Biologie des Eleonorenfalken(Falco eleonorae): 10. Der Einflu? der Horstlage auf den Bruterfolg

Zusammenfassung Der Bruterfolg des Eleonorenfalken wurde auf einer ägäischen Inselkolonie in Relation zur Horstlage untersucht. Bei Horsten mit Gratlage auf übersichtlichem Gelände war er signifikant höher (1,8 Junge/Horst) als bei den übrigen Horsten mit z. T. schlechtem Geländeüberblick (1,3 Junge/Horst). Da alle Horste gegenüber den NW-Winden geschützt lagen, waren die meisten an südlich ausgerichteten Hängen potentiell der intensiven Sonneneinstrahlung ausgesetzt. In den Horstrevieren von typisch 20 m Durchmesser gab es aber nicht immer vor Sonne geschützte Horsthöhlen, so daß bei Lufttemperaturen von 40 °C und Bodentemperaturen von bis zu 60 °C die Embryonen in den Eiern gefährdet sein können, besonders, wenn sie der direkten Sonneneinstrahlung ausgesetzt sind. Dies tritt z. B. bei einer Störung in der Brutkolonie ein. Der Bruterfolg in den sonnenexponierten Höhlen lag mit 0,8–1,3 Junge/Horst signifikant niedriger als in den sonnengeschützten Höhlen mit durchschnittlich 1,75 Junge/Horst. Neben einer normalen Infertilität von 10 % fielen weitere 8 % aller Eier in der Brutkolonie durch Sonneneinwirkung aus.

---

Biology of the Eleonora's Falcon(Falco eleonorae): 10. Breeding success in relation to nest site exposition

Summary Breeding success of the Eleonora's Falcon was studied in an Aegean island colony. In nests near cliff tops with an unobstructed view of the surroundings, a significantly higher breeding success (1.8 pulli/nest) was obtained than in other nests (1.3 pulli/nest). Since all nests were chosen protected from the wind, and as the main wind comes from NW, most nests were situated on southern slopes and are thus potentially exposed to the sun. Within a falcon territory of typically 20 m diameter in size there was not always a lime stone crevice with complete shade for the eggs. At an air temperature of 40 °C and a soil temperature of up to 60 °C, excessive sunning of an unprotected egg can be lethal for the falcon embryo. Breeding success in sun exposed nests was significantly lower (0.8–1.3 pulli/nest) than in sheltered nests (1.75 pulli/nest). In addition to a normal infertility of 10 %, about 8 % of all eggs laid were lost due to sun irradiation.

     

Childhood environmental harshness predicts coordinated health and reproductive strategies: A cross-sectional study of a nationally representative sample from France

There is considerable variation in health and reproductive behaviours within and across human populations. Drawing on principles from Life History Theory, psychosocial acceleration theory predicts that individuals developing in harsh environments decrease their level of somatic investment and accelerate their reproductive schedule. Although there is consistent empirical support for this general prediction, most studies have focused on a few isolated life history traits and few have investigated the way in which individuals apply life strategies across reproductive and somatic domains to produce coordinated behavioural responses to their environment. In our study, we thus investigate the impact of childhood environmental harshness on both reproductive strategies and somatic investment by applying structural equation modeling (SEM) to cross-sectional survey data obtained in a representative sample of the French population (n = 1015, age: 19–87 years old, both genders). This data allowed us to demonstrate that (i) inter-individual variation in somatic investment (e.g. effort in looking after health) and reproductive timing (e.g. age at first birth) can be captured by a latent fast-slow continuum, and (ii) faster strategies along this continuum are predicted by higher childhood harshness. Overall, our results support the existence of a fast-slow continuum and highlight the relevance of the life history approach for understanding variations in reproductive and health related behaviours.     

