individual lineages and total population of cells. Our results suggest that, if homeostatic control regulates the total population of memory cells, then, for a wide range of parameters, immune memory will be long-lived in the absence of persistent antigen (T1/2 > 1 year). We also show that the longevity of memory in this situation will be insensitive to the relative rates of cross-reactive stimulation, the rate of turnover of immune cells, and the functional form of the term for the maintenance of homeostasis.

A general mechanism for regulation of access to the translocon: Competition for a membrane attachment site on ribosomes

For proteins to enter the secretory pathway, the membrane attachment site (M-site) on ribosomes must bind cotranslationally to the Sec61 complex present in the endoplasmic reticulum membrane. The signal recognition particle (SRP) and its receptor (SR) are required for targeting, and the nascent polypeptide associated complex (NAC) prevents inappropriate targeting of nonsecretory nascent chains. In the absence of NAC, any ribosome, regardless of the polypeptide being synthesized, binds to the endoplasmic reticulum membrane, and even nonsecretory proteins are translocated across the endoplasmic reticulum membrane. By occupying the M-site, NAC prevents all ribosome binding unless a signal peptide and SRP are present. The mechanism by which SRP overcomes the NAC block is unknown. We show that signal peptide-bound SRP occupies the M-site and therefore keeps it free of NAC. To expose the M-site and permit ribosome binding, SR can pull SRP away from the M-site without prior release of SRP from the signal peptide.

The evolution of begging: Signaling and sibling competition

In many species, young solicit food from their parents, which respond by feeding them. Because of the difference in genetic make-up between parents and their offspring and the consequent conflict, this interaction is often studied as a paradigm for the evolution of communication. Existent theoretical models demonstrate that chick signaling and parent responding can be stable if solicitation is a costly signal. The marginal cost of producing stronger signals allows the system to converge to an equilibrium: young beg with intensity that reflects their need, and parents use this information to maximize their own inclusive fitness. However, we show that there is another equilibrium where chicks do not beg and parents’ provisioning effort is optimal with respect to the statistically probable distribution of chicks’ states. Expected fitness for parents and offspring at the nonsignaling equilibrium is higher than at the signaling equilibrium. Because nonsignaling is stable and it is likely to be the ancestral condition, we would like to know how natural systems evolved from nonsignaling to signaling. We suggest that begging may have evolved through direct sibling fighting before the establishment of a parental response, that is, that nonsignaling squabbling leads to signaling. In multiple-offspring broods, young following a condition-dependent strategy in the contest for resources provide information about their condition. Parents can use this information even though it is not an adaptation for communication, and evolution will lead the system to the signaling equilibrium. This interpretation implies that signaling evolved in multiple-offspring broods, but given that signaling is evolutionarily stable, it would also be favored in species which secondarily evolved single-chick broods.

Competition between a sterol biosynthetic enzyme and tRNA modification in addition to changes in the protein synthesis machinery causes altered nonsense suppression

The Saccharomyces cerevisiae Mod5 protein catalyzes isopentenylation of A to i6A on tRNAs in the nucleus, cytosol, and mitochondria. The substrate for Mod5p, dimethylallyl pyrophosphate, is also a substrate for Erg20p that catalyzes an essential step in sterol biosynthesis. Changing the distribution of Mod5p so that less Mod5p is present in the cytosol decreases i6A on cytosolic tRNAs and alters tRNA-mediated nonsense suppression. We devised a colony color/growth assay to assess tRNA-mediated nonsense suppression and used it to search for genes, which, when overexpressed, affect nonsense suppression. We identified SAL6, TEF4, and YDL219w, all of which likely affect nonsense suppression via alteration of the protein synthesis machinery. We also identified ARC1, whose product interacts with aminoacyl synthetases. Interestingly, we identified ERG20. Midwestern analysis showed that yeast cells overproducing Erg20p have reduced levels of i6A on tRNAs. Thus, Erg20p appears to affect nonsense suppression by competing with Mod5p for substrate. Identification of ERG20 reveals that yeast have a limited pool of dimethylallyl pyrophosphate. It also demonstrates that disrupting the balance between enzymes that use dimethylallyl pyrophosphate as substrate affects translation.

How does a β-hairpin fold/unfold? Competition between topology and heterogeneity in a solvable model

We study the competition between topological effects and sequence inhomogeneities in determining the thermodynamics and the un/folding kinetics of a β-hairpin. Our work utilizes a new exactly solvable model that allows for arbitrary configurations of native contacts. In general, the competition between heterogeneity and topology results in a crossover of the dominant transition state. Interestingly, near this crossover, the single reaction coordinate picture can be seriously misleading. Our results also suggest that inferring the folding pathway from unfolding simulations is not always justified.

Correlated effects of sperm competition and postmating female mortality

Adaptations in one sex may impair fitness in the opposite sex. Experiments with Drosophila melanogaster have shown that seminal fluid from the male accessory gland triggers a series of postmating responses in the female, including increased egg laying rate and lower remating propensity, but that accessory gland proteins also increase female death rate. Here, we tested the relationships among the longevity of females mated to males from 51 chromosome-extracted D. melanogaster lines, male-mating ability, and sperm-competitive ability. We found significant differences in longevity of females mated to males of different genotypes, and all mated females showed a higher death rate than control virgin females shortly after mating. Both the age-independent mortality parameter (the intercept of the female's survival function) and the slope of the mortality rate curve were significantly correlated with the proportion of progeny sired by the first male to mate relative to tester males (sperm-defense ability, P1). No significant correlation was found between the proportion of progeny sired by the second-mating male relative to tester males (sperm-offense ability, P2) and any mortality parameter. Our results support the hypothesis of a tradeoff between defensive sperm-competitive ability of males and life-history parameters of mated females.

