Mismatches between habitat preferences and risk avoidance for birds in intensive Mediterranean farmland

Land use intensification may create habitats that organisms perceive as suitable, but where reproduction or survival is insufficient to maintain self-sustaining populations. Such conditions may qualify as ecological traps, but their existence is often hard to prove. Here, we provide a practical framework to evaluate a potential ecological trap resulting from mismatch between habitat preferences and predation risk, focusing on ground-nesting farmland birds of conservation concern. The framework is based on species-specific associations with safe or unsafe habitat types (i.e. field and landscape types with high or low nest survival), and the occurrence of risk avoidance (i.e. negative responses to predator abundances or to nest failure rates after controlling for habitat effects). Bird densities were far more influenced by field characteristics than landscape context. Corn bunting and fan-tailed warbler were associated with tall swards (safe habitats), and did not show risk avoidance. Tawny pipit and and Galerida larks were associated with short swards (unsafe habitats), with the former avoiding fields with high nest predation rates, and the later avoiding high mongoose abundances. Short-toed lark was associated with fields with short swards and low nest trampling rates. Results suggest that short-toed lark may be the most vulnerable to ecological trapping, because it nests on unsafe habitats and did not show predation risk avoidance. Our approach provides a practical first step to infer vulnerability to a potential ecological trap, though further research is needed to confirm this effect. Management actions increasing nest survival in short sward fields will likely favour grassland bird conservation in intensive Mediterranean farmland.     

Effects of inter-annual temperature variability,including ENSO and post-ENSO events,on reproductive traits in the tunicate Pyura praeputialis

Reproduction in tunicates is considered to be particularly vulnerable to changes in seawater temperature. In the present study we investigated the effects of sea surface temperature and temperature anomalies on reproductive traits of the non-native sessile tunicate Pyura praeputialis. Reproductive traits of this species were investigated over the course of 67 months, based on samples collected at two localities (eastern and western shorelines) of the Bay of Antofagasta. The study period included years with different oceanic and atmospheric conditions: a warm event, El Niño (June 1997 to July 1998); a cold event, La Niña (August 1998 to December 2000); and post-La Niña (January 2000 to December 2002). We compared two common indices (condition and gonadosomatic) and histological sections to evaluate the maximum reproduction index of this introduced species that dominates a large part of the rocky intertidal habitat in the Bay of Antofagasta. We found sexually mature individuals all year-round and a decrease in both reproductive indices matching the reduction in the sea surface temperature during the austral autumn and winter months. The results suggest that gonad development in this species is sensitive to sea surface temperature and thermal anomalies. We conclude that future thermal anomalies or projected global average sea surface warming associated with climate change might have no negative consequences on these reproductive traits of P. praeputialis. This suggests this species is ecologically resilient and that the ecosystem services that this species provides for other invertebrate and algal species will be maintained.     

Vacuole membrane protein 1 marks endoplasmic reticulum subdomains enriched in phospholipid synthesizing enzymes and is required for phosphoinositide distribution

The multispanning membrane protein vacuole membrane protein 1 (VMP1) marks and regulates endoplasmic reticulum (ER)‐domains associated with diverse ER‐organelle membrane contact sites. A proportion of these domains associate with endosomes during their maturation and remodeling. We found that these VMP1 domains are enriched in choline/ethanolamine phosphotransferase and phosphatidylinositol synthase (PIS1), 2 ER enzymes required for the synthesis of various phospholipids. Interestingly, the lack of VMP1 impairs the formation of PIS1‐enriched ER domains, suggesting a role in the distribution of phosphoinositides. In fact, depletion of VMP1 alters the distribution of PtdIns4P and proteins involved in the trafficking of PtdIns4P. Consistently, in these conditions, defects were observed in endosome trafficking and maturation as well as in Golgi morphology. We propose that VMP1 regulates the formation of ER domains enriched in lipid synthesizing enzymes. These domains might be necessary for efficient distribution of PtdIns4P and perhaps other lipid species. These findings, along with previous reports that involved VMP1 in regulating PtdIns3P during autophagy, expand the role of VMP1 in lipid trafficking and explain the pleiotropic effects observed in VMP1‐deficient mammalian cells and other model systems.      

The sequences of MinE responsible for its subcellular localization analyzed by competitive binding method in <Emphasis Type="Italic">Escherichia coli</Emphasis>

The subcellular localization of a protein is important for its proper function. Escherichia coli MinE is a small protein with clear subcellular localization, which provides a good model to study protein localization mechanism. In the present study, a series of recombinant minEs truncated in one end or in the middle regions, fused with egfp, was constructed, and these recombinant proteins could compete to function with the chromosomal MinE. Our results showed that the sequences related to the subcellular localization of MinE span several functional domains, demonstrating that MinE positioning in cells depends on multiple factors. The eGFP fusions with some truncated MinE from N-terminal resulted in different cell phenotypes and localization features, implying that these fusions can interfere chromosomal MinE’s function, similar to MinE^36–88 phenotype in the previous report. The amino acid in the region (32–48) is sensitive to change MinE conformation and influence its dimerization. Some truncated protein structure could be unstable. Thus, the MinE localization is prerequisite for its proper anti-MinCD function and some new features of MinE were demonstrated. This approach can be extended for subcellular localization research for other essential proteins.     

