Biology subjects

Grass, I.

Publications and source records attributed to Grass, I..

3 recordsLinked to original sources

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↗