The impact of temperature on balancing immune responsiveness and growth in Arabidopsis

Plants have evolved polymorphic immune receptors to recognize pathogens causing disease. However, triggering of resistance needs to be tuned to the local environment to maintain a balance between defense and growth. We consider here the impact of temperature as a key environmental factor influencing immune pathway activation in Arabidopsis. Genetic compensatory and molecular buffering mechanisms affecting the diversification, functionality and subcellular dynamics of immune receptors, reveal multiple points at which temperature intersects with host resistance signaling systems, including a role of at least one receptor in sensing temperature change. Analysis of temperature-dependent autoimmunity caused by allelic mismatches in hybrids of evolutionary diverged Arabidopsis accessions is illuminating processes by which plants maintain 'poise' between immune responsiveness and fitness in natural populations.     

Genetic and evolutionary perspectives on the interplay between plant immunity and development

There is now ample evidence that plant development, responses to abiotic environments, and immune responses are tightly intertwined in their physiology. Thus optimization of the immune system during evolution will occur in coordination with that of plant development. Two alternative and possibly complementary forces are at play: genetic constraints due to the pleiotropic action of players in both systems, and coevolution, if developmental changes modulate the cost-benefit balance of immunity. A current challenge is to elucidate the ecological forces driving evolution of quantitative variation for defense at molecular level. The analysis of natural co-variation for developmental and immunity traits in Arabidopsis thaliana promises to bring important insights.     

A complete skull of an early cretaceous sauropod and the evolution of advanced titanosaurians

Advanced titanosaurian sauropods, such as nemegtosaurids and saltasaurids, were diverse and one of the most important groups of herbivores in the terrestrial biotas of the Late Cretaceous. However, little is known about their rise and diversification prior to the Late Cretaceous. Furthermore, the evolution of their highly-modified skull anatomy has been largely hindered by the scarcity of well-preserved cranial remains. A new sauropod dinosaur from the Early Cretaceous of Brazil represents the earliest advanced titanosaurian known to date, demonstrating that the initial diversification of advanced titanosaurians was well under way at least 30 million years before their known radiation in the latest Cretaceous. The new taxon also preserves the most complete skull among titanosaurians, further revealing that their low and elongated diplodocid-like skull morphology appeared much earlier than previously thought.     

Olanzapine-induced hyperphagia and weight gain associate with orexigenic hypothalamic neuropeptide signaling without concomitant AMPK phosphorylation

The success of antipsychotic drug treatment in patients with schizophrenia is limited by the propensity of these drugs to induce hyperphagia, weight gain and other metabolic disturbances, particularly evident for olanzapine and clozapine. However, the molecular mechanisms involved in antipsychotic-induced hyperphagia remain unclear. Here, we investigate the effect of olanzapine administration on the regulation of hypothalamic mechanisms controlling food intake, namely neuropeptide expression and AMP-activated protein kinase (AMPK) phosphorylation in rats. Our results show that subchronic exposure to olanzapine upregulates neuropeptide Y (NPY) and agouti related protein (AgRP) and downregulates proopiomelanocortin (POMC) in the arcuate nucleus of the hypothalamus (ARC). This effect was evident both in rats fed ad libitum and in pair-fed rats. Of note, despite weight gain and increased expression of orexigenic neuropeptides, subchronic administration of olanzapine decreased AMPK phosphorylation levels. This reduction in AMPK was not observed after acute administration of either olanzapine or clozapine. Overall, our data suggest that olanzapine-induced hyperphagia is mediated through appropriate changes in hypothalamic neuropeptides, and that this effect does not require concomitant AMPK activation. Our data shed new light on the hypothalamic mechanism underlying antipsychotic-induced hyperphagia and weight gain, and provide the basis for alternative targets to control energy balance.