Herbivore responses to nutrient enrichment and landscape heterogeneity in a mangrove ecosystem

Complex gradients in forest structure across the landscape of offshore mangrove islands in Belize are associated with nutrient deficiency and flooding. While nutrient availability can affect many ecological processes, here we investigate how N and P enrichment interact with forest structure in three distinct zones (fringe, transition, dwarf) to alter patterns of herbivory as a function of folivory, loss of yield, and tissue mining. The effects of nutrient addition and zone varied by functional feeding group or specific herbivore. Folivory ranged from 0 to 0.4% leaf area damaged per month, but rates did not vary by either nutrient enrichment or zone. Leaf lifetime damage ranged from 3 to 10% of the total leaf area and was caused primarily by the omnivorous tree crab Aratus pisonii. We detected two distinct spatial scales of response by A. pisonii that were unrelated to nutrient treatment, i.e., most feeding damage occurred in the fringe zone and crabs fed primarily on the oldest leaves in the canopy. Loss of yield caused by the bud moth Ecdytolopha sp. varied by zone but not by nutrient treatment. A periderm-mining Marmara sp. responded positively to nutrient enrichment and closely mirrored the growth response by Rhizophora mangle across the tree height gradient. In contrast, a leaf-mining Marmara sp. was controlled by parasitoids and predators that killed >89% of its larvae. Thus, nutrient availability altered patterns of herbivory of some but not all mangrove herbivores. These findings support the hypothesis that landscape heterogeneity of the biotic and abiotic environment has species-specific effects on community structure and trophic interactions. Predicting how herbivores respond to nutrient over-enrichment in mangrove ecosystems also requires an assessment of habitat heterogeneity coupled with feeding strategies and species-specific behavior measured on multiple scales of response.     

Mutation of E1-CONJUGATING ENZYME-RELATED1 decreases RELATED TO UBIQUITIN conjugation and alters auxin response and development

The ubiquitin-like protein RELATED TO UBIQUITIN (RUB) is conjugated to CULLIN (CUL) proteins to modulate the activity of Skp1-Cullin-F-box (SCF) ubiquitylation complexes. RUB conjugation to specific target proteins is necessary for the development of many organisms, including Arabidopsis (Arabidopsis thaliana). Here, we report the isolation and characterization of e1-conjugating enzyme-related1-1 (ecr1-1), an Arabidopsis mutant compromised in RUB conjugation. The ecr1-1 mutation causes a missense change located two amino acid residues from the catalytic site cysteine, which normally functions to form a thioester bond with activated RUB. A higher ratio of unmodified CUL1 relative to CUL1-RUB is present in ecr1-1 compared to wild type, suggesting that the mutation reduces ECR1 function. The ecr1-1 mutant is resistant to the auxin-like compound indole-3-propionic acid, produces fewer lateral roots than wild type, displays reduced adult height, and stabilizes a reporter fusion protein that is degraded in response to auxin, suggesting reduced auxin signaling in the mutant. In addition, ecr1-1 hypocotyls fail to elongate normally when seedlings are grown in darkness, a phenotype shared with certain other RUB conjugation mutants that is not general to auxin-response mutants. The suite of ecr1-1 molecular and morphological phenotypes reflects roles for RUB conjugation in many aspects of plant growth and development. Certain ecr1-1 elongation defects are restored by treatment with the ethylene-response inhibitor silver nitrate, suggesting that the short ecr1-1 root and hypocotyl result from aberrant ethylene accumulation. Further, silver nitrate supplementation in combination with various auxins and auxin-like compounds reveals that members of this growth regulator family may differentially rely on ethylene signaling to inhibit root growth.     

barren inflorescence2 Encodes a co-ortholog of the PINOID serine/threonine kinase and is required for organogenesis during inflorescence and vegetative development in maize

Organogenesis in plants is controlled by meristems. Axillary meristems, which give rise to branches and flowers, play a critical role in plant architecture and reproduction. Maize (Zea mays) and rice (Oryza sativa) have additional types of axillary meristems in the inflorescence compared to Arabidopsis (Arabidopsis thaliana) and thus provide an excellent model system to study axillary meristem initiation. Previously, we characterized the barren inflorescence2 (bif2) mutant in maize and showed that bif2 plays a key role in axillary meristem and lateral primordia initiation in the inflorescence. In this article, we cloned bif2 by transposon tagging. Isolation of bif2-like genes from seven other grasses, along with phylogenetic analysis, showed that bif2 is a co-ortholog of PINOID (PID), which regulates auxin transport in Arabidopsis. Expression analysis showed that bif2 is expressed in all axillary meristems and lateral primordia during inflorescence and vegetative development in maize and rice. Further phenotypic analysis of bif2 mutants in maize illustrates additional roles of bif2 during vegetative development. We propose that bif2/PID sequence and expression are conserved between grasses and Arabidopsis, attesting to the important role they play in development. We provide further support that bif2, and by analogy PID, is required for initiation of both axillary meristems and lateral primordia.     

