Biology subjects

Grass, I.

Publications and source records attributed to Grass, I..

6 recordsLinked to original sources

bioRxiv2024

PDK-1/S6K and mTORC1 bypass systemic growth restrictions to promote regeneration

Inflammation triggers systemic signals that induce growth restrictions in distant organs, a process well characterized in tumor cachexia. While mechanisms allowing tumors to circumvent these systemic growth restrictions have been established, the physiological processes that overcome inflammation-induced growth restrictions during regeneration remain largely unexplored. In our study, we use a model of tissue inflammation and regeneration in developing Drosophila imaginal discs to dissect key metabolic and signaling adaptations that, in physiological settings, both induce and overcome systemic growth restrictions. We find that expression of eiger, the Drosophila TNF- homolog, induces systemic insulin restriction, as evidenced by reduced expression of dILP2 and dILP5, as well as elevated nuclear dFOXO, and reduced protein translation and proliferation in peripheral tissues. Proliferating cells overcome systemic insulin restriction by upregulating Pdk1, which is both necessary and sufficient to promote phosphorylation of ribosomal protein S6 and protein translation via an Insulin/Akt-independent mechanism. We further demonstrate that JAK/STAT signaling acts upstream to increase Pdk1 levels, delineating a novel JAK/STAT-Pdk1-S6K axis essential for regenerative proliferation. The upregulation of amino acid transporters in the proliferative domain further suggests that regenerating cells preferentially import amino acids, fueling mTORC1 activation. Similar metabolic signatures are observed in a Drosophila RasV12, scrib tumor model, suggesting that tumors may co-opt these metabolic pathways to sustain growth in an insulin-restricted environment. Our findings reveal a specialized metabolic program that integrates systemic nutrient mobilization with local metabolic reprogramming, with important implications for understanding of physiological tissue repair but also pathologies such as chronic wounds and cancer.

developmental biology↗

bioRxiv2024

The neonicotinoid acetamiprid is highly toxic to wild non-target insects

Although pesticides are seen as one of the main drivers of insect decline, there are still only few studies that assess their effects on non-target species under field conditions. Here we investigated the effects of the neonicotinoid insecticide Mospilan(R)SG (active ingredient acetamiprid) on plant bugs (Heteroptera: Miridae), a dominant group of European grassland insect communities. Abundance of three focal mirid species was reduced by up to 78% two days after field exposure at concentrations expected at field margins, with mortality varying considerably among species. Follow-up feeding assays with insecticide-treated host plants in the greenhouse and controlled dose-response assays in the laboratory confirmed the strong negative effects on non-target species. Strikingly, the neonicotinoid was nearly 10,000 times more toxic to plant bugs than to honeybees. In addition, male bugs were 20 times more sensitive than females in two of the three tested species. Thus, continuous exposure to neonicotinoids in the field may reduce the plant bug populations and promote a shift towards more insecticide-tolerant species, altering community composition. We suggest that sex-specific sensitivity should be considered in risk assessment and conclude that the real risk to non-target insects is currently greatly underestimated.

ecology↗

bioRxiv2024

Stand structure as the proximate driver of endemic biodiversity and ecosystem functions in tropical mosaic landscapes

Transformation of forests into agricultural lands threatens biodiversity and ecosystem functions globally. In the biodiversity hotspot Madagascar, key ecosystem functions along with highly endemic flora and fauna are under threat. Comprehensive studies identifying proximate drivers are lacking, with no studies accounting for endemic species richness across multiple taxa. We assess how plot-scale stand structural attributes (basal area, leaf area index, diameter diversity, and tree species richness) and landscape-scale forest cover affect biodiversity (species richness of butterflies, ants, birds, amphibians, reptiles, herbaceous plants, and multidiversity) and ecosystem functions (soil organic carbon, predation rate, acoustic diversity index, and multifunctionality) in the tropical mosaic landscape of northeastern Madagascar. Across a prevalent land-use gradient in the region, we sampled five woody land-use types: old-growth forest, forest fragment, woody fallow, forest-derived and fallow-derived vanilla agroforests. Complexly structured stands with a larger basal area and higher tree species richness promoted greater endemic multidiversity and certain ecosystem functions. Landscape-scale forest cover significantly favored, particularly, endemic bird species richness. Our models explained 70% of the variance in endemic multidiversity, 26% in multidiversity, and 43% in multifunctionality. Significant effects directions of our predictors differed between taxa but were univocally positive for endemic species richness. Our findings highlight that a simplified stand structure, resulting from land-use change, substantially reduces endemic biodiversity and ecosystem functions in this historically forested region. Conservation actions should aim at maintaining complex stand structure in forests and agroforests, while restoration interventions should focus on re-building such structures.

