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Corre, M.

Publications and source records attributed to Corre, M..

2 recordsLinked to original sources

Plant Cell Wall Enzymatic Hydrolysis: Predicting Yield Dynamics from Autofluorescence and Morphological Temporal Changes

Enzymatic hydrolysis of plant cell walls into fermentable sugars is a critical step in biotechnological conversion, yet efficiency is limited by cell wall recalcitrance. Predicting conversion yields of cell wall-derived sugars during hydrolysis is challenging due to the complex underlying mechanisms and the labor-intensive nature of conventional assays. This study introduces an innovative pipeline that accurately quantifies cell wall autofluorescence intensity and morphological descriptors during enzymatic hydrolysis. The pipeline incorporates a novel adaptive drift compensation strategy which dynamically adjusts to the progression and extent of deconstruction ensuring robust analysis. Applied to time-lapse images of spruce wood enzymatic deconstruction, the pipeline revealed strong negative correlations of conversion yields during hydrolysis with both the dynamics of cell wall autofluorescence intensity and morphological descriptors. Phase-specific analysis uncovered distinct correlation patterns dependent on hydrolysis stage and sugar type. This non-destructive pipeline eliminates the need for extensive sampling and time-consuming chemical assays, establishing plant cell wall autofluorescence and morphological descriptors as accurate predictive real-time biomarkers of dynamics of sugar conversion yields. The findings provide a framework for accelerating the development of optimized biotechnological conversion processes.

biochemistry↗

Alternative splicing of the stress-sensitive regulator CIRBP sharpens the cellular response to bacterial infection

Cell autonomous responses to intracellular bacteria largely depend on gene expression reorganization. To gain isoform-level resolution into these regulations, we combined long- and short-read transcriptomic analyses of the response of intestinal epithelial cells to infection by the foodborne pathogen Listeria monocytogenes. Among the most striking isoform-based regulations, expression of the cellular stress response regulator CIRBP (cold-inducible RNA-binding protein) and of several SRSFs (serine/arginine-rich splicing factors) switched from canonical transcripts to nonsense-mediated decay-sensitive isoforms by inclusion of "poison exons". We showed that damage to host cell membranes caused by bacterial pore-forming toxins (listeriolysin O, perfringolysin, streptolysin, or aerolysin) led to the dephosphorylation of SRSF proteins via the inhibition of the kinase activity of CLK1, thereby driving CIRBP alternative splicing. CIRBP isoform usage was found to have consequences on infection, since selective repression of canonical CIRBP reduced intracellular bacterial load while that of the poison exon-containing isoform exacerbated it. Consistently, CIRBP-bound mRNAs were shifted towards stress-relevant transcripts in infected cells, with increased mRNA levels or reduced translation efficiency for some targets. Our results thus generalize the alternative splicing of CIRBP and SRSFs as a common response to biotic or abiotic stresses by extending its relevance to the context of bacterial infection.

molecular biology↗