Community structure, abundance, and morphology

The role of interspecific competition in structuring communities has been a highly debated issue for the last two decades. The nonrandom nature of morphological patterns within communities has been at the center of this controversy. Null models addressing community-wide dispersions in morphology have produced equivocal results and may be based on assumptions that are too restrictive (e.g., competitive exclusion or displacement). If morphological distinctiveness allows species to escape competitive pressures and exhibit higher densities, then a positive relationship should exist between morphological dissimilarity and abundance. We develop a suite of models that evaluates patterns in abundance that are associated with the morphological proximity of a species to other competitors. We evaluated the relationship between morphological distance and abundance from a variety of morphological perspectives, from those representing strictly diffuse interactions to those representing only interactions between a species and its nearest neighbor in morphological space. These models were sufficiently powerful to detect positive associations between abundance and morphological differences in a nocturnal desert rodent guild for which the effects of competition on structure are well established. Models such as these may be more useful than traditional models evaluating morphological dispersions for many reasons. They do not require that communities reach equilibrium before competitive interactions give rise to deterministic structure. They do not suffer from limitations of potentially inaccurate faunal pools or from phylogenetic constraints. Lastly, they may be used as a diagnostic tool in comparative studies to determine the degree to which competitive interactions structure communities.     

Long‐term development of species richness in a central European beech (Fagus sylvatica) forest affected by windthrow—Support for the intermediate disturbance hypothesis?

On the basis of long‐term surveys of permanent plots and traps, we examined the communities of saproxylic beetles, fungi, herbs, and trees on an untreated 22 ha large beech forest windthrow and asked whether the results lend support to the intermediate disturbance hypothesis (IDH). We studied species richness and the similarity of community composition. Additionally, we grouped species by their frequency trend over time to successional model types to examine whether, corresponding to the IDH, the diversity of these groups explained peak richness at intermediate intervals after the disturbance. In line with the IDH, species richness showed a hump‐backed temporal course for alpha and gamma diversity. We found evidence for a linear succession directly after the disturbance. This, however, did not continue, and in all species groups, a partial recovery of the initial community was observed. In the case of fungi, herbs, and trees, but not for saproxylic beetles, alpha diversity was driven by the diversity of the successional model types. Our results underline that the mechanisms driving species richness after disturbances are more complex than the IDH suggests and that these mechanisms vary with species group. We assumed that, besides competition, legacy effects, facilitation, habitat heterogeneity, and random saturation of the species pool are important. In case of trees and herbs, we found indications for strong legacy and competition effects. For fungi and beetles, substrate heterogeneity and microclimate were assumed to be important. We concluded that disturbances contribute to increasing species richness not only by reducing the effectiveness of competitors but also by increasing the amount and diversity of resources, as well as their rate of change over time.     

Osteogenesis imperfecta: the audiological phenotype lacks correlation with the genotype

Background

Neurofibromatosis 1 (NF1), a common autosomal dominant disorder, was shown in one study to be associated with a 15-year decrease in life expectancy. However, data on mortality in NF1 are limited. Our aim was to evaluate mortality in a large retrospective cohort of NF1 patients seen in France between 1980 and 2006.

Methods

Consecutive NF1 patients referred to the National French Referral Center for Neurofibromatoses were included. The standardized mortality ratio (SMR) with its 95% confidence interval (CI) was calculated as the ratio of observed over expected numbers of deaths. We studied factors associated with death and causes of death.

Results

Between 1980 and 2006, 1895 NF1 patients were seen. Median follow-up was 6.8 years (range, 0.4-20.6). Vital status was available for 1226 (65%) patients, of whom 1159 (94.5%) survived and 67 (5.5%) died. Overall mortality was significantly increased in the NF1 cohort (SMR, 2.02; CI, 1.6-2.6; P < 10^-4). The excess mortality occurred among patients aged 10 to 20 years (SMR, 5.2; CI, 2.6-9.3; P < 10^-4) and 20 to 40 years (SMR, 4.1; 2.8-5.8; P < 10^-4). Significant excess mortality was found in both males and females. In the 10-20 year age group, females had a significant increase in mortality compared to males (SMR, 12.6; CI, 5.7-23.9; and SMR, 1.8; CI, 0.2-6.4; respectively). The cause of death was available for 58 (86.6%) patients; malignant nerve sheath tumor was the main cause of death (60%).

