Raspail, F. | bioRxiv Science

bioRxiv2026

Urbanization drives dietary specialization in insectivorous bird communities: insights from a multi-prey cafeteria experiment monitored by innovative cameras

1. Urbanization is widely associated with functional homogenization of ecological communities, including declines in insectivorous bird species and concomitant restructuring of arthropod assemblages. While these changes are often assumed to alter ecosystem functioning through trophic interactions, it remains unclear whether bird insectivory in cities can be inferred from community composition alone, or whether it also depends on which species actively forage, on natural prey availability and on the arthropod guilds exploited. 2. We hypothesized that urbanization (i) restructures both insectivorous bird communities and arthropod prey assemblages, thereby (ii) increasing divergence between trait-based potential and realized insectivory, while (iii) prey use is shaped by natural prey availability and active prey selection. 3. We used 25 plots distributed along a controlled urbanization gradient in Montreal, Canada. We combined acoustic monitoring of insectivorous bird communities, arthropod surveys, and camera-monitored cafeteria-like experiments deployed on 73 trees to quantify trait-based potential insectivory, realized insectivory through direct foraging interactions, natural prey availability and prey selection among three arthropod guilds (lepidopteran larvae, spiders and ants). 4. Urbanization reduced bird functional diversity while also decreasing the availability of high-quality prey, particularly lepidopteran larvae and spiders. Realized insectivory was consistently decoupled from community-based expectations, with actively foraging assemblages systematically less insect-specialized than predicted by broader community compositions (potential insectivory). This mismatch was non-random and only weakly related to urban and vegetation gradients. Prey use was largely independent of natural prey availability and instead reflected consistent preferences for larval prey over other guilds, with some indication that the functional composition of bird foraging assemblages further shaped which prey were exploited. 5. Our results show that realized trophic interactions emerge through successive ecological filters rather than directly from community composition: environmental conditions restructure bird communities and prey availability, subsequent foraging filters determine which species actively participate, and prey selection governs which guilds are consumed. Predicting ecosystem functioning in cities therefore requires considering not only biodiversity patterns but also the ecological processes linking community composition to realized trophic interactions.

ecology↗

bioRxiv2018

High-quality SNPs from genic regions highlight introgression patterns among European white oaks (Quercus petraea and Q. robur).

The Src homology-2 domain containing phosphatase SHP2 is a critical regulator of signal transduction, being implicated in cell growth and differentiation. Activating mutations cause developmental disorders and act as oncogenic drivers in hematologic cancers. SHP2 is activated by phosphopeptide binding to the N-SH2 domain, triggering the release of N-SH2 from the catalytic PTP domain. Based on early crystallographic data, it has been widely accepted that opening of the binding cleft of N-SH2 serves as the key "allosteric switch" driving SHP2 activation. To test the putative coupling between binding cleft opening and SHP2 activation as assumed by the "allosteric switch" model, we critically reviewed structural data of SHP2 and we used extensive molecular dynamics (MD) simulation and free energy calculations of isolated N-SH2 in solution, SHP2 in solution, and SHP2 in a crystal environment. Our results demonstrate that the binding cleft in N-SH2 is constitutively flexible and open in solution, and that a closed cleft found in certain structures is a consequence of crystal contacts. The degree of opening of the binding cleft has only a negligible effect on the free energy of SHP2 activation. Instead, SHP2 activation is greatly favored by the opening of the central {beta}- sheet of N-SH2. We conclude that opening of the N-SH2 binding cleft is not the key allosteric switch triggering SHP2 activation. Significance StatementSHP2 is a multi-domain protein, playing an important role in up-regulating cellular processes such as cell survival, proliferation, and programmed cell death. SHP2 mutations cause developmental disorders and were found in many cancer types, including neuroblastoma, breast cancer, and leukemia. In healthy cells, SHP2 mainly takes an autoinhibited, inactive form, and SHP2 is activated upon binding of phosphopeptides to the N-SH2 domain. For the past two decades, the widening of the binding cleft upon peptide binding has been considered as the key event driving SHP2 activation. Here, by analyzing crystallographic data and molecular simulations, we demonstrate that the binding cleft in N-SH2 is, instead, already open and accessible in solution, and its degree of opening does not influence SHP2 activation.

evolutionary biology↗