Evolution of a quadripartite hybrid virus by interspecific exchange and recombination between replicase components of two related tripartite RNA viruses

Cucumber mosaic virus (CMV) and tomato aspermy virus (TAV) belong to the Cucumovirus genus. They have a tripartite genome consisting of single-stranded RNAs, designated 1, 2, and 3. Previous studies have shown that viable pseudorecombinants could be created in vitro by reciprocal exchanges between CMV and TAV RNA 3, but exchanges of RNAs 1 and 2 were replication deficient. When we coinoculated CMV RNAs 2 and 3 along with TAV RNAs 1 and 2 onto Nicotiana benthamiana, a hybrid quadripartite virus appeared that consisted of TAV RNA 1, CMV RNAs 2 and 3, and a distinctive chimeric RNA originating from a recombination between CMV RNA 2 and the 3′-terminal 320 nucleotides of TAV RNA 2. This hybrid arose by means of segment reassortment and RNA recombination to produce an interspecific hybrid with the TAV helicase subunit and the CMV polymerase subunit. To our knowledge, this is the first report demonstrating the evolution of a new plant or animal virus strain containing an interspecific hybrid replicase complex.

Invariant scaling relationships for interspecific plant biomass production rates and body size

The allometric relationships for plant annualized biomass production (“growth”) rates, different measures of body size (dry weight and length), and photosynthetic biomass (or pigment concentration) per plant (or cell) are reported for multicellular and unicellular plants representing three algal phyla; aquatic ferns; aquatic and terrestrial herbaceous dicots; and arborescent monocots, dicots, and conifers. Annualized rates of growth G scale as the 3/4-power of body mass M over 20 orders of magnitude of M (i.e., G ∝ M3/4); plant body length L (i.e., cell length or plant height) scales, on average, as the 1/4-power of M over 22 orders of magnitude of M (i.e., L ∝ M1/4); and photosynthetic biomass Mp scales as the 3/4-power of nonphotosynthetic biomass Mn (i.e., Mp ∝ Mn3/4). Because these scaling relationships are indifferent to phylogenetic affiliation and habitat, they have far-reaching ecological and evolutionary implications (e.g., net primary productivity is predicted to be largely insensitive to community species composition or geological age).

Competition for Microtubule-binding with Dual Expression of Tau Missense and Splice Isoforms

How tau mutations lead to neurodegeneration is unknown but may be related to altered microtubule binding properties of mutant tau protein. The tendency for the mutations to cluster around the microtubule-binding domain of tau or to alter the ratios of those splice isoforms that affect binding supports the view that the tau/microtubule interaction is critical and finely regulated. In cells transfected with both mutant and wild-type tau isoforms fused to either yellow fluorescent protein or cyan fluorescent protein we can observe tau fusion proteins that differ by a single amino acid or by the inclusion or exclusion of exon 10. With coexpression of mutant and wild-type tau, the mutant isoform appears diffuse throughout the cytoplasm; however, when mutant tau is expressed alone, it appears mostly bound to the microtubules. Dual imaging of the three- and four-repeat tau isoforms indicated that the expression of four-repeat tau displaced three-repeat tau from the microtubules. These results suggest that altered kinetic competition among the isoforms for microtubule binding could be a disease precipitant.

A model of self-thinning through local competition.

Explanations of self-thinning in plant populations have focused on plant shape and packing. A dynamic model based on the structure of local interactions successfully reproduces the pattern and can be approximated to identify key parameters and relationships. The approach generates testable new explanations for differences between species and populations, unifies self-thinning with other patterns in plant population dynamics, and indicates why organisms other than plants can follow the law.

Competition between noggin and bone morphogenetic protein 4 activities may regulate dorsalization during Xenopus development.

Bone morphogenetic protein 4 (BMP-4) induces ventral mesoderm but represses dorsal mesoderm formation in Xenopus embryos. We show that BMP-4 inhibits two signaling pathways regulating dorsal mesoderm formation, the induction of dorsal mesoderm (Spemann organizer) and the dorsalization of ventral mesoderm. Ectopic expression of BMP-4 RNA reduces goosecoid and forkhead-1 transcription in whole embryos and in activin-treated animal cap explants. Embryos and animal caps overexpressing BMP-4 transcribe high levels of genes expressed in ventral mesoderm (Xbra, Xwnt-8, Xpo, Mix.1, XMyoD). The Spemann organizer is ventralized in these embryos; abnormally high levels of Xwnt-8 mRNA and low levels of goosecoid mRNA are detected in the organizer. In addition, the organizer loses the ability to dorsalize neighboring ventral marginal zone to muscle. Overexpression of BMP-4 in ventral mesoderm inhibits its response to dorsalization signals. Ventral marginal zone explants ectopically expressing BMP-4 form less muscle when treated with soluble noggin protein or when juxtaposed to a normal Spemann organizer in comparison to control explants. Endogenous BMP-4 transcripts are downregulated in ventral marginal zone explants dorsalized by noggin, in contrast to untreated explants. Thus, while BMP-4 inhibits noggin protein activity, noggin downregulates BMP-4 expression by dorsalizing ventral marginal zone to muscle. Noggin and BMP-4 activities may control the lateral extent of dorsalization within the marginal zone. Competition between these two molecules may determine the final degree of muscle formation in the marginal zone, thus defining the border between dorsolateral and ventral mesoderm.