ecology↗

bioRxiv2023

Scale-dependent landscape-biodiversity relationships shape multi-taxa diversity in an oil palm monoculture under restoration

Enhancing biodiversity in monoculture-dominated landscapes is a pressing restoration challenge. Tree islands can enhance biodiversity locally, but the role of scale-dependent processes on local biodiversity remains unclear. Using a multi-scale approach, we explored how scale-dependent processes influence the diversity of seven taxa (woody plants, understory arthropods, birds, herbaceous plants and soil bacteria, fauna, and fungi) within 52 experimental tree islands embedded in an oil palm landscape. We show that local, metacommunity (between islands), and landscape properties shaped above- and below-ground taxa diversity, with the stronger effects on above-ground taxa. The spatial extent that best-predicted diversity ranged from 150 m for woody plants to 700 m for understory arthropods with below-ground taxa responding at large spatial extents. Our results underscore the need for multi-scale approaches to restoration. Additionally, our findings contribute to understanding the complex processes shaping multi-taxa diversity and offer insights for targeted conservation and restoration strategies.

ecology↗

bioRxiv2022

Landscape heterogeneity and soil biota are central to multi-taxa diversity for landscape restoration

How to enhance biodiversity in monoculture-dominated landscapes is a key sustainability question that requires considering the spatial organization of ecological communities (beta diversity). Here, we experimentally tested if increasing landscape heterogeneity - through tree islands - is a suitable landscape restoration strategy when aiming to enhance multi-taxa diversity. We found that multi-taxa diversity resulted from islands fostering unique species (turnover: between 0.18 - 0.73) rather than species losses and gains (nestedness: between 0.03 - 0.34), suggesting that tree islands enhance diversity at the landscape scale. Through partial correlation networks, we revealed that landscape heterogeneity is associated with multi-taxa diversity (strength = 0.84). Soil biota were also central to the overall community by connecting beta diversity patterns across taxa. Our results show that increasing landscape heterogeneity enhances multi-taxa diversity in monoculture-dominant landscapes. Furthermore, we highlight that strategies aiming to enhance multi-taxa diversity should consider that spatial distributions of above- and below-ground communities are associated.

ecology↗

bioRxiv2022

Mutual repression between JNK/AP-1 and JAK/STAT stratifies cell behaviors during tissue regeneration

Epithelial repair relies on the activation of stress signaling pathways to coordinate cellular repair behaviors. Their deregulation is implicated in chronic wound and cancer pathologies. Despite such translational importance, an understanding of how spatial patterns of signaling pathways and repair behaviors arise in damaged tissues remains elusive. Using TNF-/Eiger-mediated inflammatory damage to Drosophila imaginal discs, we uncover that JNK/AP-1 signaling cells act as paracrine organizers and initiate a mutual repression network that spatially segregates JNK/AP-1 and JAK/STAT signaling cells into distinct populations. While JNK/AP-1 signaling cells produce JAK/STAT-activating Upd ligands, these signal-sending cells suppress activation of JAK/STAT via Ptp61F. Conversely, responding cells with activated JAK/STAT suppress JNK activation via Zfh2. The resulting bistable segregation of signaling domains is associated with distinct cellular tasks and regenerative potential. While JNK/AP-1 signaling cells at the wound center act as paracrine organizers, their cell cycle is senescently arrested. Thus, compensatory proliferation occurs exclusively in JAK/STAT signaling cells at the wound periphery. This spatial stratification is essential for proper tissue repair, as co-activation of JNK/AP-1 and JAK/STAT in the same cells creates conflicting inputs on cell cycle progression, leading to excess apoptosis of senescently arrested organizer cells. Finally, we demonstrate that bistable spatial segregation of JNK/AP-1 and JAK/STAT drives senescent and proliferative behaviors in transient as well as chronic tissue damage models, and importantly, in RasV12, scrib tumors under the influence of JNK/AP-1 activity. Revealing this previously uncharacterized regulatory network between JNK/AP-1, JAK/STAT and associated cell behaviors have important implications for our conceptual understanding of tissue repair, chronic wound pathologies and tumor microenvironments, where both pathways are strongly implicated.

developmental biology↗