Homotypic and Heterotypic Adhesion Induced by Odorant Receptors and the β2-Adrenergic Receptor

In the mouse olfactory system regulated expression of a large family of G Protein-Coupled Receptors (GPCRs), the Odorant Receptors (ORs), provides each sensory neuron with a single OR identity. In the wiring of the olfactory sensory neuron projections, a complex axon sorting process ensures the segregation of >1,000 subpopulations of axons of the same OR identity into homogeneously innervated glomeruli. ORs are critical determinants in axon sorting, and their presence on olfactory axons raises the intriguing possibility that they may participate in axonal wiring through direct or indirect trans-interactions mediating adhesion or repulsion between axons. In the present work, we used a biophysical assay to test the capacity of ORs to induce adhesion of cell doublets overexpressing these receptors. We also tested the β2 Adrenergic Receptor, a non-OR GPCR known to recapitulate the functions of ORs in olfactory axon sorting. We report here the first evidence for homo- and heterotypic adhesion between cells overexpressing the ORs MOR256-17 or M71, supporting the hypothesis that ORs may contribute to olfactory axon sorting by mediating differential adhesion between axons.     

Atypical and distinct microtubule radial symmetries in the centriole and the axoneme of Lecudina tuzetae

The centriole is a minute cylindrical organelle present in a wide range of eukaryotic species. Most centrioles have a signature ninefold radial symmetry of microtubules that is imparted to the axonemes of the cilia and flagella they template, with nine centriolar microtubule doublets growing into nine axonemal microtubule doublets. There are exceptions to the ninefold symmetrical arrangement of axonemal microtubules in some species, with lower or higher fold symmetries. In the few cases where this has been examined, such alterations in axonemal symmetries are grounded in similar alterations in centriolar symmetries. Here, we examine the question of microtubule number continuity between centriole and axoneme in flagellated gametes of the gregarine Lecudina tuzetae, which have been reported to exhibit a sixfold radial symmetry of axonemal microtubules. We used time-lapse differential interference microscopy to identify the stage at which flagellated gametes are present. Thereafter, using electron microscopy and ultrastructure-expansion microscopy coupled to stimulated emission depletion superresolution imaging, we uncover that a six- or fivefold radial symmetry in the axoneme is accompanied by an eightfold radial symmetry in the centriole. We conclude that the transition between centriolar and axonemal microtubules can be characterized by unexpected plasticity.     

The spatio-temporal dynamics of PKA activity profile during mitosis and its correlation to chromosome segregation

The cyclic adenosine monophosphate dependent kinase protein (PKA) controls a variety of cellular processes including cell cycle regulation. Here, we took advantages of genetically encoded FRET-based biosensors, using an AKAR-derived biosensor to characterize PKA activity during mitosis in living HeLa cells using a single-cell approach. We measured PKA activity changes during mitosis. HeLa cells exhibit a substantial increase during mitosis, which ends with telophase. An AKAREV T>A inactive form of the biosensor and H89 inhibitor were used to ascertain for the specificity of the PKA activity measured. On a spatial point of view, high levels of activity near to chromosomal plate during metaphase and anaphase were detected. By using the PKA inhibitor H89, we assessed the role of PKA in the maintenance of a proper division phenotype. While this treatment in our hands did not impaired cell cycle progression in a drastic manner, inhibition of PKA leads to a dramatic increase in chromososme misalignement on the spindle during metaphase that could result in aneuploidies. Our study emphasizes the insights that can be gained with genetically encoded FRET-based biosensors, which enable to overcome the shortcomings of classical methologies and unveil in vivo PKA spatiotemporal profiles in HeLa cells.     