Conclusions

We found significantly increased SMRs indicating excess mortality in NF1 patients compared to the general population. The definitive diagnosis of NF1 in all patients is a strength of our study, and the high rate of death related to malignant transformation is consistent with previous work. The retrospective design and hospital-based recruitment are limitations of our study. Mortality was significantly increased in NF1 patients aged 10 to 40 years and tended to be higher in females than in males.     

Two-color STED microscopy of living synapses using a single laser-beam pair

The advent of superresolution microscopy has opened up new research opportunities into dynamic processes at the nanoscale inside living biological specimens. This is particularly true for synapses, which are very small, highly dynamic, and embedded in brain tissue. Stimulated emission depletion (STED) microscopy, a recently developed laser-scanning technique, has been shown to be well suited for imaging living synapses in brain slices using yellow fluorescent protein as a single label. However, it would be highly desirable to be able to image presynaptic boutons and postsynaptic spines, which together form synapses, using two different fluorophores. As STED microscopy uses separate laser beams for fluorescence excitation and quenching, incorporation of multicolor imaging for STED is more difficult than for conventional light microscopy. Although two-color schemes exist for STED microscopy, these approaches have several drawbacks due to their complexity, cost, and incompatibility with common labeling strategies and fluorophores. Therefore, we set out to develop a straightforward method for two-color STED microscopy that permits the use of popular green-yellow fluorescent labels such as green fluorescent protein, yellow fluorescent protein, Alexa Fluor 488, and calcein green. Our new (to our knowledge) method is based on a single-excitation/STED laser-beam pair to simultaneously excite and quench pairs of these fluorophores, whose signals can be separated by spectral detection and linear unmixing. We illustrate the potential of this approach by two-color superresolution time-lapse imaging of axonal boutons and dendritic spines in living organotypic brain slices.     

STED nanoscopy of actin dynamics in synapses deep inside living brain slices

It is difficult to investigate the mechanisms that mediate long-term changes in synapse function because synapses are small and deeply embedded inside brain tissue. Although recent fluorescence nanoscopy techniques afford improved resolution, they have so far been restricted to dissociated cells or tissue surfaces. However, to study synapses under realistic conditions, one must image several cell layers deep inside more-intact, three-dimensional preparations that exhibit strong light scattering, such as brain slices or brains in vivo. Using aberration-reducing optics, we demonstrate that it is possible to achieve stimulated emission depletion superresolution imaging deep inside scattering biological tissue. To illustrate the power of this novel (to our knowledge) approach, we resolved distinct distributions of actin inside dendrites and spines with a resolution of 60–80 nm in living organotypic brain slices at depths up to 120 μm. In addition, time-lapse stimulated emission depletion imaging revealed changes in actin-based structures inside spines and spine necks, and showed that these dynamics can be modulated by neuronal activity. Our approach greatly facilitates investigations of actin dynamics at the nanoscale within functionally intact brain tissue.     

A Complex Metacommunity Structure for Gastropods Along an Elevational Gradient

The metacommunity framework integrates species‐specific responses to environmental gradients to detect emergent patterns of mesoscale organization. Abiotic characteristics (temperature, precipitation) and associated vegetation types change with elevation in a predictable fashion, providing opportunities to decouple effects of environmental gradients per se from those of biogeographical or historical origin. Moreover, expected structure is different if a metacommunity along an elevational gradient is molded by idiosyncratic responses to abiotic variables (expectation=Gleasonian structure) than if such a metacommunity is molded by strong habitat preferences or specializations (expectation=Clementsian structure). We evaluated metacommunity structure for 13 species of gastropod from 15 sites along an elevational transect in the Luquillo Experimental Forest of Puerto Rico. Analyses were conducted separately for the primary axis and for the secondary axis of correspondence extracted via reciprocal averaging. The metacommunity exhibited quasi‐Clementsian structure along the primary axis, which represented a gradient of gastropod species specialization that was unassociated with elevation. The secondary axis represented environmental variation associated with elevation. Along this axis, the metacommunity exhibited Clementsian structure, with specialists characterizing each of three suites of sites that corresponded to three distinct forest types. These forest types are associated with low (tabonuco forest), mid‐ (palo colorado forest), or high (elfin forest) elevations. Thus, variation among sites in species composition reflected two independent processes: the first decoupled from elevational variation and its environmental correlates, and the second highly associated with environmental variation correlated with elevation. Abstract in Spanish is available at http://www.blackwell‐synergy.com/loi/btp .     

