Density-Dependence in Space and Time: Opposite Synchronous Variations in Population Distribution and Body Condition in the Baltic Sea Sprat (Sprattus sprattus) over Three Decades

Spatio-temporal density-dependent processes are crucial regulatory factors for natural populations. However, there is a lack of studies addressing spatial density-dependence in fish growth. A previous investigation has suggested spatio-temporal density-dependence in body condition of Baltic sprat. Here, we used different techniques, such as centre of gravity, distance, and homogeneity indices, to better characterize the spatial and temporal variations in sprat density and body condition in the Baltic Proper. Our results evidenced a negative spatio-temporal co-variation between the centres of gravity of density and maximum condition. In the 1980s-early 1990s both centres were located in the middle of the Baltic Proper. From the mid 1990s the centres progressively separated in space, as the sprat population moved towards the north-eastern Baltic Proper, and the centre of maximum condition towards the south-western areas. Moreover, at low abundances, sprat density and condition were homogeneously distributed in space, whereas at high abundances both density and condition showed pronounced geographical gradients. The ecological processes potentially explaining the observed patterns were discussed in the light of the Ideal Free Distribution theory. We provide evidence that the shift in the spatial distribution of cod, the main predator of sprat, has been the main factor triggering the overall spatial changes in sprat density, and thus condition, during the past thirty years. The spatial indices shown here, synthesizing the spatio-temporal patterns of fish distribution, can support the implementation of the EU Marine Strategy Framework Directive.     

NirN Protein from Pseudomonas aeruginosa is a Novel Electron-bifurcating Dehydrogenase Catalyzing the Last Step of Heme d1 Biosynthesis

Heme d₁ plays an important role in denitrification as the essential cofactor of the cytochrome cd₁ nitrite reductase NirS. At present, the biosynthesis of heme d₁ is only partially understood. The last step of heme d₁ biosynthesis requires a so far unknown enzyme that catalyzes the introduction of a double bond into one of the propionate side chains of the tetrapyrrole yielding the corresponding acrylate side chain. In this study, we show that a Pseudomonas aeruginosa PAO1 strain lacking the NirN protein does not produce heme d₁. Instead, the NirS purified from this strain contains the heme d₁ precursor dihydro-heme d₁ lacking the acrylic double bond, as indicated by UV-visible absorption spectroscopy and resonance Raman spectroscopy. Furthermore, the dihydro-heme d₁ was extracted from purified NirS and characterized by UV-visible absorption spectroscopy and finally identified by high-resolution electrospray ionization mass spectrometry. Moreover, we show that purified NirN from P. aeruginosa binds the dihydro-heme d₁ and catalyzes the introduction of the acrylic double bond in vitro. Strikingly, NirN uses an electron bifurcation mechanism for the two-electron oxidation reaction, during which one electron ends up on its heme c cofactor and the second electron reduces the substrate/product from the ferric to the ferrous state. On the basis of our results, we propose novel roles for the proteins NirN and NirF during the biosynthesis of heme d₁.     

Baricitinib treatment resolves lower-airway macrophage inflammation and neutrophil recruitment in SARS-CoV-2-infected rhesus macaques

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Effects of asymmetry on the strength of the chelonian shell: A comparison of three species

A major focus of the field of organismal biology is to understand how morphology impacts performance. Although the functional implications of certain aspects of shape have been widely examined, the functional implications of a related parameter, symmetry, remain mostly unknown. We used finite‐element models to examine the effects of turtle shell asymmetry on shell strength across three morphologically distinct emydid species. The goals of this study were to: 1) test the hypothesis that increased asymmetry (independent of differences in shape) is associated with increased stress levels for a given load, and thus with weaker shells, 2) ascertain how asymmetry and the position of load application interact to influence shell strength, and 3) determine how interspecific differences in shape influence the effect of asymmetry. We found that increased asymmetry does produce higher stresses for both midline and non‐midline loads. Non‐midline loads produce slightly larger and more variable stresses. Species‐specific shell shape can mitigate the effects of asymmetry; stronger shapes are potentially more resistant to the negative effects of asymmetry. Our findings indicate that changes in asymmetry associated with relatively small changes in shape can have as much of an effect on stress incurred by the shell as the changes in shape themselves. J. Morphol. 274:901–908, 2013. © 2013 Wiley Periodicals, Inc.     