Cross‐talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury

Scar formation after brain injury is still poorly understood. To further elucidate such processes, here, we examine the interplay between astrocyte proliferation taking place predominantly at the vascular interface and monocyte invasion. Using genetic mouse models that decrease or increase reactive astrocyte proliferation, we demonstrate inverse effects on monocyte numbers in the injury site. Conversely, reducing monocyte invasion using CCR2^?/? mice causes a strong increase in astrocyte proliferation, demonstrating an intriguing negative cross‐regulation between these cell types at the vascular interface. CCR2^?/? mice show reduced scar formation with less extracellular matrix deposition, smaller lesion site and increased neuronal coverage. Surprisingly, the GFAP⁺ scar area in these mice is also significantly decreased despite increased astrocyte proliferation. Proteomic analysis at the peak of increased astrocyte proliferation reveals a decrease in extracellular matrix synthesizing enzymes in the injury sites of CCR2^?/? mice, highlighting how early key aspects of scar formation are initiated. Taken together, we provide novel insights into the cross‐regulation of juxtavascular proliferating astrocytes and invading monocytes as a crucial mechanism of scar formation upon brain injury.     

Contrasting genetic metrics and patterns among naturalized rainbow trout (Oncorhynchus mykiss) in two Patagonian lakes differentially impacted by trout aquaculture

Different pathways of propagation and dispersal of non‐native species into new environments may have contrasting demographic and genetic impacts on established populations. Repeated introductions of rainbow trout (Oncorhynchus mykiss) to Chile in South America, initially through stocking and later through aquaculture escapes, provide a unique setting to contrast these two pathways. Using a panel of single nucleotide polymorphisms, we found contrasting genetic metrics and patterns among naturalized trout in Lake Llanquihue, Chile's largest producer of salmonid smolts for nearly 50 years, and Lake Todos Los Santos (TLS), a reference lake where aquaculture has been prohibited by law. Trout from Lake Llanquihue showed higher genetic diversity, weaker genetic structure, and larger estimates for the effective number of breeders (N_b) than trout from Lake TLS. Trout from Lake TLS were divergent from Lake Llanquihue and showed marked genetic structure and a significant isolation‐by‐distance pattern consistent with secondary contact between documented and undocumented stocking events in opposite shores of the lake. Multiple factors, including differences in propagule pressure, origin of donor populations, lake geomorphology, habitat quality or quantity, and life history, may help explain contrasting genetic metrics and patterns for trout between lakes. We contend that high propagule pressure from aquaculture may not only increase genetic diversity and N_b via demographic effects and admixture, but also may impact the evolution of genetic structure and increase gene flow, consistent with findings from artificially propagated salmonid populations in their native and naturalized ranges.     

P2RY1/ALK3-Expressing Cells within the Adult Human Exocrine Pancreas Are BMP-7 Expandable and Exhibit Progenitor-like Characteristics

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Citrus tristeza virus co-opts glyceraldehyde 3-phosphate dehydrogenase for its infectious cycle by interacting with the viral-encoded protein p23

Key message

Citrus tristeza virus encodes a unique protein, p23, with multiple functional roles that include co-option of the cytoplasmic glyceraldehyde 3-phosphate dehydrogenase to facilitate the viral infectious cycle.

Abstract

The genome of citrus tristeza virus (CTV), genus Closterovirus family Closteroviridae, is a single-stranded (+) RNA potentially encoding at least 17 proteins. One (p23), an RNA-binding protein of 209 amino acids with a putative Zn-finger and some basic motifs, displays singular features: (i) it has no homologues in other closteroviruses, (ii) it accumulates mainly in the nucleolus and Cajal bodies, and in plasmodesmata, and (iii) it mediates asymmetric accumulation of CTV RNA strands, intracellular suppression of RNA silencing, induction of some CTV syndromes and enhancement of systemic infection when expressed as a transgene ectopically or in phloem-associated cells in several Citrus spp. Here, a yeast two-hybrid screening of an expression library of Nicotiana benthamiana (a symptomatic experimental host for CTV), identified a transducin/WD40 domain protein and the cytosolic glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as potential host interactors with p23. Bimolecular fluorescence complementation corroborated the p23-GAPDH interaction in planta and showed that p23 interacts with itself in the nucleolus, Cajal bodies and plasmodesmata, and with GAPDH in the cytoplasm (forming aggregates) and in plasmodesmata. The latter interaction was preserved in a p23 deletion mutant affecting the C-terminal domain, but not in two others affecting the Zn-finger and one internal basic motif. Virus-induced gene silencing of GAPDH mRNA resulted in a decrease of CTV titer as revealed by real-time RT-quantitative PCR and RNA gel-blot hybridization. Thus, like other viruses, CTV seems to co-opt GAPDH, via interaction with p23, to facilitate its infectious cycle.