Irisin immunohistochemistry in gastrointestinal system cancers

Cancer is the leading cause of morbidity and mortality worldwide. Some studies have shown that high heat kills cancer cells. Irisin is a protein involved in heat production by converting white into brown adipose tissue, but there is no information about how its expression changes in cancerous tissues. We used irisin antibody immunohistochemistry to investigate changes in irisin expression in gastrointestinal cancers compared to normal tissues. Irisin was found in human brain neuroglial cells, esophageal epithelial cells, esophageal epidermoid carcinoma, esophageal adenocarcinoma and neuroendocrine esophageal carcinoma, gastric glands, gastric adenosquamous carcinoma, gastric neuroendocrine carcinoma, gastric signet ring cell carcinoma, neutrophils in vascular tissues, intestinal glands of colon, colon adenocarcinoma, mucinous colon adenocarcinoma, hepatocytes, hepatocellular carcinoma, islets of Langerhans, exocrine pancreas, acinar cells and interlobular and interlobular ducts of normal pancreas, pancreatic ductal adenocarcinoma, and intra- and interlobular ducts of cancerous pancreatic tissue. Histoscores (area × intensity) indicated that irisin was increased significantly in gastrointestinal cancer tissues, except liver cancers. Our findings suggest that the relation of irisin to cancer warrants further investigation.     

Phosphorylation of Photosystem II Controls Functional Macroscopic Folding of Photosynthetic Membranes in Arabidopsis

