Biology subjects

Baonza, A.

Publications and source records attributed to Baonza, A..

5 recordsLinked to original sources

bioRxiv2025

Cytoneme-mediated signalling coordinates the development of glial cells and neurons in the Drosophila eye

Effective cell communication is essential for the development and maintenance of the nervous system, where neurons and glial cells must interact closely. While cytoneme-mediated signalling is well-documented in various biological contexts, its role in coordinating neuron-glia development remains poorly understood. In this study, we investigated the function of cytonemes in neuron-glia coordination using the Drosophila eye imaginal disc as a model. This is a well-established system for examining the orchestrated development of glial and neuronal cells. Our results reveal that glial cells produce two distinct types of cytonemes based on their spatial orientation: one set extends toward nascent photoreceptors, while the other targets the morphogenetic furrow (MF). We have characterised the dynamics of glial cytonemes and demonstrated that disrupting these structures has a significant impact on glial cell migration and differentiation. This highlights the critical role of cytoneme-mediated signalling in regulating glial behaviour. Our findings also demonstrate that cytoneme function is essential for activating the Hedgehog (Hh) pathway in glial cells, with Hh ligand produced by photoreceptors. This pathway is necessary for glial differentiation, uncovering a previously unrecognised role for Hh signalling in this process. Overall, our results suggest that cytoneme-mediated Hh signalling is key to coordinating the development of both glial and neuronal populations.

developmental biology↗

bioRxiv2023

Cell proliferation and Notch signaling coordinate the formation of epithelial folds in the Drosophila leg

The formation of complex three-dimensional organs during development requires the precise coordination between patterning networks and mechanical forces. In particular, tissue folding is a crucial process that relies on a combination of local and tissue-wide mechanical forces. Here, we investigate the contribution of cell proliferation to epithelial morphogenesis using the Drosophila leg tarsal folds as a model. We reveal that tissue-wide compression forces generated by cell proliferation, in coordination with Notch signaling pathway, are essential for the formation of epithelial folds in precise locations along the proximo-distal axis of the leg. As cell numbers increase, compressive stresses arise, promoting the buckling of the epithelium and reinforcing the apical constriction of invaginating cells. Additionally, the Notch target dysfusion (dysf) plays a key function specifying the location of the folds, through the apical accumulation of F-actin and the apico-basal shortening of invaginating cells. These findings provide new insights into the intricate mechanisms involved in epithelial morphogenesis, highlighting the critical role of tissue-wide forces in shaping a three-dimensional organ in a reproducible manner.

developmental biology↗

bioRxiv2023

Temporal Dynamics of Apoptosis-Induced Proliferation in Pupal Wing Development: Implications for Regenerative Ability

The ability of animals to regenerate damaged tissue is a complex process that involves various cellular mechanisms. As animals age, they lose their regenerative abilities, making it essential to understand the underlying mechanisms that limit regenerative ability during aging. Drosophila melanogaster wing imaginal discs are epithelial structures that can regenerate after tissue injury. While significant research has focused on investigating regenerative responses during larval stages, particularly regarding the regulation and function of the JNK pathway, our comprehension of the regenerative potential of pupal wings and the underlying mechanisms contributing to the decline of regenerative responses remains limited. This study explores the temporal dynamics during pupal development of the proliferative response triggered by the induction of cell death, a typical regenerative response. Our results indicate that the apoptosis-induced proliferation response can be initiated as late as 30 hours after pupa formation (APF), when in normal circumstances cell proliferation ceases at around 20 hours APF. Furthermore, our data revealed that after 35 hours APF, cell death alone fails to induce further proliferation. Interestingly, the failure of reinitiating the cell cycle beyond this time point is not attributed to an incapacity to activate the JNK pathway. Instead, one of the constraining factors in the apoptotic-induced proliferation process during pupal development seems to be the activity level of ecdysone-responsive genes. Author SummaryAnimals have the remarkable ability to regenerate damaged tissues, but this regenerative potential diminishes with age. Understanding the mechanisms underlying age-related decline in regenerative abilities is crucial. Drosophila melanogaster wing imaginal discs provide a valuable model for studying tissue regeneration. While significant research has focused on regenerative responses during larval stages, our understanding of the regenerative potential and mechanisms in pupal wings remains limited. In this study, we investigate the temporal dynamics of the proliferative response triggered by cell death during late during the development, in pupal development. Our findings reveal that the apoptosis-induced proliferation response can occur during pupal development, even after normal cell proliferation has ceased. However, at late stages of pupal development this response does not occur. We have found that, the inability to reinitiate the cell cycle beyond this time point is influenced by the activity of the hormone ecdysone and its-responsive genes. These findings shed light on the dynamic processes involved in tissue regeneration during pupal development. This study expands our understanding of the complex interplay between cell death, proliferation, and gene activity during tissue regeneration, providing valuable insights for future research in regenerative biology.

developmental biology↗

bioRxiv2021

p53 pro-apoptotic activity is regulated by the G2/M promoting factor Cdk1 in response to DNA damage

Exposure to genotoxic stress promotes cell-cycle arrest and DNA repair or apoptosis. These "life" or "death" cell fate decisions often rely on the activity of the tumor suppressor gene p53. Therefore, how p53 activity is precisely regulated is essential to maintain tissue homeostasis and to prevent cancer development. Here we demonstrate that Drosophila p53 pro-apoptotic activity is regulated by the G2/M kinase Cdk1. We find that cell cycle arrested or endocycle-induced cells are refractory to ionizing radiation induced apoptosis. We show that the p53 protein is not able to bind to and to activate the expression of the pro-apoptotic genes in experimentally arrested cells. Our results indicate that p53 genetically and physically interacts with Cdk1 and that p53 pro-apoptotic role is regulated by the cell cycle status of the cell. We propose a model in which cell cycle progression and p53 pro-apoptotic activity are molecularly connected to coordinate the appropriate response after DNA damage.

developmental biology↗

bioRxiv2020

Dpp and Hedgehog promote the Glial response to neuronal damage in the developing Drosophila Visual system

Damage in the nervous system induces a stereotypical response that is mediated by glial cells. Here, we use the eye disc to explore the mechanisms involved in promoting glial cell response after neural injuries. We demonstrate that eye glia cells rapidly respond to neuronal injury by increasing in number and undergoing morphological changes, which grant them phagocytic abilities. We found that this glial response is controlled by the activity of the long-range signalling pathways, decapentaplegic (dpp) and hedgehog (hh). These pathways are activated in the damaged region and their functions are necessary for inducing glial cell proliferation and migration to the eye discs. The latter of these two processes depends on the function of the JNK pathway, which is cooperatively activated by dpp and hh signalling.

neuroscience↗