Intestinal Cell Tight Junctions Limit Invasion of Candida albicans through Active Penetration and Endocytosis in the Early Stages of the Interaction of the Fungus with the Intestinal Barrier

C. albicans is a commensal yeast of the mucous membranes in healthy humans that can also cause disseminated candidiasis, mainly originating from the digestive tract, in vulnerable patients. It is necessary to understand the cellular and molecular mechanisms of the interaction of C. albicans with enterocytes to better understand the basis of commensalism and pathogenicity of the yeast and to improve the management of disseminated candidiasis. In this study, we investigated the kinetics of tight junction (TJ) formation in parallel with the invasion of C. albicans into the Caco-2 intestinal cell line. Using invasiveness assays on Caco-2 cells displaying pharmacologically altered TJ (i.e. differentiated epithelial cells treated with EGTA or patulin), we were able to demonstrate that TJ protect enterocytes against invasion of C. albicans. Moreover, treatment with a pharmacological inhibitor of endocytosis decreased invasion of the fungus into Caco-2 cells displaying altered TJ, suggesting that facilitating access of the yeast to the basolateral side of intestinal cells promotes endocytosis of C. albicans in its hyphal form. These data were supported by SEM observations of differentiated Caco-2 cells displaying altered TJ, which highlighted membrane protrusions engulfing C. albicans hyphae. We furthermore demonstrated that Als3, a hypha-specific C. albicans invasin, facilitates internalization of the fungus by active penetration and induced endocytosis by differentiated Caco-2 cells displaying altered TJ. However, our observations failed to demonstrate binding of Als3 to E-cadherin as the trigger mechanism of endocytosis of C. albicans into differentiated Caco-2 cells displaying altered TJ.     

Recessive Mutations in COL25A1 Are a Cause of Congenital Cranial Dysinnervation Disorder

Abnormal ocular motility is a common clinical feature in congenital cranial dysinnervation disorder (CCDD). To date, eight genes related to neuronal development have been associated with different CCDD phenotypes. By using linkage analysis, candidate gene screening, and exome sequencing, we identified three mutations in collagen, type XXV, alpha 1 (COL25A1) in individuals with autosomal-recessive inheritance of CCDD ophthalmic phenotypes. These mutations affected either stability or levels of the protein. We further detected altered levels of sAPP (neuronal protein involved in axon guidance and synaptogenesis) and TUBB3 (encoded by TUBB3, which is mutated in CFEOM3) as a result of null mutations in COL25A1. Our data suggest that lack of COL25A1 might interfere with molecular pathways involved in oculomotor neuron development, leading to CCDD phenotypes.     

Treatment of Chronic Experimental Autoimmune Encephalomyelitis with Epigallocatechin-3-Gallate and Glatiramer Acetate Alters Expression of Heme-Oxygenase-1

We previously demonstrated that epigallocatechin-3-gallate (EGCG) synergizes with the immunomodulatory agent glatiramer acetate (GA) in eliciting anti-inflammatory and neuroprotective effects in the relapsing-remitting EAE model. Thus, we hypothesized that mice with chronic EAE may also benefit from this combination therapy. We first assessed how a treatment with a single dose of GA together with daily application of EGCG may modulate EAE. Although single therapies with a suboptimal dose of GA or EGCG led to disease amelioration and reduced CNS inflammation, the combination therapy had no effects. While EGCG appeared to preserve axons and myelin, the single GA dose did not improve axonal damage or demyelination. Interestingly, the neuroprotective effect of EGCG was abolished when GA was applied in combination. To elucidate how a single dose of GA may interfere with EGCG, we focused on the anti-inflammatory, iron chelating and anti-oxidant properties of EGCG. Surprisingly, we observed that while EGCG induced a downregulation of the gene expression of heme oxygenase-1 (HO-1) in affected CNS areas, the combined therapy of GA+EGCG seems to promote an increased HO-1 expression. These data suggest that upregulation of HO-1 may contribute to diminish the neuroprotective benefits of EGCG alone in this EAE model. Altogether, our data indicate that neuroprotection by EGCG in chronic EAE may involve regulation of oxidative processes, including downmodulation of HO-1. Further investigation of the re-dox balance in chronic neuroinflammation and in particular functional studies on HO-1 are warranted to understand its role in disease progression.