Biology subjects

Rhiner, C.

Publications and source records attributed to Rhiner, C..

6 recordsLinked to original sources

bioRxiv2026

Longitudinal analysis of visuomotor orientation after optic lobe lesions reveals brain plasticity in Drosophila

Acute brain injury disrupts neuro-glial networks leading to impaired brain function. Although injury induces diverse forms of plasticity, their contributions to brain injury outcome remain poorly understood. We previously showed that targeted stab lesions to the optic lobe (OL) of the adult fly brain induce proliferation of glial and neural progenitor cells. Here, we examined the effect of OL lesions on distinct features of fly behavior, which revealed a specific drop in visual stripe fixation performance acutely after injury, whereas locomotor behavior remained mostly unaffected. Using longitudinal studies of injured individuals, we found that flies significantly regain stripe fixation capacity and idiosyncratic traits one week post injury, suggesting a role for plasticity mechanisms. When the proliferation of adult neural progenitor cells is specifically blocked prior to injury, individuals showed no significant improvements of visual orientation during the identified plasticity window suggesting that progenitor activation may support recovery of stripe approach behavior. Hence the individual tracking of orientation behavior emerges as a suitable quantitative framework for studying functional recovery and interindividual variability in the adult Drosophila brain following brain injury.

neuroscience↗

bioRxiv2026

A whole-genome screen identifies a bilateral Flower-Grindelwald/TNFR-Veli/LIN-7 communication module in cell competition

Viable yet suboptimal ("loser") cells can be recognized and selectively eliminated when in the presence of neighboring fitter ("winner") cells through cell competition, thereby promoting optimal tissue fitness and homeostasis. One mechanism through which cells compare their relative fitness levels relies on isoforms of the conserved transmembrane protein Flower (Fwe). Despite the role of Fwe-dependent cell selection in several pathophysiological processes, little is known about downstream components of this pathway. In this study, we develop a versatile clonal interaction assay in Drosophila, the Easy Win Assay. By overexpressing human FWE1 Lose isoform to trigger cell competition, we perform an unbiased whole-genome RNAi screen and identify new pathway modulators. We show that the receptor Grindelwald/TNFR is necessary in either winner or loser cells to drive Eiger/TNF--independent elimination of losers, whereas the scaffolding protein Veli/LIN-7 is simultaneously required in both cell populations. We further demonstrate that Fwe, Grindelwald and Veli redistribute to establish a previously undescribed bilateral communication module at winner-loser interfaces, promoting intercellular communication and elimination of loser cells. These findings show that distinct cell elimination pathways converge on a common execution module while remaining independently regulated upstream, enabling flexible recognition and elimination of diverse damaged or dangerous cells.

cell biology↗

bioRxiv2026

A shared extracellular plasticity program drives brain repair and tumor progression

Injury induces complex multicellular repair responses that restore tissue integrity and replenish lost cells. In the brain, regeneration is limited and depends on the proliferation of neural and glial progenitors. But how these cells remodel the microenvironment to support repair remains poorly understood. Here, we profile dividing cells in the injured fruit fly brain revealing signatures of neural stem cell activation and ECM remodeling. We find that rapid activation of a Heparan Sulfate-binding factor (Hpsl) and changes in glypicans condition the extracellular space for proliferation. Hpsl promotes signalling of scarce Dpp/BMP ligands in brain cells with latent proliferative capacity and regulates organismal resilience to brain injury. We further show that malignant cells in fly and mouse brains promote similar HS-interactions to support tumor progression. Together, our findings identify extracellular proteoglycan remodeling as a key regulator of brain repair and uncover a common plasticity program engaged by brain damage and tumorigenesis.

cell biology↗

bioRxiv2025

Hbs and Rst adhesion molecules provide a regional code that regulates cell elimination during epithelial remodelling

Cell-cell interactions and mechanical forces are fundamental in shaping epithelial tissue architecture. For example, tissue compression promotes cell elimination by downregulating compaction-sensitive EGFR/ERK signalling. However, a subgroup of cells that are eliminated do not show EGFR/ERK downregulation, suggesting the involvement of additional mechanisms. Here, we conducted a multi-step RNAi screen in the Drosophila notum and identified 47 diverse regulators of epithelial remodelling. Among them, we focused on two membrane proteins, Hibris (Hbs) and Roughest (Rst), which mediate heterophilic cell adhesion. We show that Hbs and Rst exhibit region-specific expression patterns in the developing notum, showing elevated protein levels in zones of cell survival and reduced expression in regions undergoing cell pruning. Uniform knock-down of hbs and rst or homogenous overexpression of hbs, disrupts normal cell elimination during morphogenesis and results in adult tissue malformations. Remarkably, local suppression of Hbs and Rst in Hbshigh /Rsthigh territories triggers ectopic cell elimination, indicating that a surface code defined by Hbs/Rst can instruct cell removal. We further demonstrate that Hbs, but not Rst, is regulated by compaction-sensitive EGFR signalling, positioning Hbs as a potential integrator of mechanical cues and cell property signals, possibly via its interaction with Rst. These findings uncover a novel adhesive code that shapes the thorax midline and potentially other organs.

cell biology↗

bioRxiv2019

Blood cells of adult Drosophila do not expand, but control survival after bacterial infection by induction of Drosocin around their reservoir at the respiratory epithelia

Drosophila melanogaster has been an excellent model for innate immunity, but the role and regulation of adult blood cells and organismal immunity have remained incompletely understood. Here we address these questions in a comprehensive investigation of the blood cell system in adult Drosophila. As a central finding, we reveal the largest reservoir of blood cells (hemocytes) at the respiratory epithelia (tracheal air sacs) and fat body of the thorax and head. We show that most hemocytes of adult Drosophila are phagocytic macrophages (plasmatocytes), derived by more than 60% from the embryonic lineage that parallels vertebrate tissue macrophages. Surprisingly, in contrast to hemocytes at the larval stage, we find no capacity of the adult blood cell system to expand. Instead, we demonstrate its central role in relaying an innate immune response to tissues surrounding the blood cell reservoir: Hemocytes, through Imd signaling and the Jak/Stat pathway ligand Upd3, act as sentinels of bacterial infection that induce expression of the antimicrobial peptide gene Drosocin in the respiratory epithelia and colocalizing domains of the fat body. We demonstrate that endogenous Drosocin expression in these tissues promotes animal survival after bacterial infection. Our work identifies the first molecular step in a new relay of organismal immunity, establishing adult Drosophila as model to dissect mechanisms of inter-organ immunity.

immunology↗

bioRxiv2018

Culling less fit neurons protects against amyloid-β induced brain damage and cognitive and motor decline

Alzheimers disease (AD) is the most common form of dementia, impairing cognitive and motor functions. One of the pathological hallmarks of AD is neuronal loss, which is not reflected in mouse models of AD. Therefore, the role of neuronal death is still uncertain. Here, we used a Drosophila AD model expressing a secreted form of human amyloid-{beta}42 peptide and show that it recapitulates key aspects of AD pathology, including neuronal death and impaired long-term memory. We found that neuronal apoptosis is mediated by cell fitness-driven neuronal culling, which selectively eliminates impaired neurons from brain circuits. We show that removal of less fit neurons delays amyloid-{beta}42-induced brain damage and protects against cognitive and motor decline, suggesting that - contrary to common knowledge - neuronal death may have a beneficial effect in AD.

developmental biology↗