Comparison of spatially implicit and explicit approaches to model plant infestation by insect pests

Spatial heterogeneities have been explored in many different ways in population dynamic models. We investigate here the way in which space should be considered in the dynamics of an aphid–parasitoid system in a melon greenhouse, in order to plan a biological control program at a wide scale. By comparing a non-spatial model with a spatially explicit model (a lattice one), we show a strong difference between predictions and we thus confirm that it is essential to take space into account in such closed and structured environments when describing the spatial heterogeneities observed in the field. The way in which space should be considered in such system is tested by comparing the spatially explicit model with a new implicit approach, which describes the level of plant infestation by a continuous variable corresponding to the number of plants with a given density of pests at a given time. When the explicit model needs as many equations as plants in the greenhouse, our novel approach has only a partial differential equation. We infer from the comparisons between the two spatial models that the predicted host–parasitoid dynamics are similar under most conditions. Some differences occur when local dispersal (considered only in the explicit model) is high and it can have a strong impact on population dynamics but does not change the conclusions for crop protection. We conclude that the new spatially implicit model thus generate relevant predictions with a more synthetic formalism than the common plant-by-plant model and it will thus be more adapted to test biological control strategies at a higher scale than the greenhouse.     

Loss of alpha6 integrins in keratinocytes leads to an increase in TGFbeta and AP1 signaling and in expression of differentiation genes

Mice lacking the alpha6 integrin chain die at birth with severe skin blistering. To further study the function of alpha6 integrin in skin, we generated conditionally immortalized cell lines from the epidermis of wild-type and alpha6 deficient mouse embryos. Mutant cells presented a decreased adhesion on laminin 5, the major component of the basement membrane in the skin, and on laminins 10/11 and 2. A DNA array analysis revealed alterations in the expression of extracellular matrix (ECM) components including laminin 5, cytoskeletal elements, but also membrane receptors like the hemidesmosomal components integrin beta4 and collagen XVII, or growth factors and signaling molecules of the TGFbeta, EGF, and Wnt pathways. Finally, an increase of several epidermal differentiation markers was observed in cells and tissue at the protein level. Further examination of the mutant tissue revealed alterations in the filaggrin signal. These differences may be linked to an upregulation of the TGFbeta and the Jun/Fos pathways in mutant keratinocytes. These results are in favor of a role for integrin alpha6beta4 in the maintenance of basal keratinocyte properties and epidermal homeostasis.     

Molecular evolution of the Rab-escort-protein/guanine-nucleotide-dissociation-inhibitor superfamily

Prenylation of Rab GTPases regulating vesicle traffic by Rab geranylgeranyltransferase (RabGGTase) requires a complex formed by the association of newly synthesized Rab proteins with Rab-escort-protein (REP), the choroideremia-gene-product that is mutated in disease, leading to loss of vision. After delivery to the membrane by the REP-Rab complex, subsequent recycling to the cytosol requires the REP-related guanine-nucleotide-dissociation-inhibitor (GDI). Although REP and GDI share common Rab-binding properties, GDI cannot assist in Rab prenylation and REP cannot retrieve Rab proteins from the membranes. We have now isolated REP mutant proteins that are able to partially function as both REP and GDI. These results provide molecular insight into the functional and evolutionary organization of the REP/GDI superfamily.     

CK2‐regulated schwannomin‐interacting protein IQCJ‐SCHIP‐1 association with AnkG contributes to the maintenance of the axon initial segment

The axon initial segment (AIS) plays a central role in electrogenesis and in the maintenance of neuronal polarity. Its molecular organization is dependent on the scaffolding protein ankyrin (Ank) G and is regulated by kinases. For example, the phosphorylation of voltage‐gated sodium channels by the protein kinase CK2 regulates their interaction with AnkG and, consequently, their accumulation at the AIS. We previously showed that IQ motif containing J‐Schwannomin‐Interacting Protein 1 (IQCJ‐SCHIP‐1), an isoform of the SCHIP‐1, accumulated at the AIS in vivo. Here, we analyzed the molecular mechanisms involved in IQCJ‐SCHIP‐1‐specific axonal location. We showed that IQCJ‐SCHIP‐1 accumulation in the AIS of cultured hippocampal neurons depended on AnkG expression. Pull‐down assays and surface plasmon resonance analysis demonstrated that AnkG binds to CK2‐phosphorylated IQCJ‐SCHIP‐1 but not to the non‐phosphorylated protein. Surface plasmon resonance approaches using IQCJ‐SCHIP‐1, SCHIP‐1a, another SCHIP‐1 isoform, and their C‐terminus tail mutants revealed that a segment including multiple CK2‐phosphorylatable sites was directly involved in the interaction with AnkG. Pharmacological inhibition of CK2 diminished both IQCJ‐SCHIP‐1 and AnkG accumulation in the AIS. Silencing SCHIP‐1 expression reduced AnkG cluster at the AIS. Finally, over‐expression of IQCJ‐SCHIP‐1 decreased AnkG concentration at the AIS, whereas a mutant deleted of the CK2‐regulated AnkG interaction site did not. Our study reveals that CK2‐regulated IQJC‐SCHIP‐1 association with AnkG contributes to AIS maintenance.