The crystal structure of the catalytic domain of the ser/thr kinase PknA from M. tuberculosis shows an Src‐like autoinhibited conformation

Signal transduction mediated by Ser/Thr phosphorylation in Mycobacterium tuberculosis has been intensively studied in the last years, as its genome harbors eleven genes coding for eukaryotic‐like Ser/Thr kinases. Here we describe the crystal structure and the autophosphorylation sites of the catalytic domain of PknA, one of two protein kinases essential for pathogen's survival. The structure of the ligand‐free kinase domain shows an auto‐inhibited conformation similar to that observed in human Tyr kinases of the Src‐family. These results reinforce the high conservation of structural hallmarks and regulation mechanisms between prokaryotic and eukaryotic protein kinases. Proteins 2015; 83:982–988. © 2015 Wiley Periodicals, Inc.     

Variations in type III effector repertoires,pathological phenotypes and host range of Xanthomonas citri pv. citri pathotypes

The mechanisms determining the host range of Xanthomonas are still undeciphered, despite much interest in their potential roles in the evolution and emergence of plant pathogenic bacteria. Xanthomonas citri pv. citri (Xci) is an interesting model of host specialization because of its pathogenic variants: pathotype A strains infect a wide range of Rutaceous species, whereas pathotype A*/A^W strains have a host range restricted to Mexican lime (Citrus aurantifolia) and alemow (Citrus macrophylla). Based on a collection of 55 strains representative of Xci worldwide diversity assessed by amplified fragment length polymorphism (AFLP), we investigated the distribution of type III effectors (T3Es) in relation to host range. We examined the presence of 66 T3Es from xanthomonads in Xci and identified a repertoire of 28 effectors, 26 of which were shared by all Xci strains, whereas two (xopAG and xopC1) were present only in some A*/A^W strains. We found that xopAG (=avrGf1) was present in all A^W strains, but also in three A* strains genetically distant from A^W, and that all xopAG‐containing strains induced the hypersensitive response (HR) on grapefruit and sweet orange. The analysis of xopAD and xopAG suggested horizontal transfer between X. citri pv. bilvae, another citrus pathogen, and some Xci strains. A strains were genetically less diverse, induced identical phenotypic responses and possessed indistinguishable T3E repertoires. Conversely, A*/A^W strains exhibited a wider genetic diversity in which clades correlated with geographical origin and T3E repertoire, but not with pathogenicity, according to T3E deletion experiments. Our data outline the importance of taking into account the heterogeneity of Xci A*/A^W strains when analysing the mechanisms of host specialization.     

Impact of stone removal on renal function: a review

Stone removal can improve renal function by eradicating obstruction and, in certain cases, an underlying infection. Stone-removing procedures, however, may negatively impact functional integrity. Many things may impact the latter, including the procedures used, the methods of assessing function, the time when these assessments are made, the occurrence of complications, the baseline condition of the kidney, and patient-related factors. In the majority of cases, little significant functional impairment occurs. However, there are gaps in our knowledge of this subject, including the cumulative effects of multiple procedures violating the renal parenchyma and long-term functional outcomes.     

Nodal dependent differential localisation of dishevelled-2 demarcates regions of differing cell behaviour in the visceral endoderm

The anterior visceral endoderm (AVE), a signalling centre within the simple epithelium of the visceral endoderm (VE), is required for anterior-posterior axis specification in the mouse embryo. AVE cells migrate directionally within the VE, thereby properly positioning the future anterior of the embryo and orientating the primary body axis. AVE cells consistently come to an abrupt stop at the border between the anterior epiblast and extra-embryonic ectoderm, which represents an end-point to their proximal migration. Little is known about the underlying basis for this barrier and how surrounding cells in the VE respond to or influence AVE migration. We use high-resolution 3D reconstructions of protein localisation patterns and time-lapse microscopy to show that AVE cells move by exchanging neighbours within an intact epithelium. Cell movement and mixing is restricted to the VE overlying the epiblast, characterised by the enrichment of Dishevelled-2 (Dvl2) to the lateral plasma membrane, a hallmark of Planar Cell Polarity (PCP) signalling. AVE cells halt upon reaching the adjoining region of VE overlying the extra-embryonic ectoderm, which displays reduced neighbour exchange and in which Dvl2 is excluded specifically from the plasma membrane. Though a single continuous sheet, these two regions of VE show distinct patterns of F-actin localisation, in cortical rings and an apical shroud, respectively. We genetically perturb PCP signalling and show that this disrupts the localisation pattern of Dvl2 and F-actin and the normal migration of AVE cells. In Nodal null embryos, membrane localisation of Dvl2 is reduced, while in mutants for the Nodal inhibitor Lefty1, Dvl2 is ectopically membrane localised, establishing a role for Nodal in modulating PCP signalling. These results show that the limits of AVE migration are determined by regional differences in cell behaviour and protein localisation within an otherwise apparently uniform VE. In addition to coordinating global cell movements across epithelia (such as during convergence extension), PCP signalling in interplay with TGFβ signalling can demarcate regions of differing behaviour within epithelia, thereby modulating the movement of cells within them.