Intestinal pH profile in rainbow trout Oncorhynchus mykiss and microhabitat preference of the flagellate Spironucleus salmonis (Diplomonadida)

In farmed rainbow trout Oncorhynchus mykiss, the flagellate Spironucleus salmonis (Diplomonadida) is often found in the pyloric region of the intestine. While previous in vitro studies report a pH of 7.5 to 8.0 as optimal for presumed S. salmonis, no previous in vivo studies have investigated the relationship between pH and microhabitat preference. Therefore, in 698 rainbow trout (75% were 5 to 6 mo old juveniles, 10 to 20 cm total length), we recorded occurrence and density of S. salmonis, and pH, in the pyloric, anterior, middle, and posterior intestine. There were no significant differences in total length or weight between infected and uninfected fish. S. salmonis preferred the pyloric region, with occurrence and density decreasing significantly from pyloric to posterior regions. In infected fish, pH in pyloric (6.8 to 7.9, mean 7.3) and posterior regions (6.5 to 8.0, mean 7.1) was significantly lower than in anterior (6.5 to 8.5, mean 7.7) and middle (6.8 to 8.2, mean 7.7) regions; in uninfected fish, the pH profile was similar. At the individual level, 90 % of infected fish and 79% of uninfected fish showed this pH profile. In the pyloric region, pH was not significantly different among uninfected fish, and fish with light, moderate, or heavy infections. Our in vivo study suggests the optimal pH for S. salmonis is between 7.1 and 7.5, possibly close to 7.3 (the mean in pyloric region of infected fish). We conclude that while the presence of S. salmonis reflected tolerable pH, density of infection was not correlated with pH, and thus a causal relationship between microhabitat preference and pH is unlikely.     

Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle

The aims of this investigation were 1) to determine whether endurance exercise training could reverse impairments in insulin-stimulated compartmentalization and/or activation of aPKCzeta/lambda and Akt2 in skeletal muscle from high-fat-fed rodents and 2) to assess whether the PPARgamma agonist rosiglitazone could reverse impairments in skeletal muscle insulin signaling typically observed after high-fat feeding. Sprague-Dawley rats were placed on chow (NORCON, n = 16) or high-fat (n = 64) diets for 4 wk. During a subsequent 4-wk experimental period, high-fat-fed rats were allocated (n = 16/group) to either sedentary control (HFC), exercise training (HFX), rosiglitazone treatment (HFRSG), or a combination of both exercise training and rosiglitazone (HFRX). Following the 4-wk experimental period, animals underwent hindlimb perfusions. Insulin-stimulated plasma membrane-associated aPKCzeta and -lambda protein concentration, aPKCzeta/lambda activity, GLUT4 protein concentration, cytosolic Akt2, and aPKCzeta/lambda activities were reduced (P < 0.05) in HFC compared with NORCON. Cytosolic Akt2, aPKCzeta, and aPKClambda protein concentrations were not affected in HFC compared with NORCON. Exercise training reversed the deleterious effects of the high-fat diet such that insulin-stimulated compartmentalization and activation of components of the insulin-signaling cascade in HFX were normalized to NORCON. High-fat diet-induced impairments to skeletal muscle glucose metabolism were not reversed by rosiglitazone administration, nor did rosiglitazone augment the effect of exercise. Our findings indicate that chronic exercise training, but not rosiglitazone, reverses high-fat diet induced impairments in compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle.     

Critical negative regulation of type 1 T cell immunity and immunopathology by signaling adaptor DAP12 during intracellular infection

Transmembrane signaling adaptor DAP12 has increasingly been recognized for its important role in innate responses. However, its role in the regulation of antimicrobial T cell responses has remained unknown. In our current study, we have examined host defense, T cell responses, and tissue immunopathology in models of intracellular infection established in wild-type and DAP12-deficient mice. During mycobacterial infection, lack of DAP12 leads to pronounced proinflammatory and Th1 cytokine responses, overactivation of Ag-specific CD4 and CD8 T cells of type 1 phenotype, and heightened immunopathology both in the lung and lymphoid organs. DAP12-deficient airway APC display enhanced NF-kappaB activation and cytokine responses upon TLR stimulation or mycobacterial infection in vitro. Of importance, adoptive transfer of Ag-loaded DAP12-deficient APC alone could lead to overactivation of transferred transgenic or endogenous wild-type T cells in vivo. We have further found that the immune regulatory role by DAP12 is not restricted only to intracellular bacterial infection, since lack of this molecule also leads to uncontrolled type 1 T cell activation and severe immunopathology and tissue injury during intracellular viral infection. Our study thus identifies DAP12 as an important novel immune regulatory molecule that acts, via APC, to control the level of antimicrobial type 1 T cell activation and immunopathology.     

TLR signaling mediated by MyD88 is required for a protective innate immune response by neutrophils to Citrobacter rodentium

Enteropathogenic Escherichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and effacing pathogens based on their ability to adhere to intestinal epithelium via actin-filled membranous protrusions (pedestals). Infection of mice with C. rodentium causes breach of the colonic epithelial barrier, a vigorous Th1 inflammatory response, and colitis. Ultimately, an adaptive immune response leads to clearance of the bacteria. Whereas much is known about the adaptive response to C. rodentium, the role of the innate immune response remains unclear. In this study, we demonstrate for the first time that the TLR adaptor MyD88 is essential for survival and optimal immunity following infection. MyD88(-/-) mice suffer from bacteremia, gangrenous mucosal necrosis, severe colitis, and death following infection. Although an adaptive response occurs, MyD88-dependent signaling is necessary for efficient clearance of the pathogen. Based on reciprocal bone marrow transplants in conjunction with assessment of intestinal mucosal pathology, repair, and cytokine production, our findings suggest a model in which TLR signaling in hemopoietic and nonhemopoietic cells mediate three distinct processes: 1) induction of an epithelial repair response that maintains the protective barrier and limits access of bacteria to the lamina propria; 2) production of KC or other chemokines that attract neutrophils and thus facilitate killing of bacteria; and 3) efficient activation of an adaptive response that facilitates Ab-mediated clearance of the infection. Taken together, these experiments provide evidence for a protective role of innate immune signaling in infections caused by attaching and effacing pathogens.