Photosynthetic thylakoid membranes in plants contain highly folded membrane layers enriched in photosystem II, which uses light energy to oxidize water and produce oxygen. The sunlight also causes quantitative phosphorylation of major photosystem II proteins. Analysis of the Arabidopsis thaliana stn7xstn8 double mutant deficient in thylakoid protein kinases STN7 and STN8 revealed light-independent phosphorylation of PsbH protein and greatly reduced N-terminal phosphorylation of D2 protein. The stn7xstn8 and stn8 mutants deficient in light-induced phosphorylation of photosystem II had increased thylakoid membrane folding compared with wild-type and stn7 plants. Significant enhancement in the size of stacked thylakoid membranes in stn7xstn8 and stn8 accelerated gravity-driven sedimentation of isolated thylakoids and was observed directly in plant leaves by transmission electron microscopy. Increased membrane folding, caused by the loss of light-induced protein phosphorylation, obstructed lateral migration of the photosystem II reaction center protein D1 and of processing protease FtsH between the stacked and unstacked membrane domains, suppressing turnover of damaged D1 in the leaves exposed to high light. These findings show that the high level of photosystem II phosphorylation in plants is required for adjustment of macroscopic folding of large photosynthetic membranes modulating lateral mobility of membrane proteins and sustained photosynthetic activity.The use of captured sunlight energy to split water and drive oxygenic photosynthesis by photosystem II (PSII) (Barber, 2006) inevitably generates reactive oxygen species and causes oxidative damage to the PSII protein pigment complex. The light-induced damage to PSII, in particular to the D1 reaction center protein, requires PSII repair to sustain its photosynthetic function (Takahashi and Murata, 2008). Impairment and degradation of D1 increase with rising light intensities, and this protein has the fastest turnover rate among the photosynthetic proteins of plants, algae, and cyanobacteria (Yokthongwattana and Melis, 2006). However, in plants, the PSII is segregated in highly stacked membrane layers of very large thylakoid membranes (Andersson and Anderson, 1980; Kirchhoff et al., 2008), which are densely folded to fit inside chloroplasts (Mullineaux, 2005; Shimoni et al., 2005). As a consequence, the PSII repair cycle in plants is slower than in cyanobacteria (Yokthongwattana and Melis, 2006), and it includes migration of the PSII complex from the stacked membrane domains (grana) to the unstacked membranes (stroma lamellae), where proteolysis and insertion of a newly synthesized D1 protein occurs (Baena-Gonzalez and Aro, 2002; Yokthongwattana and Melis, 2006). High light also causes quantitative phosphorylation of the membrane surface–exposed regions of D1, D2, CP43, and PsbH proteins of PSII in plants (Rintamäki et al., 1997; Vener et al., 2001), but the function of this phosphorylation is largely unknown and reports on its importance for the D1 protein turnover are conflicting (Bonardi et al., 2005; Tikkanen et al., 2008).Phosphorylation of the PSII proteins in Arabidopsis thaliana depends mostly on the light-activated protein kinase STN8 (Vainonen et al., 2005), while the STN7 kinase is essential for phosphorylation of the light-harvesting proteins of PSII (Bellafiore et al., 2005; Bonardi et al., 2005; Tikkanen et al., 2006). An earlier study on Arabidopsis mutants lacking both STN7 and STN8 (stn7xstn8), as well as only STN8, concluded that protein phosphorylation was not essential for PSII repair (Bonardi et al., 2005), while more recent work revealed a dramatic retardation in D1 degradation under high light in the stn8 and stn7xstn8 mutants (Tikkanen et al., 2008). Moreover, it was shown that the lack of PSII phosphorylation resulted in accumulation of photodamaged PSII complexes and in general oxidative damage of photosynthetic proteins in the thylakoid membranes under high light (Tikkanen et al., 2008). The other study revealed that the stn7xstn8 double mutant grown under natural field conditions produced 41% less seeds than wild-type plants (Frenkel et al., 2007), which also indicated physiological importance of thylakoid protein phosphorylation in maintenance of plant fitness.To uncover the function of light-dependent protein phosphorylation in plant photosynthetic membranes, we performed a detailed analysis of the Arabidopsis mutants deficient in the protein kinases STN7 and STN8. The earlier published results on protein phosphorylation analyses in the stn7xstn8 mutant of Arabidopsis were restricted to antiphosphothreonine antibody-based immunodetection and did not reveal any phosphorylation of PSII core proteins (Bonardi et al., 2005; Tikkanen et al., 2008). Using a mass spectrometry (MS) approach and immunoblot analyses with two complementary antiphosphothreonine antibodies, we find remaining light-independent phosphorylation of PsbH and D2 proteins of PSII in stn7xstn8. We demonstrate that degradation and aggregation patterns of the D1 protein in stn7xstn8 differ from those in wild-type, stn7, and stn8 plants. We also observe a reproducible delay in the degradation of D1 in high light–treated leaves of stn7xstn8 and stn8 compared with the wild-type and stn7 plants. Finally, we show that phosphorylation of PSII proteins modulates macroscopic rearrangements of the entire membrane network of plant thylakoids, which facilitates lateral mobility of membrane proteins, required for repair and sustained activity of PSII.     

Analysis of the Chloroplast Protein Kinase Stt7 during State Transitions

State transitions allow for the balancing of the light excitation energy between photosystem I and photosystem II and for optimal photosynthetic activity when photosynthetic organisms are subjected to changing light conditions. This process is regulated by the redox state of the plastoquinone pool through the Stt7/STN7 protein kinase required for phosphorylation of the light-harvesting complex LHCII and for the reversible displacement of the mobile LHCII between the photosystems. We show that Stt7 is associated with photosynthetic complexes including LHCII, photosystem I, and the cytochrome b₆f complex. Our data reveal that Stt7 acts in catalytic amounts. We also provide evidence that Stt7 contains a transmembrane region that separates its catalytic kinase domain on the stromal side from its N-terminal end in the thylakoid lumen with two conserved Cys that are critical for its activity and state transitions. On the basis of these data, we propose that the activity of Stt7 is regulated through its transmembrane domain and that a disulfide bond between the two lumen Cys is essential for its activity. The high-light–induced reduction of this bond may occur through a transthylakoid thiol–reducing pathway driven by the ferredoxin-thioredoxin system which is also required for cytochrome b₆f assembly and heme biogenesis.