     

Control of vertebrate multiciliogenesis by miR-449 through direct repression of the Delta/Notch pathway

Multiciliated cells lining the surface of some vertebrate epithelia are essential for various physiological processes, such as airway cleansing. However, the mechanisms governing motile cilia biosynthesis remain poorly elucidated. We identify miR-449 microRNAs as evolutionarily conserved key regulators of vertebrate multiciliogenesis. In human airway epithelium and Xenopus laevis embryonic epidermis, miR-449 microRNAs strongly accumulated in multiciliated cells. In both models, we show that miR-449 microRNAs promote centriole multiplication and multiciliogenesis by directly repressing the Delta/Notch pathway. We established Notch1 and its ligand Delta-like 1(DLL1) as miR-449 bona fide targets. Human DLL1 and NOTCH1 protein levels were lower in multiciliated cells than in surrounding cells, decreased after miR-449 overexpression and increased after miR-449 inhibition. In frog, miR-449 silencing led to increased Dll1 expression. Consistently, overexpression of Dll1 mRNA lacking miR-449 target sites repressed multiciliogenesis, whereas both Dll1 and Notch1 knockdown rescued multiciliogenesis in miR-449-deficient cells. Antisense-mediated protection of miR-449-binding sites of endogenous human Notch1 or frog Dll1 strongly repressed multiciliogenesis. Our results unravel a conserved mechanism whereby Notch signalling must undergo miR-449-mediated inhibition to permit differentiation of ciliated cell progenitors.     

Group Release of Sanctuary Chimpanzees (<Emphasis Type="Italic">Pan troglodytes</Emphasis>) in the Haut Niger National Park,Guinea, West Africa: Ranging Patterns and Lessons So Far

The release of wild or captive-bred mammals within their historical ranges typically aims to reestablish populations in areas where they have become extinct or extirpated, to reinforce natural populations, or to resolve human–wildlife conflicts. Such programs, which also typically in parallel help foster the protection of the release site, concern a wide range of endangered mammalian species, including our closest living relatives: chimpanzees. In June 2008, the Chimpanzee Conservation Center (CCC), which is located in the High Niger National Park (HNNP) in Guinea, released a group of 12 chimpanzees (Pan troglodytes verus) comprised of 6 females and 6 males (8–20 yr old). The selected release site lies 32 km from the sanctuary in the Mafou, a core area of HNNP where wild chimpanzees are also known to occur. The purpose of this release was therefore to reinforce the natural chimpanzee population within the Mafou core area and to promote the protection of the HNNP. Nearly 2 yr postrelease, 9 chimpanzees still remain free-living. Two thirds of the release chimpanzees were equipped with VHF-GPS store-on-board tracking collars. We used data from retrieved collars to explore the release chimpanzees’ habitat use, individual day range, and core area use (50% and 80%) during the first year of the release. Males traveled significantly further than females. Although minimum day range did not differ between the sexes or vary seasonally, some release males were active for longer during the day than the females. Males also ranged over larger areas and used a wider network of core areas than the females. Habitat use was similar to that recorded in wild chimpanzees in the HNNP. As of September 2010, 2 males and 3 females form a group at the release site. Two of these females gave birth to healthy offspring respectively 16 and 20 mo postrelease. Another female successfully immigrated into a wild chimpanzee community. We suggest that the success of this chimpanzee release can be attributed to the CCC’s lengthy rehabilitation process and the savanna-mosaic habitat of the HNNP. This release demonstrates that under special socioecological circumstances, the release of wild-born adult chimpanzees of both sexes is a viable strategy, which can also function as an effective conservation tool.