Does Drought Influence the Relationship Between Biodiversity and Ecosystem Functioning in Boreal Forests?

In mixed forests, interactions among species influence ecosystem functioning but environmental conditions also play an important role in shaping relationships between biodiversity and ecosystem functioning. In the context of climate change, the carbon and water balance in pure versus mixed forest stands may be differentially influenced by changing soil water availability. To test this hypothesis, we compared the influence of biodiversity on stand water use efficiency (WUE_S) in boreal forests between wet and dry years. We assessed the carbon isotope composition (δ ¹³C) of tree rings in Betula pendula, Pinus sylvestris, and Picea abies growing in pure versus mixed stands. In addition, we tested whether differences in WUE_S affected patterns of stand basal area increment (BAI_S). No biodiversity effect was found for stand δ ¹³C (δ ¹³C_S) during the wet year. However, there was a significant increase in δ ¹³C_S between the wet and the dry year and a significant effect of biodiversity on δ ¹³C_S in the dry year. The increase in δ ¹³C_S in mixed stands was associated with both selection and complementarity effects. Although BAI_S decreased significantly in the dry year, changes in δ ¹³C_S did not translate into variations in BAI_S along the biodiversity gradient. Our results confirmed that the physiological response of boreal forest ecosystems to changing soil water conditions is influenced by species interactions and that during dry growing seasons, species interactions in mixed stands can lead to lower soil moisture availability. This illustrates that biodiversity effects can also be negative in mixed stands in the sense that soil resources can be more intensively exhausted. Overall, our results confirm that in boreal forests, the biodiversity–ecosystem functioning relationship depends on local environmental conditions.     

Assessment of phosphorylation in Toxoplasma glideosome assembly and function

Members of the phylum Apicomplexa possess a highly conserved molecular motor complex anchored in the parasite pellicle and associated with gliding motility, invasion and egress from infected cells. This machinery, called the glideosome, is structured around the acylated gliding‐associated protein GAP45 that recruits the motor complex composed of myosin A and two associated myosin light chains (TgMLC1 and TgELC1). This motor is presumably firmly anchored to the inner membrane complex underneath the plasma membrane via an interaction with two integral membrane proteins, GAP50 and GAP40. To determine if the previously mapped phosphorylation sites on TgGAP45 and TgMLC1 have a direct significance for glideosome assembly and function, a series of phospho‐mimetic and phospho‐null mutants were generated. Neither the overexpression nor the allelic replacement of TgMLC1 with phospho‐mutants impacted on glideosome assembly and parasite motility. TgGAP45 phosphorylation mutants were functionally investigated using a complementation strategy in a TgGAP45 inducible knockout background. The loss of interaction with TgGAP50 by one previously reported GAP45‐mutant appeared to depend only on the presence of a remaining competing wild type copy of TgGAP45. Accordingly, this mutant displayed no phenotype in complementation experiments. Unexpectedly, GAP45 lacking the region encompassing the cluster of twelve phosphorylation sites did not impact on its dual function in motor recruitment and pellicle integrity. Despite the extensive phosphorylation of TgMLC1 and TgGAP45, this post‐translational modification does not appear to be critical for the assembly and function of the glideosome.     

The Timing of Timezyme Diversification in Vertebrates

All biological functions in vertebrates are synchronized with daily and seasonal changes in the environment by the time keeping hormone melatonin. Its nocturnal surge is primarily due to the rhythmic activity of the arylalkylamine N-acetyl transferase AANAT, which thus became the focus of many investigations regarding its evolution and function. Various vertebrate isoforms have been reported from cartilaginous fish to mammals but their origin has not been clearly established. Using phylogeny and synteny, we took advantage of the increasing number of available genomes in order to test whether the various rounds of vertebrate whole genome duplications were responsible for the diversification of AANAT. We highlight a gene secondary loss of the AANAT2 in the Sarcopterygii, revealing for the first time that the AAANAT1/2 duplication occurred before the divergence between Actinopterygii (bony fish) and Sarcopterygii (tetrapods, lobe-finned fish, and lungfish). We hypothesize the teleost-specific whole genome duplication (WDG) generated the appearance of the AANAT1a/1b and the AANAT2/2′paralogs, the 2′ isoform being rapidly lost in the teleost common ancestor (ray-finned fish). We also demonstrate the secondary loss of the AANAT1a in a Paracantopterygii (Atlantic cod) and of the 1b in some Ostariophysi (zebrafish and cave fish). Salmonids present an even more diverse set of AANATs that may be due to their specific WGD followed by secondary losses. We propose that vertebrate AANAT diversity resulted from 3 rounds of WGD followed by previously uncharacterized secondary losses. Extant isoforms show subfunctionalized localizations, enzyme activities and affinities that have increased with time since their emergence.     

Differences in visible light‐induced pigmentation according to wavelengths: a clinical and histological study in comparison with UVB exposure

The visible light spectrum is wide, and it can be hypothesized that all the wavelengths between 400–700 nm do not induce the same photobiological effects on pigmentation. We assessed the potential pro‐pigmenting effects of two single wavelengths located at both extremities of the visible spectrum: the blue/violet line (λ = 415 nm) and the red line (λ = 630 nm). We made colorimetric, clinical, and histological assessments with increasing doses of those lights on healthy volunteers. Then, we compared these irradiations to non‐exposed and UVB‐exposed skin. Colorimetric and clinical assessments showed a clear dose effect with the 415‐nm irradiation, in both skin type III and IV subjects, whereas the 630 nm did not induce hyperpigmentation. When compared to UVB irradiation, the blue–violet light induced a significantly more pronounced hyperpigmentation that lasted up to 3 months. Histological examination showed a significant increase of keratinocyte necrosis and p53 with UVB, as compared to 415‐ and 630‐nm exposures.     

