A negative feedback loop controls ROS production in plant immunity

Non peer reviewe

Externalities in a Life-Cycle Model with Endogenous Survival

We study socially vs. individually optimal lifecycle allocations of consumption and health care, when individual health expenditure curbs own mortality but also has a spillover effect on other persons' survival. Such spillovers arise, for instance, when health care activity at aggregate level triggers improvements in treatment through learningbydoing (positive externality) or a deterioration in the quality of care through congestion (negative externality). We combine an agestructured optimal control model at population level with a conventional lifecycle model to derive the social and private value of life. We then examine how individual incentives deviate from social incentives and how they can be aligned by way of a transfer scheme. The agepatterns of socially and individually optimal health expenditure and the transfer rate are derived. Numerical analysis illustrates the workings of our model.Demand for health, externality, life-cycle-model, optimal control, tax-subsidy, value of life.

The reproductive value as part of the shadow price of population

The reproductive value (see Fisher [10]) arises as part of the shadow price of the population in a large class of age-structured optimal control models.life history, reproductive value

The Reproductive Value in Distributed Optimal Control Models

We show that in a large class of distributed optimal control models (DOCM), where population is described by a McKendrick type equation with an endogenous number of newborns, the reproductive value of Fisher shows up as part of the shadow price of the population. Depending on the objective function, the reproductive value may be negative. Moreover, we show results of the reproductive value for changing vital rates. To motivate and demonstrate the general framework, we provide examples in health economics, epidemiology, and population biology.Reproductive value, distributed optimal control theory, McKendrick, shadow price, indirect effect, health economics, epidemiology, population biology.

The Reproductive Value as Part of the Shadow Price of Population

The reproductive value (see Fisher 1930) arises as part of the shadow price of the population in a large class of age-structured optimal control models.Reproductive value, distributed optimal control theory, McKendrick equation, shadow price, indirect effect.

R&D for green technologies in a dynamic oligopoly: Schumpeter, Arrow and inverted-U’s

We extend a well known differential oligopoly game to encompass the possibility for production to generate a negative environmental externality, regulated through Pigouvian taxation and price caps. We show that, if the price cap is set so as to fix the tolerable maximum amount of emissions, the resulting equilibrium investment in green R&D is indeed concave in the structure of the industry. Our analysis appears to indicate that inverted-U-shaped investment curves are generated by regulatory measures instead of being a "natural" feature of firms’ decisions

Arabidopsis GRI is involved in the regulation of cell death induced by extracellular ROS

Reactive oxygen species (ROS) have important functions in plant stress responses and development. In plants, ozone and pathogen infection induce an extracellular oxidative burst that is involved in the regulation of cell death. However, very little is known about how plants can perceive ROS and regulate the initiation and the containment of cell death. We have identified an Arabidopsis thaliana protein, GRIM REAPER (GRI), that is involved in the regulation of cell death induced by extracellular ROS. Plants with an insertion in GRI display an ozone-sensitive phenotype. GRI is an Arabidopsis ortholog of the tobacco flower-specific Stig1 gene. The GRI protein appears to be processed in leaves with a release of an N-terminal fragment of the protein. Infiltration of the N-terminal fragment of the GRI protein into leaves caused cell death in a superoxide-and salicylic acid-dependent manner. Analysis of the extracellular GRI protein yields information on how plants can initiate ROS-induced cell death during stress response and development.Reactive oxygen species (ROS) have important functions in plant stress responses and development. In plants, ozone and pathogen infection induce an extracellular oxidative burst that is involved in the regulation of cell death. However, very little is known about how plants can perceive ROS and regulate the initiation and the containment of cell death. We have identified an Arabidopsis thaliana protein, GRIM REAPER (GRI), that is involved in the regulation of cell death induced by extracellular ROS. Plants with an insertion in GRI display an ozone-sensitive phenotype. GRI is an Arabidopsis ortholog of the tobacco flower-specific Stig1 gene. The GRI protein appears to be processed in leaves with a release of an N-terminal fragment of the protein. Infiltration of the N-terminal fragment of the GRI protein into leaves caused cell death in a superoxide-and salicylic acid-dependent manner. Analysis of the extracellular GRI protein yields information on how plants can initiate ROS-induced cell death during stress response and development.Reactive oxygen species (ROS) have important functions in plant stress responses and development. In plants, ozone and pathogen infection induce an extracellular oxidative burst that is involved in the regulation of cell death. However, very little is known about how plants can perceive ROS and regulate the initiation and the containment of cell death. We have identified an Arabidopsis thaliana protein, GRIM REAPER (GRI), that is involved in the regulation of cell death induced by extracellular ROS. Plants with an insertion in GRI display an ozone-sensitive phenotype. GRI is an Arabidopsis ortholog of the tobacco flower-specific Stig1 gene. The GRI protein appears to be processed in leaves with a release of an N-terminal fragment of the protein. Infiltration of the N-terminal fragment of the GRI protein into leaves caused cell death in a superoxide-and salicylic acid-dependent manner. Analysis of the extracellular GRI protein yields information on how plants can initiate ROS-induced cell death during stress response and development.Peer reviewe

