Biology subjects

Malandain, G.

Publications and source records attributed to Malandain, G..

6 recordsLinked to original sources

bioRxiv2026

Taming complexity in enzymatic saccharification: A predictive hierarchical modeling framework

Lignocellulosic biomass biotechnological conversion relies on enzymatic hydrolysis of recalcitrant plant cell walls, which limits conversion efficiency and economic viability and renders sugar-release dynamics difficult to predict. Mathematical modeling has therefore emerged as a key approach for elucidating the mechanisms governing enzymatic hydrolysis and predicting its dynamics. Here, a hierarchical adsorption-inhibition framework is developed, beginning with a detailed Dynamic Adsorption-Inhibition Model (DyAIM). This model is then simplified into a Reduced Adsorption-Inhibition Model (ReAIM) by pruning weak adsorption and inhibition interactions. Finally, ReAIM is further simplified into an Effective Activity Model (EAM), in which nonproductive enzyme adsorption onto lignin is represented by a reduction in effective enzymatic activity. Plant cell wall composition is expressed as four structural polymers coupled to six soluble products, with inhibition by mono- and oligosaccharides acting on five functional enzyme pools. Using glucose, xylose and mannose release at two enzyme loadings, the model hierarchy is validated in reproducing saccharification dynamics and in delivering a quantitative product-enzyme inhibition network consistent with literature trends. The model framework was further validated by prediction of saccharification dynamics at an unseen enzyme loading, demonstrating robust performance beyond the calibration conditions. Sensitivity analysis further supported the progressive simplifications adopted in ReAIM and EAM. Maintaining predictive performance across increasing levels of simplification indicates that the hierarchy effectively distinguishes essential mechanisms from dispensable complexity, enabling rational model selection.

biochemistry↗

bioRxiv2025

Automated cell naming reveals reproducible and variable features of ascidian embryogenesis

Ascidians develop with highly reproducible cell lineages, making them ideal models for quantitative comparisons of morphogenesis between individuals and species. Yet, identifying corresponding cells across embryos has so far relied on slow, manual annotation following the Conklin nomenclature, which limits scalability and consistency. We present an automated framework that assigns cell identities in three-dimensional time-lapse reconstructions of ascidian embryos by transferring names from a reference set of manually curated embryos. The process operates in two steps: an initiation phase, which globally aligns early embryos to establish initial correspondences, and a propagation phase, which propagates names through time and cell divisions by comparing the pattern of contacts each cell forms with its neighbors. Applied to eight wild-type Phallusia mammillata and one Ascidiella aspersa embryo, the pipeline assigns consistent names up to stages containing about 700 cells, corrects inconsistencies in earlier datasets, and extends Conklins rules to internal tissues beyond gastrulation. Using this unified reference, we quantify natural variability in division timing and orientation, confirming the global robustness and revealing local variability of ascidian morphogenesis. The same framework also demonstrates its use to quantitatively phenotype experimentally perturbed embryos, such as those with inhibited ERK signaling. This work provides both a validated collection of coherently named ascidian embryos and open-source tools for automated cell identification and phenotypic comparison, establishing a foundation for systematic, quantitative, and evolutionary analyses of animal development.

developmental biology↗

bioRxiv2024

A Distinct Autofluorescence Distribution Pattern Marks Enzymatic Deconstruction of Plant Cell Wall

Achieving an economically viable transformation of plant cell walls into bioproducts requires a comprehensive understanding of enzymatic deconstruction. Microscale quantitative analysis offers a relevant approach to enhance our understanding of cell wall hydrolysis, but becomes challenging under high deconstruction conditions. This study comprehensively addresses the challenges of quantifying the impact of extensive enzymatic deconstruction on plant cell wall at microscale. Investigation of highly deconstructed spruce wood provided spatial profiles of cell walls during hydrolysis with a remarkable precision. A distinct cell wall autofluorescence distribution pattern marking enzymatic hydrolysis along with an asynchronous impact of hydrolysis on cell wall structure, with cell wall volume reduction preceding cell wall accessible surface area decrease, were revealed. This study provides novel insights into enzymatic deconstruction of cell wall at under-investigated cell scale, and a robust computational pipeline applicable to diverse biomass species and pretreatment types for assessing hydrolysis impact and efficiency.

biochemistry↗

bioRxiv2021

Embryo-scale epithelial buckling forms a propagating furrow that initiates gastrulation

Cell apical constriction driven by actomyosin contraction forces is a conserved mechanism during tissue folding in embryo development. While much effort has been made to better understand the molecular mechanisms responsible for apical constriction, it is still not clear if apical actomyosin contraction forces are necessary or sufficient per se to drive tissue folding. To tackle this question, we use the Drosophila embryo model system that forms a furrow on the ventral side, initiating mesoderm internalization. Past computational models support the idea that cell apical contraction forces may not be sufficient and that active or passive cell apico-basal forces may be necessary to drive cell wedging and tissue furrowing. By using 3D computational modelling and in toto embryo image analysis and manipulation, we now challenge this idea and show that embryo-scale force balance of the tissue surface, rather than cell-autonomous shape changes, is necessary and sufficient to drive a buckling of the epithelial surface forming a furrow which propagates and initiates embryo gastrulation.

developmental biology↗

bioRxiv2020

A multiscale analysis of early flower development in Arabidopsis provides an integrated view of molecular regulation and growth control

The link between gene regulation and morphogenesis of multicellular organisms is a fundamental problem in biology. We address this question in the floral meristem of Arabidopsis, which generates new tissues and organs through complex changes in growth patterns. Starting from high-resolution time-lapse images, we generated a comprehensive 4-D atlas of early flower development including cell lineage, cellular growth rates and the expression patterns of 28 regulatory genes. This information was introduced in MorphoNet, a web-based open-access platform. The application of mechanistic computational models indicated that the molecular network based on the literature only explained a minority of the expression patterns. This was substantially improved by adding single regulatory hypotheses for individual genes. We next used the integrated information to correlate growth with the combinatorial expression of multiple genes. This led us to propose a set of hypotheses for the action of individual genes in morphogenesis, not visible by simply correlating gene expression and growth. This identified the central transcription factor LEAFY as a potential regulator of heterogeneous growth, which was supported by quantifying growth patterns in a leafy mutant. By providing an integrated, multiscale view of flower development, this atlas should represent a fundamental step towards mechanistic multiscale-scale models of flower development.

developmental biology↗

bioRxiv2017

Contact-dependent cell communications drive morphological invariance during ascidian embryogenesis

Canalization of developmental processes ensures the reproducibility and robustness of embryogenesis within each species. In its extreme form, found in ascidians, early embryonic cell lineages are invariant between embryos within and between species, despite rapid genomic divergence. To resolve this paradox, we used live light-sheet imaging to quantify individual cell behaviors in digitalized embryos and explore the forces that canalize their development. This quantitative approach revealed that individual cell geometries and cell contacts are strongly constrained, and that these constraints are tightly linked to the control of fate specification by local cell inductions. While in vertebrates ligand concentration usually controls cell inductions, we found that this role is fulfilled in ascidians by the area of contacts between signaling and responding cells. We propose that the duality between geometric and genetic control of inductions contributes to the counterintuitive inverse correlation between geometric and genetic variability during embryogenesis.

developmental biology↗