Heterogeneous Intracellular Trafficking Dynamics of Brain-Derived Neurotrophic Factor Complexes in the Neuronal Soma Revealed by Single Quantum Dot Tracking

Accumulating evidence underscores the importance of ligand-receptor dynamics in shaping cellular signaling. In the nervous system, growth factor-activated Trk receptor trafficking serves to convey biochemical signaling that underlies fundamental neural functions. Focus has been placed on axonal trafficking but little is known about growth factor-activated Trk dynamics in the neuronal soma, particularly at the molecular scale, due in large part to technical hurdles in observing individual growth factor-Trk complexes for long periods of time inside live cells. Quantum dots (QDs) are intensely fluorescent nanoparticles that have been used to study the dynamics of ligand-receptor complexes at the plasma membrane but the value of QDs for investigating ligand-receptor intracellular dynamics has not been well exploited. The current study establishes that QD conjugated brain-derived neurotrophic factor (QD-BDNF) binds to TrkB receptors with high specificity, activates TrkB downstream signaling, and allows single QD tracking capability for long recording durations deep within the soma of live neurons. QD-BDNF complexes undergo internalization, recycling, and intracellular trafficking in the neuronal soma. These trafficking events exhibit little time-synchrony and diverse heterogeneity in underlying dynamics that include phases of sustained rapid motor transport without pause as well as immobility of surprisingly long-lasting duration (several minutes). Moreover, the trajectories formed by dynamic individual BDNF complexes show no apparent end destination; BDNF complexes can be found meandering over long distances of several microns throughout the expanse of the neuronal soma in a circuitous fashion. The complex, heterogeneous nature of neuronal soma trafficking dynamics contrasts the reported linear nature of axonal transport data and calls for models that surpass our generally limited notions of nuclear-directed transport in the soma. QD-ligand probes are poised to provide understanding of how the molecular mechanisms underlying intracellular ligand-receptor trafficking shape cell signaling under conditions of both healthy and dysfunctional neurological disease models.     

Fluctuations in chick diet of the Squacco Heron Ardeola ralloides in southern France: changes over the last 30 years

Capsule The composition varied between colony site, month and year.

Aims To determine the diet composition of chicks and its variations in 2000 and 2001. To look for any changes over the last 30 years.

Methods Chick regurgitates were analysed to determine which Order contributed most to the diet, by frequency and by biomass.

Results During 2000 and 2001 chick diet was dominated by insects (92% and 70% by biomass, respectively), mainly Coleoptera (60% and 41%) and Orthoptera (27% in both years). The dry mass of Orthoptera, Coleoptera adults, Odonata and amphibians differed significantly between breeding sites, months and years.The proportion of invertebrates (in biomass) increased from 36.5% in 1970 and 31% in 1971 to 95% in 2000 and 90% in 2001 whereas the proportion of amphibians decreased in the same time from 49% and 33% in 1970 and 1971 to 5.0% and 9.5% in 2000 and 2001, respectively.

Conclusion The proportion of prey types differed bewteen colony sites and months. Major changes were found in the diet composition between the early 1970s and 2000s. The possible hypotheses for the observed differences are discussed.     

α-Catenin and Vinculin Cooperate to Promote High E-cadherin-based Adhesion Strength

Maintaining cell cohesiveness within tissues requires that intercellular adhesions develop sufficient strength to support traction forces applied by myosin motors and by neighboring cells. Cadherins are transmembrane receptors that mediate intercellular adhesion. The cadherin cytoplasmic domain recruits several partners, including catenins and vinculin, at sites of cell-cell adhesion. Our study used force measurements to address the role of αE-catenin and vinculin in the regulation of the strength of E-cadherin-based adhesion. αE-catenin-deficient cells display only weak aggregation and fail to strengthen intercellular adhesion over time, a process rescued by the expression of αE-catenin or chimeric E-cadherin·αE-catenins, including a chimera lacking the αE-catenin dimerization domain. Interestingly, an αE-catenin mutant lacking the modulation and actin-binding domains restores cadherin-dependent cell-cell contacts but cannot strengthen intercellular adhesion. The expression of αE-catenin mutated in its vinculin-binding site is defective in its ability to rescue cadherin-based adhesion strength in cells lacking αE-catenin. Vinculin depletion or the overexpression of the αE-catenin modulation domain strongly decreases E-cadherin-mediated adhesion strength. This supports the notion that both molecules are required for intercellular contact maturation. Furthermore, stretching of cell doublets increases vinculin recruitment and α18 anti-αE-catenin conformational epitope immunostaining at cell-cell contacts. Taken together, our results indicate that αE-catenin and vinculin cooperatively support intercellular adhesion strengthening, probably via a mechanoresponsive link between the E-cadherin·β-catenin complexes and the underlying actin cytoskeleton.