Reactive Oxygen in Abiotic Stress Perception-From Genes to Proteins

Peer reviewe

Poly(ADP-ribose)-binding protein RCD1 is a plant PARylation reader regulated by Photoregulatory Protein Kinases

Poly(ADP-ribosyl)ation (PARylation) is a reversible post-translational protein modification that has profound regulatory functions in metabolism, development and immunity, and is conserved throughout the eukaryotic lineage. Contrary to metazoa, many components and mechanistic details of PARylation have remained unidentified in plants. Here we present the transcriptional co-regulator RADICAL-INDUCED CELL DEATH1 (RCD1) as a plant PAR-reader. RCD1 is a multidomain protein with intrinsically disordered regions (IDRs) separating its domains. We have reported earlier that RCD1 regulates plant development and stress-tolerance by interacting with numerous transcription factors (TFs) through its C-terminal RST domain. This study suggests that the N-terminal WWE and PARP-like domains, as well as the connecting IDR play an important regulatory role for RCD1 function. We show that RCD1 binds PAR in vitro via its WWE domain and that PAR-binding determines RCD1 localization to nuclear bodies (NBs) in vivo. Additionally, we found that RCD1 function and stability is controlled by Photoregulatory Protein Kinases (PPKs). PPKs localize with RCD1 in NBs and phosphorylate RCD1 at multiple sites affecting its stability. This work proposes a mechanism for negative transcriptional regulation in plants, in which RCD1 localizes to NBs, binds TFs with its RST domain and is degraded after phosphorylation by PPKs

The optimal momentum of population growth and decline

About 50 years ago, Keyfitz (1971) asked how much further a growing human population would increase if its fertility rate were immediately to be reduced to replacement level and remain there forever. The reason for demographic momentum is an age–structure inertia due to relatively many potential parents because of past high fertility. Although nobody expects such a miraculous reduction in reproductive behavior, a gradual decline in fertility in rapidly growing populations seems inevitable. As any delay in fertility decline to a stationary level leads to an increase in the momentum, it makes sense to think about the timing and the quantum of the reduction in reproduction. More specifically, we consider an intertemporal trade-off between costly pro- and anti-natalistic measures and the demographic momentum at the end of the planning period. This paper uses the McKendrick–von Foerster partial differential equation of age–structured population dynamics to study a sketched problem in a distributed parameter control framework. Among the results obtained by applying an appropriate extension of Pontryagin’s Maximum Principle are the following: (i) monotony of adaptation efforts to net reproduction rate and convex decrease/concave increase (if initial net reproduction rate exceeds 1/is below 1); and (ii) oscillating efforts and reproduction rate if, additionally, the size of the total population does not deviate from a fixed level